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'''This page contains general information about Glomerular disease. For more information on specific types, please visit the pages on [[hematuria]], [[proteinuria]], [[minimal change disease]], [[focal segmental glomerulosclerosis]], [[membranous glomerulonephritis]], [[IgA nephropathy]], [[rapidly progressive glomerulonephritis]], [[membranoproliferative glomerulonephritis]], [[Goodpasture syndrome]], [[Granulomatosis with polyangiitis]], [[Eosinophilic granulomatosis with polyangiitis]], and [[Microscopic polyangiitis]]. '''
__NOTOC__
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Glomerulonephritis_pathophysiology]]
{{CMG}}; {{AE}}{{MJ}}, {{HK}}


<div style="-webkit-user-select: none;">
'''This page contains general information about Glomerular disease.'''
__NOTOC__
<br>'''For more information on specific types, please visit the pages on:'''
{{Infobox_Disease |
:'''[[Nephritic syndrome]]'''
  Name          = {{PAGENAME}} |
:'''[[Nephrotic syndrome]]'''
  Image          = Acute GN 2.jpg|
:'''[[Fabry's disease]]'''
  Caption        = Acute Glomerulonephritis: Micro H&E high mag; an  excellent example of acute exudative glomerulonephritis. <br> <small> [http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] </small>|
:'''[[Post-streptococcal glomerulonephritis]]'''
:'''[[Lupus nephritis|Lupus nephritis]]'''
:'''[[Goodpasture syndrome|Antiglomerular basement membrane disease]]'''
:'''[[Goodpasture syndrome|(Goodpasture's syndrome)]]'''
:'''[[Cryoglobulinemia]]'''
:'''[[Henoch-Schönlein purpura]]'''
:'''[[Amyloidosis]]'''
:'''Pulmonary-renal syndromes ([[vasculitis]])'''
:'''[[Thin basement membrane disease]]'''
:'''[[Alport syndrome|Alport's Syndrome]]'''
:'''[[Goodpasture syndrome|anti-GBM Disease]]'''
:'''[[Hypertensive nephrosclerosis]]'''
:'''[[Subacute bacterial endocarditis]]'''


}}
{{Glomerular disease}}
{{CMG}}; {{AE}}{{MJ}}, {{HK}}


==Overview==
==Overview==
Glomerular disease is a condition that affects the [[glomerulus]]. It consists of different diseases with different clinical courses and treatment options. Glomerular disease can be isolated hematuria, isolated proteinuria; acute or chronic glomerulonephritis, and nephrotic or nephritic features of glomerulonephritis. The end stage of all of these diseases will be glomerulosclerosi swhich is characterized by [[fibrosis]] of the [[glomerulus]], and end-stage renal disease.
Glomerular disease is a condition that affects the [[glomerulus]]. It consists of different diseases with different clinical courses and treatment options. Glomerular disease can be isolated [[hematuria]], isolated [[proteinuria]]; [[acute]] or [[chronic]] glomerulonephritis, and [[nephrotic]] or [[Nephritic syndrome|nephritic]] features of glomerulonephritis. The end stage of all of these diseases will be [[glomerulosclerosis]] which is characterized by [[fibrosis]] of the [[glomerulus]], and [[end-stage renal disease]].
 


==Classification==
==Classification==
Glomerular diseases can be classified by their presentation as below:


=== Acute nephritic syndromes ===
=== Glomerular dieseases can be classified into several clinical and pathological syndromes as below: ===
Poststreptococcal Glomerulonephritis
{| class="wikitable"
!Syndrome
!Disease
|-
|Acute nephritic syndromes
|
* [[Poststreptococcal glomerulonephritis]]
* [[Subacute bacterial endocarditis]]
* [[Lupus nephritis]]
* [[Goodpasture syndrome|Antiglomerular basement membrane disease]]
* [[IgA nephropathy]]
* [[Vasculitis|ANCA Small-Vessel Vasculitis]]


Subacute Bacterial Endocarditis
** [[Granulomatosis with polyangiitis|Granulomatosis with Polyangiitis (Wegener's)]]
** [[Microscopic polyangiitis|Microscopic Polyangiitis]]
** [[Eosinophilic granulomatosis with polyangiitis|Churg-Strauss Syndrome]]


Lupus Nephritis
* [[Membranoproliferative glomerulonephritis|Membranoproliferative Glomerulonephritis]]
 
* Mesangioproliferative Glomerulonephritis
Antiglomerular Basement Membrane Disease
|-
 
|Nephrotic syndrome
IgA Nephropathy
|
 
* [[Minimal change disease|Minimal Change Disease]]
ANCA Small-Vessel Vasculitis
* [[Focal segmental glomerulosclerosis|Focal Segmental Glomerulosclerosis]]
 
* [[Membranous glomerulonephritis|Membranous Glomerulonephritis]]
Granulomatosis with Polyangiitis (Wegener's)
* [[Diabetic nephropathy|Diabetic Nephropathy]]
 
|-
Microscopic Polyangiitis
|Glomerular Deposition Diseases
 
|
Churg-Strauss Syndrome
* [[Light chain disease|Light Chain Deposition Disease]]
 
* [[Amyloidosis|Renal Amyloidosis]]
Membranoproliferative Glomerulonephritis
* Fibrillary-Immunotactoid Glomerulopathy
 
* [[Fabry's disease|Fabry's Disease]]
Mesangioproliferative Glomerulonephritis
|-
 
|Pulmonary-Renal Syndromes:
=== Nephrotic syndrome ===
|
Minimal Change Disease
* [[Goodpasture syndrome|Goodpasture's syndrome]]
 
* [[Granulomatosis with polyangiitis|Granulomatosis with polyangiitis (Wegener's)]]
Focal Segmental Glomerulosclerosis
* [[Microscopic polyangiitis]]
 
* [[Churg-Strauss syndrome|Churg-Strauss vasculitis]]
Membranous Glomerulonephritis
* [[Henoch-Schönlein purpura]]
 
* [[Cryoglobulinemia]]
Diabetic Nephropathy
|-
 
|Basement Membrane Syndromes
=== Glomerular Deposition Diseases ===
|
Light Chain Deposition Disease
* [[Anti-glomerular basement membrane antibody|Anti-GBM Disease]]
 
* [[Alport syndrome|Alport's Syndrome]]
Renal Amyloidosis
* [[Thin basement membrane disease|Thin Basement Membrane Disease]]
 
* [[Nail-patella syndrome|Nail-Patella Syndrome]]
Fibrillary-Immunotactoid Glomerulopathy
|-
 
|Glomerular-Vascular Syndromes
Fabry's Disease
|
 
* Atherosclerotic Nephropathy
=== Pulmonary-Renal Syndromes: ===
* [[Hypertensive nephropathy|Hypertensive nephrosclerosis]]
Goodpasture's syndrome
* [[Cholesterol emboli syndrome|Cholesterol Emboli]]
 
* [[Sickle-cell disease|Sickle Cell Disease]]
granulomatosis with polyangiitis (Wegener's)
* [[Thrombotic microangiopathies|Thrombotic Microangiopathies]]
 
* [[Antiphospholipid syndrome|Antiphospholipid Antibody Syndrome]] 
microscopic polyangiitis
|-
 
|Infectious Disease–Associated Syndromes
Churg-Strauss vasculitis
|
 
* [[Post-streptococcal glomerulonephritis|Post-Streptococcal Glomerulonephritis]]
Henoch-Schönlein purpura  
* [[Endocarditis|Subacute bacterial endocarditis]]
 
* [[Human Immunodeficiency Virus (HIV)|Human Immunodeficiency Virus]]
cryoglobulinemia
* [[Hepatitis|Hepatitis B and C]]
 
* Other Viruses
=== Basement Membrane Syndromes ===
* [[Syphilis]]
Anti-GBM Disease
* [[Leprosy]]
 
* [[Malaria]]
Alport's Syndrome
* [[Schistosomiasis]]
 
* Other Parasites
Thin Basement Membrane Disease
|}
 
Nail-Patella Syndrome
 
=== Glomerular-Vascular Syndromes ===
Atherosclerotic Nephropathy
 
Hypertensive Nephrosclerosis
 
Cholesterol Emboli
 
Sickle Cell Disease
 
Thrombotic Microangiopathies
 
Antiphospholipid Antibody Syndrome 
 
=== Infectious Disease–Associated Syndromes ===
Post-Streptococcal Glomerulonephritis
 
Subacute Bacterial Endocarditis


Human Immunodeficiency Virus
=== Also, glomerular diseases can be classified based on their clinical and urinary pattern in to below types: ===


Hepatitis B and C
==== Mild nephritc: ====
This category include mild nephritic sediment that is associated with less than half involvement of glomeruli.


Other Viruses
==== Severe nephritic: ====
More severe clinical features such as edema, heavy [[proteinuria]], hypertension, and/or [[renal failure]] may occur.


Syphilis
==== Nephrotic: ====
This syndrome is associated with heavy proteinuria and lipiduria.


Leprosy
=== Glomerular diseases also may classified by their presentation as below: ===


Malaria
====== Glomerular [[hematuria]]: ======
1- Isolated [[hematuria]]


Schistosomiasis
2- Glomerulonephritis ([[nephritic syndrome]])


Other Parasites
====== [[Proteinuria]]: ======
1-Isolated non-nephrotic [[proteinuria]] 


=== Glomerular hematuria: ===
2- [[Nephrotic syndrome]]


==== 1- Isolated hematuria ====
====== [[Rapidly progressive glomerulonephritis]] ======


==== 2- Glomerulonephritis (nephritic syndrome) ====
=== Glomerulonephritis ===
Glomerulonephritis which is inflammation of the glomeruli can be classified based on pathogenic type into three subtypes:  
Glomerulonephritis which is inflammation of the glomeruli can be classified based on pathogenic type into three subtypes:
* Immune complex glomerulonephritis: Granular deposit of immune complex.
* '''Immune complex glomerulonephritis: Granular deposit of immune complex.'''
*# Infection mediated types
*# Infection mediated types
*# Autoimmune types, eg [[SLE]]
*# Autoimmune types, eg [[SLE]]
Line 129: Line 136:
*# [[Membranous nephropathy]]
*# [[Membranous nephropathy]]


* Anti-GBM disease: Linear deposit  
* '''Anti-GBM disease: Linear deposit'''
*# [[Goodpasture syndrome]] (renal and lung involvement)
*# [[Goodpasture syndrome]] (renal and lung involvement)
*# Renal involvement alone
*# Renal involvement alone
*# Lung involvement alone
*# Lung involvement alone


* ANCA associated, small vessels vasculitis: Few or no deposit
* '''ANCA associated, small vessels vasculitis: Few or no deposit'''
*# [[Granulomatosis with polyangiitis]] ([[Granulomatosis with polyangiitis|Wegener granulomatosis]])
*# [[Granulomatosis with polyangiitis]] ([[Granulomatosis with polyangiitis|Wegener granulomatosis]])
*# [[Eosinophilic granulomatosis with polyangiitis]] ([[Churg-Strauss syndrome]])
*# [[Eosinophilic granulomatosis with polyangiitis]] ([[Churg-Strauss syndrome]])
Line 140: Line 147:


Glomerulonephritis (nephritic syndrome) also may be classified based on disease course into [[Acute nephritic syndrome|acute]] or [[chronic nephritic syndrome]]; primary vs secondary causes; or systemic vs renal limited disease. '''''For more information about nephritic syndrome classifications click [[Nephritic syndrome classification|here]].'''''
Glomerulonephritis (nephritic syndrome) also may be classified based on disease course into [[Acute nephritic syndrome|acute]] or [[chronic nephritic syndrome]]; primary vs secondary causes; or systemic vs renal limited disease. '''''For more information about nephritic syndrome classifications click [[Nephritic syndrome classification|here]].'''''
=== Proteinuria: ===
==== 1-Isolated non-nephrotic proteinuria ====
==== 2- Nephrotic syndrome ====
=== Rapidly progressive glomerulonephritis ===
==Pathophysiology==
===Microscopic Pathology===
[http://www.peir.net Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
image:Acute GN 1.jpg|Glomerulonephritis: Micro H&E med mag; an excellent example of AGN with many neutrophils
image:Acute GN 2.jpg|Acute Glomerulonephritis: Micro H&E high mag; an  excellent example of acute exudative glomerulonephritis.
</gallery>
</div>
<br>
===Glomerulonephritis Videos===
====Rapidly progressive glomerulonephritis====
{{#ev:youtube|CqSyj4cVZPE}}
====Chronic glomerulonephritis====
{{#ev:youtube|eA1vYarRAWo}}
===Images===
[http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 1.jpg|This is a low-power photomicrograph of a saggital section of end stage chronic glomerulonephritis (GN). Note the marked thinning of the cortex (arrow).
Image:Glomerulonephritis case 2.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (arrows) and glomeruli with thick basement membranes.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 3.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).
Image:Glomerulonephritis case 4.jpg|This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 5.jpg|This is an immunofluorescent photomicrograph of granular membranous immunofluorescence (immune complex disease). The antibody used for these studies was specific for IgG.
Image:Glomerulonephritis case 6.jpg|This is an electron micrograph of subepithelial granular electron dense deposits (arrows) which correspond to the granular immunofluorescence seen in the previous image.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 7.jpg|This is a photomicrograph of a glomerulus from another case with acute poststreptococcal glomerulonephritis. In this case the immune complex glomerular disease is ongoing with necrosis and accumulation of neutrophils in the glomerulus.
Image:Glomerulonephritis case 8.jpg|This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 9.jpg|This electron micrograph demonstrates scattered subepithelial dense deposits (arrows) and a polymorphonuclear leukocyte in the lumen.
Image:Glomerulonephritis case 10.jpg|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.
</gallery>
</div>
===Images:===
*[http://www.pathologyatlas.ro/Crescentic%20Glomerulonephritis.html Crescentic GN]
*[http://www.pathologyatlas.ro/Chronic%20Glomerulonephritis1.html Chronic GN]


==Differential Diagnosis==
==Differential Diagnosis==
The various types of glomerular diseases should be differentiated from each other based on associations, presence of [[pitting edema]], [[hematuria]], [[hypertension]], [[hemoptysis]], [[oliguria]], peri-orbital edema, [[hyperlipidemia]], type of [[antibodies]], [[Light microscope|light]] and [[Electron microscopy|electron microscopic]] features. The following table differentiates between various types of glumerular diseases:


{| class="wikitable"
{| class="wikitable"
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerular diseases
! rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Glomerular diseases
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Sub-entity
! colspan="2" rowspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes and associations
! colspan="9" style="background:#4479BA; color: #FFFFFF;" align="center" + |History and Symtoms
! colspan="7" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Laboratory Findings
! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
! colspan="3" style="background:#4479BA; color: #FFFFFF;" align="center" + |Pathology
|-
|-
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |ANCA
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Anti-glomerular basement membrane antibody (Anti-GBM antibody)
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immune complex formation
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
|-
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! rowspan="13" style="background:#4479BA; color: #FFFFFF;" align="center" + |Acute Nephritic Syndromes
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! colspan="2" |[[Post-streptococcal glomerulonephritis|Poststreptococcal Glomerulonephritis]]<ref name="pmid13022878">{{cite journal| author=GERMUTH FG| title=A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type. | journal=J Exp Med | year= 1953 | volume= 97 | issue= 2 | pages= 257-82 | pmid=13022878 | doi= | pmc=PMC2136196 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13022878 }}</ref><ref name="pmid5031005">{{cite journal| author=Germuth FG, Senterfit LB, Dreesman GR| title=Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system. | journal=Johns Hopkins Med J | year= 1972 | volume= 130 | issue= 6 | pages= 344-57 | pmid=5031005 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5031005 }}</ref><ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 | volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }}</ref>
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia (pre-dominantly microscopic)
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemoptysis
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Peri-orbital edema
|-
| rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Acute Nephritic Syndromes
![[Minimal change disease]]
|
|
* [[Idiopathic]]
* [[Streptococcal infections|Streptococcal]] [[skin]] [[infections]]
* [[Protein]] [[Protein tyrosine phosphatase|tyrosine phosphatase]] receptor type O (glomerular epithelial protein 1- GLEPP1)
* [[Streptococcus|Streptococcal]] [[pharyngitis]]
* 2-3 weeks after [[infection]]
|
|
* Young children
* [[Fever]]
* Recent [[infection]] and [[immunization]]
* [[Fatigue]]
* [[Atopy]]
* Skin [[rash]]
* [[Hodgkin's lymphoma|Hodgkin lymphoma]]
|<nowiki>+/-</nowiki>
* [[Thrombosis]] (due to [[Urinary system|urinary]] loss of [[Antithrombin III|antithrombin-III]])
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
|
+
* [[Anti-dsDNA antibody|Anti-dsDNA antibodies]]
* Anti-C1q antibodies
* [[Antineutrophil cytoplasmic antibodies]] ([[ANCA]])
|
|
-
* Hypercellular and [[inflamed]] [[glomeruli]]
|
|
-
* Sub-[[epithelial]] [[immune complex]] deposits
* Obliteration of epithelial cell foot processes
|
|
-
* [[Immune]] complex GN
* Granular deposit
|-
! colspan="2" |[[Renal]] disease due to [[Endocarditis|Subacute Bacterial Endocarditis]], or [[cardiac shunt]] (Atrioventricular)<ref name="pmid6380288">{{cite journal |vauthors=Neugarten J, Baldwin DS |title=Glomerulonephritis in bacterial endocarditis |journal=Am. J. Med. |volume=77 |issue=2 |pages=297–304 |date=August 1984 |pmid=6380288 |doi= |url=}}</ref><ref name="pmid6831779">{{cite journal |vauthors=Arze RS, Rashid H, Morley R, Ward MK, Kerr DN |title=Shunt nephritis: report of two cases and review of the literature |journal=Clin. Nephrol. |volume=19 |issue=1 |pages=48–53 |date=January 1983 |pmid=6831779 |doi= |url=}}</ref>
|
|
+/-
* History of [[infective endocarditis]] mostly due to ''[[Staphylococcus aureus|S. aureus]]''
* [[Cardiac shunt]]
|
|
-
* [[Fever]]
* [[Fatigue]]
* Weight loss
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
|
+
* [[Myeloperoxidase (MPO)|ANCA (myeloperoxidase)]] positive in 1/3
* Activation of the [[alternative complement pathway]] (Decreased [[C3 (complement)|C3]], C4)
* Positive [[RF]]
* Positive [[Anti-glomerular basement membrane antibody|anti-GBM autoantibodies]]
|
|
+
* [[Rapidly progressive glomerulonephritis|Crescentic]] GN is the most common pathological features
 
* [[Membranoproliferative glomerulonephritis|Diffuse membranoproliferative glomerulonephritis]] features
* Focal proliferative GN
* Mesangial proliferative GN 
|
|
-
* [[Mesangial cell|Mesangial]] deposits,
* Subendothelial deposits
* Subepithelial "humps," in minority of cases
|
|
-
* Pauci-immune GN
|
-
|
-
|
* Normal
|
* Fusion of [[podocytes]]
|
-
|-
|-
![[Focal segmental glomerulosclerosis]]
! colspan="2" |[[Lupus nephritis|Lupus Nephritis]]<ref name="pmid14717922">{{cite journal |vauthors=Weening JJ, D'Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M |title=The classification of glomerulonephritis in systemic lupus erythematosus revisited |journal=Kidney Int. |volume=65 |issue=2 |pages=521–30 |date=February 2004 |pmid=14717922 |doi=10.1111/j.1523-1755.2004.00443.x |url=}}</ref>
|
|
* Idiopathic
* History of [[SLE]] features
* [[Human Immunodeficiency Virus (HIV)|HIV]]
* [[Heroine hydrochloride|Heroine]] use
* [[Sickle-cell disease|Sickle cell disease]]
* [[Interferon]]
* Severe [[obesity]]
* [[Cryoglobulinemia|Mixed cryoglobulinemia]] ([[Hepatitis C]])
|
|
* Adults
* [[Systemic lupus erythematosus|Lupus]] criteria:
|<nowiki>+</nowiki>
** [[Malar rash]]
|<nowiki>-</nowiki>
** [[Arthritis]]
|<nowiki>-</nowiki>
** [[Arthralgia]]
|<nowiki>-</nowiki>
** [[Anemia]]
** Easy bruising
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
* Anti-C1q antibodies
* [[Anti-dsDNA antibody|Anti-dsDNA]]
|
* Differs based on the disease classification
|
|
* Focal (some [[glomeruli]]) and segmental (only part of [[glomerulus]])
* Differs based on the disease classification
|
|
* Effacement of [[podocytes]]
* Differs based on the disease classification, mostly immune complex GN
|<nowiki>-</nowiki>
* Granular deposit
|-
|-
![[Membranous glomerulonephritis]]
! colspan="2" |[[Goodpasture syndrome|Antiglomerular Basement Membrane Disease]] [[Goodpasture syndrome|(Goodpasture's syndrome)]]<ref name="pmid8914046">{{cite journal |vauthors=Bolton WK |title=Goodpasture's syndrome |journal=Kidney Int. |volume=50 |issue=5 |pages=1753–66 |date=November 1996 |pmid=8914046 |doi= |url=}}</ref><ref name="pmid1090223">{{cite journal |vauthors=Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P |title=Goodpasture's syndrome: normal renal diagnostic findings |journal=Ann. Intern. Med. |volume=82 |issue=2 |pages=215–8 |date=February 1975 |pmid=1090223 |doi= |url=}}</ref>
|
|
* [[Idiopathic]]
* Young adults
* [[Hepatitis B]] and [[Hepatitis C|C]]
* [[Solid tumors]]
* [[Systemic lupus erythematosus]]
* Drugs ([[NSAIDS]], pencilamine, [[gold]], [[captopril]])
|
|
* Dry [[cough]]
* [[Hemoptysis]]
* [[Malaise]] 
* [[Fever]] and chills
* [[Arthralgia]] 
* [[Fatigue]]
* [[Lethargy]]
* [[Pallor]]
* [[Anorexia]]
* Easy [[bruising]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
|
* Thick [[glomerular basement membrane]]
* [[Myeloperoxidase (MPO)|ANCA (myeloperoxidase)]]
* Positive [[Anti-glomerular basement membrane antibody|anti-GBM autoantibodies]]
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation) 
|Diffuse thickening of the [[glomerular basement membrane]] with absence of sub-[[Epithelial cells|epithelial]] and sub-[[endothelial]] deposits 
|
|
* Sub-[[Epithelial cells|epithelial]] [[immune complex]] depositis with 'spike and dome' appearance
* Immune complex GN
|<nowiki>-</nowiki>
* Linear deposit
|-
|-
| rowspan="7" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic Syndrome
! colspan="2" |[[IgA nephropathy|IgA Nephropathy]]<ref name="pmid21949093">{{cite journal |vauthors=Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA |title=The pathophysiology of IgA nephropathy |journal=J. Am. Soc. Nephrol. |volume=22 |issue=10 |pages=1795–803 |date=October 2011 |pmid=21949093 |pmc=3892742 |doi=10.1681/ASN.2011050464 |url=}}</ref><ref name="pmid23782179">{{cite journal |vauthors=Wyatt RJ, Julian BA |title=IgA nephropathy |journal=N. Engl. J. Med. |volume=368 |issue=25 |pages=2402–14 |date=June 2013 |pmid=23782179 |doi=10.1056/NEJMra1206793 |url=}}</ref>
![[IgA nephropathy]]
|
* [[Idiopathic]]
* [[Viral infections]]
|
|
* Young children
* Young children
* History of [[mucosal]] [[infections]] (e.g. [[gastroenteritis]]) and [[upper respiratory tract infection]]
* History of [[mucosal]] [[infections]] (e.g. [[gastroenteritis]]) and [[upper respiratory tract infection]]
* 2-3 days after [[infection]] (synpharyngitic)
* 2-3 days after [[infection]] (synpharyngitic)
|
* Low grade [[fever]]
* [[Flank pain]]
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| -
| -
|<nowiki>-</nowiki>
|
|<nowiki>+</nowiki>
* Immune complex deposition
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|
|
* Crescent formation
* Crescent formation
|
|
* [[Mesangial cell|Mesangial]] proliferation
* [[Mesangial cell|Mesangial]] proliferation
|<nowiki>-</nowiki>
|
* Immune complex GN, granular deposite
|-
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
|-
! rowspan="5" |[[Rapidly progressive glomerulonephritis]]
! rowspan="3" |[[Vasculitis|ANCA Small-Vessel Vasculitis]]<ref name="pmid8746284">{{cite journal |vauthors=Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC |title=Vasculitis and rapidly progressive glomerulonephritis in the elderly |journal=Postgrad Med J |volume=72 |issue=843 |pages=41–4 |date=January 1996 |pmid=8746284 |pmc=2398323 |doi= |url=}}</ref><ref name="pmid12631105">{{cite journal |vauthors=Jennette JC |title=Rapidly progressive crescentic glomerulonephritis |journal=Kidney Int. |volume=63 |issue=3 |pages=1164–77 |date=March 2003 |pmid=12631105 |doi=10.1046/j.1523-1755.2003.00843.x |url=}}</ref>
! colspan="1" |[[Granulomatosis with polyangiitis|Granulomatosis with Polyangiitis (Wegener's)]]<ref name="pmid18172777">{{cite journal |vauthors=Renaudineau Y, Le Meur Y |title=Renal involvement in Wegener's granulomatosis |journal=Clin Rev Allergy Immunol |volume=35 |issue=1-2 |pages=22–9 |date=October 2008 |pmid=18172777 |doi=10.1007/s12016-007-8066-6 |url=}}</ref><ref name="pmid6384024">{{cite journal |vauthors=Weiss MA, Crissman JD |title=Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis |journal=Hum. Pathol. |volume=15 |issue=10 |pages=943–56 |date=October 1984 |pmid=6384024 |doi= |url=}}</ref><ref name="pmid18524109">{{cite journal |vauthors=Pagnoux C |title=[Wegener's granulomatosis and microscopic polyangiitis] |language=French |journal=Rev Prat |volume=58 |issue=5 |pages=522–32 |date=March 2008 |pmid=18524109 |doi= |url=}}</ref>
|
|
* [[Goodpasture syndrome]]
* Middle age male
|
|
* Young adults
* Constitutional symptoms
|<nowiki>+/-</nowiki>
* [[Dyspnea]]
|<nowiki>+</nowiki>
* [[Purpura]]
* [[Arthralgia|Arthralgias]]
* Neurologic dysfunction
* [[Rhinosinusitis|Sinusitis]]
* [[Otitis media]]
* [[Epistaxis]].
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| -
| -
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* [[ANCA]]
|
|
*  Diffuse thickening of the [[glomerular basement membrane]] with absence of sub-[[Epithelial cells|epithelial]] and sub-[[endothelial]] deposits 
* [[Necrotizing]] and [[Crescentic glomerulonephritis|crescentic]] glomerulonephritis
|<nowiki>+ (Linear)</nowiki>
|-
|
|
* [[Poststreptococcal glomerulonephritis|Post infectious glomerulonephritis]]
* Subendothelial [[edema]]
 
* Microthrombosis
* [[Degranulation]] of [[neutrophils]]
|
|
* [[Streptococcal infections|Streptococcal]] [[skin]] [[infections]]
* Pauci-immune GN
* [[Streptococcus|Streptococcal]] [[pharyngitis]]
|-
* 2-3 weeks after [[infection]]
! colspan="1" |[[Microscopic polyangiitis|Microscopic Polyangiitis]]<ref name="pmid20688249">{{cite journal |vauthors=Chung SA, Seo P |title=Microscopic polyangiitis |journal=Rheum. Dis. Clin. North Am. |volume=36 |issue=3 |pages=545–58 |date=August 2010 |pmid=20688249 |pmc=2917831 |doi=10.1016/j.rdc.2010.04.003 |url=}}</ref>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|
* Constitutional symptoms
* [[Dyspnea]]
* [[Purpura]]
* [[Arthralgia|Arthralgias]]
* Neurologic dysfunction
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>-</nowiki>
|
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
|
* Hypercellular and [[inflamed]] [[glomeruli]]
* [[P-ANCA]]
|
|
* Sub-[[epithelial]] [[immune complex]] deposits
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
| + (Granular)
|-
|
|
* [[Granulomatosis with polyangiitis|Granulomatosis with polyangitis]] ([[Wegener's granulomatosis|Wegner's granulomatosis]])
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|
|
* [[Necrotizing]] [[granulomas]] ([[Nasopharynx]], [[lungs]], [[kidneys]])
* Pauci-immune GN
* [[Conjunctivitis]]
|-
* Ulceration of the [[cornea]]
! colspan="1" |[[Eosinophilic granulomatosis with polyangiitis|Churg-Strauss Syndrome]]<ref name="pmid16632015">{{cite journal |vauthors=Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C |title=Renal involvement in Churg-Strauss syndrome |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=770–9 |date=May 2006 |pmid=16632015 |doi=10.1053/j.ajkd.2006.01.026 |url=}}</ref>
* [[Episcleritis]]
* [[Peripheral neuropathy]]
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
| + ([[C-ANCA]])
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|<nowiki>-  (pauci-immune)</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|-
|
|
* [[Churg-Strauss syndrome|Churg Strauss syndrome]]
*  [[Asthma]]
|
* [[Rhinosinusitis|Sinusitis]]
* [[Necrotizing]] [[granulomas]] ([[Lungs]] and [[kidneys]])
* [[Myalgia]] 
* [[Asthma]]
* [[Arthralgia]]
* [[Purpura]]
* [[Cardiac arrhythmia|Arrythmias]]
* [[Peripheral neuropathy]]
* [[Peripheral neuropathy]]
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|
|
+ ([[C-ANCA]])
[[C-ANCA]]
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
|
|
* [[Microscopic polyangiitis]]
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|
* [[Necrotizing]] [[vasculitis]] (no [[granuloma]])
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|
|
+ ([[P-ANCA]])
* Pauci-immune GN
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
|-
![[Membranoproliferative glomerulonephritis]]
! colspan="2" |[[Membranoproliferative glomerulonephritis|Membranoproliferative Glomerulonephritis]]<ref name="pmid19908070">{{cite journal |vauthors=Alchi B, Jayne D |title=Membranoproliferative glomerulonephritis |journal=Pediatr. Nephrol. |volume=25 |issue=8 |pages=1409–18 |date=August 2010 |pmid=19908070 |pmc=2887509 |doi=10.1007/s00467-009-1322-7 |url=}}</ref><ref name="pmid657595">{{cite journal |vauthors=Davis AE, Schneeberger EE, Grupe WE, McCluskey RT |title=Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children |journal=Clin. Nephrol. |volume=9 |issue=5 |pages=184–93 |date=May 1978 |pmid=657595 |doi= |url=}}</ref>
|
|
* [[Idiopathic]]
* [[Idiopathic]]
Line 499: Line 437:
* [[Periorbital edema]]
* [[Periorbital edema]]
* [[Hypertension]]
* [[Hypertension]]
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
* Thick [[glomerular basement membrane]] (Tram-track appearance)
|
* [[Mesangial cell|Mesangial]] proliferation
* [[Leukocytes|Leukocyte]] infiltration
|
* Immune complex GN
* Granular deposite
|-
! colspan="2" |[[Henoch-Schönlein purpura]] <ref name="pmid8023818">{{cite journal |vauthors=Jennette JC, Falk RJ |title=The pathology of vasculitis involving the kidney |journal=Am. J. Kidney Dis. |volume=24 |issue=1 |pages=130–41 |date=July 1994 |pmid=8023818 |doi= |url=}}</ref>
|
* Most common in young male, following [[Upper respiratory tract|upper respiratory]]  [[infections]]
|
* '''Skin manifestations-''' Palpable [[purpura]] on buttocks
* '''Gastrointestinal''' '''manifestations-'''
** [[Abdominal pain]]
** [[Melena]]
** [[Dysentery|Bloody diarrhea]]
** [[Hematemesis]]
* '''Joints'''  '''manifestations-'''
** [[Arthralgia]]
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| -
|<nowiki>+</nowiki>
|
* Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
|
|
* Thick [[glomerular basement membrane]] (Tram-track appearance)
* Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
|
|
* [[Mesangial cell|Mesangial]] proliferation and [[Leukocytes|leukocyte]] infiltration
* Immune complex GN, granular deposite
|<nowiki>+ (Granular)</nowiki>
|-
|}
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
! colspan="2" |[[Cryoglobulinemia]]<ref name="pmid26802335">{{cite journal |vauthors=Fogo AB, Lusco MA, Najafian B, Alpers CE |title=AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis |journal=Am. J. Kidney Dis. |volume=67 |issue=2 |pages=e5–7 |date=February 2016 |pmid=26802335 |doi=10.1053/j.ajkd.2015.12.007 |url=}}</ref>
|Patients having [[cryoglobulinemia]] may have positive history of:
* [[Hepatitis C|Hepatitis C infection]]
* [[Hepatitis B|Hepatitis B infection]]
* Leg ulcers
* Recurrent [[thrombosis]]
|'''Pulmonary symptoms:'''
* [[Difficulty breathing]]


Glomerulonephritis may be proliferative or non-proliferative and may be associated with [[Nephrotic syndrome|nephrotic]] or [[Nephritic syndrome|nephritic]] features. The various types of glomerulonephritides should be differentiated from each other based on associations, presence of [[pitting edema]], hemeturia, [[hypertension]], [[hemoptysis]], [[oliguria]], peri-orbital edema, [[hyperlipidemia]], type of [[antibodies]], [[Light microscope|light]] and [[Electron microscopy|electron microscopic]] features.
* Cough
The following table differentiates between various types of glomerulonephritides:<ref name="pmid17195422">{{cite journal |vauthors=Saha TC, Singh H |title=Minimal change disease: a review |journal=South. Med. J. |volume=99 |issue=11 |pages=1264–70 |date=November 2006 |pmid=17195422 |doi=10.1097/01.smj.0000243183.87381.c2 |url=}}</ref><ref name="pmid27092244">{{cite journal |vauthors=Saleem MA, Kobayashi Y |title=Cell biology and genetics of minimal change disease |journal=F1000Res |volume=5 |issue= |pages= |date=2016 |pmid=27092244 |pmc=4821284 |doi=10.12688/f1000research.7300.1 |url=}}</ref><ref name="pmid26064510">{{cite journal |vauthors=Keskar V, Jamale TE, Kulkarni MJ, Kiggal Jagadish P, Fernandes G, Hase N |title=Minimal-change disease in adolescents and adults: epidemiology and therapeutic response |journal=Clin Kidney J |volume=6 |issue=5 |pages=469–72 |date=October 2013 |pmid=26064510 |pmc=4438390 |doi=10.1093/ckj/sft063 |url=}}</ref><ref name="pmid21974967">{{cite journal |vauthors=Chugh SS, Clement LC, Macé C |title=New insights into human minimal change disease: lessons from animal models |journal=Am. J. Kidney Dis. |volume=59 |issue=2 |pages=284–92 |date=February 2012 |pmid=21974967 |pmc=3253318 |doi=10.1053/j.ajkd.2011.07.024 |url=}}</ref><ref name="pmid28242845">{{cite journal |vauthors=Rosenberg AZ, Kopp JB |title=Focal Segmental Glomerulosclerosis |journal=Clin J Am Soc Nephrol |volume=12 |issue=3 |pages=502–517 |date=March 2017 |pmid=28242845 |pmc=5338705 |doi=10.2215/CJN.05960616 |url=}}</ref><ref name="pmid25168829">{{cite journal |vauthors=Jefferson JA, Shankland SJ |title=The pathogenesis of focal segmental glomerulosclerosis |journal=Adv Chronic Kidney Dis |volume=21 |issue=5 |pages=408–16 |date=September 2014 |pmid=25168829 |pmc=4149756 |doi=10.1053/j.ackd.2014.05.009 |url=}}</ref><ref name="pmid2429634">{{cite journal |vauthors=Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT |title=Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens |journal=Arch. Pathol. Lab. Med. |volume=110 |issue=10 |pages=902–5 |date=October 1986 |pmid=2429634 |doi= |url=}}</ref><ref name="pmid25558821">{{cite journal |vauthors=Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ |title=Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment |journal=J. Formos. Med. Assoc. |volume=114 |issue=2 |pages=102–11 |date=February 2015 |pmid=25558821 |doi=10.1016/j.jfma.2014.11.002 |url=}}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref><ref name="pmid21949093">{{cite journal |vauthors=Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA |title=The pathophysiology of IgA nephropathy |journal=J. Am. Soc. Nephrol. |volume=22 |issue=10 |pages=1795–803 |date=October 2011 |pmid=21949093 |pmc=3892742 |doi=10.1681/ASN.2011050464 |url=}}</ref><ref name="pmid23782179">{{cite journal |vauthors=Wyatt RJ, Julian BA |title=IgA nephropathy |journal=N. Engl. J. Med. |volume=368 |issue=25 |pages=2402–14 |date=June 2013 |pmid=23782179 |doi=10.1056/NEJMra1206793 |url=}}</ref><ref name="pmid22373436">{{cite journal |vauthors=He S, Wu Z |title=Gene-based Higher Criticism methods for large-scale exonic single-nucleotide polymorphism data |journal=BMC Proc |volume=5 Suppl 9 |issue= |pages=S65 |date=November 2011 |pmid=22373436 |pmc=3287904 |doi=10.1186/1753-6561-5-S9-S65 |url=}}</ref><ref name="pmid8746284">{{cite journal |vauthors=Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC |title=Vasculitis and rapidly progressive glomerulonephritis in the elderly |journal=Postgrad Med J |volume=72 |issue=843 |pages=41–4 |date=January 1996 |pmid=8746284 |pmc=2398323 |doi= |url=}}</ref><ref name="pmid12631105">{{cite journal |vauthors=Jennette JC |title=Rapidly progressive crescentic glomerulonephritis |journal=Kidney Int. |volume=63 |issue=3 |pages=1164–77 |date=March 2003 |pmid=12631105 |doi=10.1046/j.1523-1755.2003.00843.x |url=}}</ref><ref name="pmid8914046">{{cite journal |vauthors=Bolton WK |title=Goodpasture's syndrome |journal=Kidney Int. |volume=50 |issue=5 |pages=1753–66 |date=November 1996 |pmid=8914046 |doi= |url=}}</ref><ref name="pmid1090223">{{cite journal |vauthors=Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P |title=Goodpasture's syndrome: normal renal diagnostic findings |journal=Ann. Intern. Med. |volume=82 |issue=2 |pages=215–8 |date=February 1975 |pmid=1090223 |doi= |url=}}</ref><ref name="pmid18172777">{{cite journal |vauthors=Renaudineau Y, Le Meur Y |title=Renal involvement in Wegener's granulomatosis |journal=Clin Rev Allergy Immunol |volume=35 |issue=1-2 |pages=22–9 |date=October 2008 |pmid=18172777 |doi=10.1007/s12016-007-8066-6 |url=}}</ref><ref name="pmid6384024">{{cite journal |vauthors=Weiss MA, Crissman JD |title=Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis |journal=Hum. Pathol. |volume=15 |issue=10 |pages=943–56 |date=October 1984 |pmid=6384024 |doi= |url=}}</ref><ref name="pmid16632015">{{cite journal |vauthors=Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C |title=Renal involvement in Churg-Strauss syndrome |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=770–9 |date=May 2006 |pmid=16632015 |doi=10.1053/j.ajkd.2006.01.026 |url=}}</ref><ref name="pmid21325353">{{cite journal |vauthors=Cartin-Ceba R, Keogh KA, Specks U, Sethi S, Fervenza FC |title=Rituximab for the treatment of Churg-Strauss syndrome with renal involvement |journal=Nephrol. Dial. Transplant. |volume=26 |issue=9 |pages=2865–71 |date=September 2011 |pmid=21325353 |pmc=3218640 |doi=10.1093/ndt/gfq852 |url=}}</ref><ref name="pmid20688249">{{cite journal |vauthors=Chung SA, Seo P |title=Microscopic polyangiitis |journal=Rheum. Dis. Clin. North Am. |volume=36 |issue=3 |pages=545–58 |date=August 2010 |pmid=20688249 |pmc=2917831 |doi=10.1016/j.rdc.2010.04.003 |url=}}</ref><ref name="pmid18524109">{{cite journal |vauthors=Pagnoux C |title=[Wegener's granulomatosis and microscopic polyangiitis] |language=French |journal=Rev Prat |volume=58 |issue=5 |pages=522–32 |date=March 2008 |pmid=18524109 |doi= |url=}}</ref><ref name="pmid19908070">{{cite journal |vauthors=Alchi B, Jayne D |title=Membranoproliferative glomerulonephritis |journal=Pediatr. Nephrol. |volume=25 |issue=8 |pages=1409–18 |date=August 2010 |pmid=19908070 |pmc=2887509 |doi=10.1007/s00467-009-1322-7 |url=}}</ref><ref name="pmid657595">{{cite journal |vauthors=Davis AE, Schneeberger EE, Grupe WE, McCluskey RT |title=Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children |journal=Clin. Nephrol. |volume=9 |issue=5 |pages=184–93 |date=May 1978 |pmid=657595 |doi= |url=}}</ref>
'''Cutaneous symptoms:'''
* [[Purpura]] 
* [[Skin ulcer]]
'''Gastrointestinal symptoms:'''
* Abdominal pain
'''General symptoms:'''
* Fever
* [[Arthralgia]],  
* [[Myalgia]]
* [[Fatigue]]


{| class="wikitable"
* [[Blurred vision|Blurring]]/loss of vision
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Glomerulonephritis
* [[Diplopia]]
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Sub-entity
* [[Confusion]]
! rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes and associations
|<nowiki>+/-</nowiki>
! colspan="7" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |History and Symtoms
| +
! colspan="9" align="center" style="background:#4479BA; color: #FFFFFF;" + |Laboratory Findings
|<nowiki>+/-</nowiki>
|-
|<nowiki>+</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Hyperlipidemia and hypercholesterolemia
|<nowiki>+/-</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephrotic features
|<nowiki>+/-</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Nephritic features
|<nowiki>+/-</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |ANCA
|<nowiki>+/-</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Anti-glomerular basement membrane antibody (Anti-GBM antibody)
|<nowiki>+/-</nowiki>
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immune complex formation
|
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Light microscope
* [[Membranoproliferative glomerulonephritis]]
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Electron microscope
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Immunoflourescence pattern
|-
! align="center" style="background:#4479BA; color: #FFFFFF;" + |History
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Pitting edema
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemeturia (pre-dominantly microscopic)
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hypertension
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Hemoptysis
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Oliguria
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Peri-orbital edema
|-
| rowspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Non-proliferative
![[Minimal change disease]]
|
|
* [[Idiopathic]]
* [[Mesangial cell|Mesangial]] and subendothelial deposits
* [[Protein]] [[Protein tyrosine phosphatase|tyrosine phosphatase]] receptor type O (glomerular epithelial protein 1- GLEPP1)
|
|
* Prominent [[IgM]] and C3
|-
! rowspan="9" style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic Syndrome
! colspan="2" |[[Minimal change disease|Minimal Change Disease]]<ref name="pmid17195422">{{cite journal |vauthors=Saha TC, Singh H |title=Minimal change disease: a review |journal=South. Med. J. |volume=99 |issue=11 |pages=1264–70 |date=November 2006 |pmid=17195422 |doi=10.1097/01.smj.0000243183.87381.c2 |url=}}</ref><ref name="pmid27092244">{{cite journal |vauthors=Saleem MA, Kobayashi Y |title=Cell biology and genetics of minimal change disease |journal=F1000Res |volume=5 |issue= |pages= |date=2016 |pmid=27092244 |pmc=4821284 |doi=10.12688/f1000research.7300.1 |url=}}</ref>
| colspan="2" |
* Young children
* Young children
* Recent [[infection]] and [[immunization]]
* Recent [[infection]] and [[immunization]]
Line 557: Line 548:
* [[Hodgkin's lymphoma|Hodgkin lymphoma]]
* [[Hodgkin's lymphoma|Hodgkin lymphoma]]
* [[Thrombosis]] (due to [[Urinary system|urinary]] loss of [[Antithrombin III|antithrombin-III]])
* [[Thrombosis]] (due to [[Urinary system|urinary]] loss of [[Antithrombin III|antithrombin-III]])
| -
| +
| -
| +
| +/-
| +
| -
| +
|
|
+
|
-
|
-
|
-
|
+/-
|
-
|
+
|
+
|
-
|
-
|
-
|
-
|
|
* Normal
* Normal
|
|
* Fusion of [[podocytes]]
* Fusion of [[podocytes]]
|
| -
-
|-
|-
![[Focal segmental glomerulosclerosis]]
! colspan="2" |[[Focal segmental glomerulosclerosis|Focal Segmental Glomerulosclerosis]]<ref name="pmid28242845">{{cite journal |vauthors=Rosenberg AZ, Kopp JB |title=Focal Segmental Glomerulosclerosis |journal=Clin J Am Soc Nephrol |volume=12 |issue=3 |pages=502–517 |date=March 2017 |pmid=28242845 |pmc=5338705 |doi=10.2215/CJN.05960616 |url=}}</ref><ref name="pmid25168829">{{cite journal |vauthors=Jefferson JA, Shankland SJ |title=The pathogenesis of focal segmental glomerulosclerosis |journal=Adv Chronic Kidney Dis |volume=21 |issue=5 |pages=408–16 |date=September 2014 |pmid=25168829 |pmc=4149756 |doi=10.1053/j.ackd.2014.05.009 |url=}}</ref><ref name="pmid2429634">{{cite journal |vauthors=Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT |title=Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens |journal=Arch. Pathol. Lab. Med. |volume=110 |issue=10 |pages=902–5 |date=October 1986 |pmid=2429634 |doi= |url=}}</ref>
|
| colspan="2" |
* Idiopathic
* Idiopathic
* [[Human Immunodeficiency Virus (HIV)|HIV]]
* [[Human Immunodeficiency Virus (HIV)|HIV]]
Line 597: Line 572:
* Severe [[obesity]]
* Severe [[obesity]]
* [[Cryoglobulinemia|Mixed cryoglobulinemia]] ([[Hepatitis C]])
* [[Cryoglobulinemia|Mixed cryoglobulinemia]] ([[Hepatitis C]])
|
* Adults
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +
|
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
|
* Focal (some [[glomeruli]]) and segmental (only part of [[glomerulus]])
* Focal (some [[glomeruli]]) and segmental (only part of [[glomerulus]])
Line 617: Line 587:
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|-
|-
![[Membranous glomerulonephritis]]
! colspan="2" |[[Membranous glomerulonephritis|Membranous Glomerulonephritis]]<ref name="pmid25558821">{{cite journal |vauthors=Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ |title=Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment |journal=J. Formos. Med. Assoc. |volume=114 |issue=2 |pages=102–11 |date=February 2015 |pmid=25558821 |doi=10.1016/j.jfma.2014.11.002 |url=}}</ref><ref name="pmid10495797">{{cite journal |vauthors=Wasserstein AG |title=Membranous glomerulonephritis |journal=J. Am. Soc. Nephrol. |volume=8 |issue=4 |pages=664–74 |date=April 1997 |pmid=10495797 |doi= |url=}}</ref>
|
| colspan="2" |
* [[Idiopathic]]
* [[Idiopathic]]
* [[Hepatitis B]] and [[Hepatitis C|C]]
* [[Hepatitis B]] and [[Hepatitis C|C]]
Line 624: Line 594:
* [[Systemic lupus erythematosus]]
* [[Systemic lupus erythematosus]]
* Drugs ([[NSAIDS]], pencilamine, [[gold]], [[captopril]])
* Drugs ([[NSAIDS]], pencilamine, [[gold]], [[captopril]])
|
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|Immune complex deposition
|
* Thick [[glomerular basement membrane]]
|
* Sub-[[Epithelial cells|epithelial]] [[immune complex]] depositis with 'spike and dome' appearance
|Immune complex GN, granular deposite
|-
! colspan="2" |[[Diabetic nephropathy|Diabetic Nephropathy]]<ref name="pmid11978659">{{cite journal| author=Drummond K, Mauer M, International Diabetic Nephropathy Study Group| title=The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes. | journal=Diabetes | year= 2002 | volume= 51 | issue= 5 |pages= 1580-7 | pmid=11978659 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11978659  }}</ref><ref name="pmid3699305">{{cite journal| author=Hørlyck A, Gundersen HJ, Osterby R| title=The cortical distribution pattern of diabetic glomerulopathy. | journal=Diabetologia | year= 1986 | volume= 29| issue= 3 | pages= 146-50 | pmid=3699305 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3699305  }}</ref><ref name="pmid21422926">{{cite journal| author=Alpers CE, Hudkins KL| title=Mouse models of diabetic nephropathy. | journal=Curr Opin Nephrol Hypertens | year= 2011 | volume= 20 | issue= 3 |pages= 278-84 | pmid=21422926 | doi=10.1097/MNH.0b013e3283451901 | pmc=PMC3658822 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21422926  }}</ref><ref name="pmid19970254">{{cite journal| author=Kimmelstiel P, Wilson C| title=Intercapillary Lesions in the Glomeruli of the Kidney. | journal=Am J Pathol | year= 1936 | volume= 12 | issue= 1 |pages= 83-98.7 | pmid=19970254 | doi= | pmc=PMC1911022 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19970254  }}</ref><ref name="pmid2766585">{{cite journal| author=Alpers CE, Biava CG| title=Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity. | journal=Clin Nephrol | year= 1989 | volume= 32 | issue= 2 | pages= 68-74 | pmid=2766585 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2766585  }}</ref><ref name="pmid17536064">{{cite journal| author=Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M| title=Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. | journal=Diabetes | year= 2007 | volume= 56 | issue= 8 | pages= 2155-60 |pmid=17536064 | doi=10.2337/db07-0019 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17536064  }}</ref><ref name="pmid16565248">{{cite journal| author=Najafian B, Crosson JT, Kim Y, Mauer M| title=Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes. | journal=J Am Soc Nephrol | year= 2006 | volume= 17 | issue= 4 Suppl 2 | pages= S53-60| pmid=16565248 | doi=10.1681/ASN.2005121342 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16565248  }}</ref><ref name="pmid12660325">{{cite journal| author=Najafian B, Kim Y, Crosson JT, Mauer M| title=Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy. | journal=J Am Soc Nephrol | year= 2003 | volume= 14 | issue= 4 | pages= 908-17 | pmid=12660325 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12660325  }}</ref><ref name="pmid21659756">{{cite journal| author=Najafian B, Alpers CE, Fogo AB| title=Pathology of human diabetic nephropathy. |journal=Contrib Nephrol | year= 2011 | volume= 170 | issue=  | pages= 36-47 | pmid=21659756 |doi=10.1159/000324942 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21659756  }}</ref><ref name="pmid216597562">{{cite journal| author=Najafian B, Alpers CE, Fogo AB| title=Pathology of human diabetic nephropathy. |journal=Contrib Nephrol | year= 2011 | volume= 170 | issue=  | pages= 36-47 | pmid=21659756 |doi=10.1159/000324942 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21659756  }}</ref>
| colspan="2" |'''''For more information on diabetes [[Diabetes mellitus|click here]]'''.''
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| +
|
|
* Diffuse [[Mesangial cell|mesangial]] matrix expansion (nodular glomerulosclerosis)
* Increased [[Mesangial cell|mesangial]] hypercellularity
* Prominent glomerular basement membranes
* Thick [[basement membrane]] without any deposit
|
* Nodular glomerulosclerosis
| -
|-
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
! rowspan="4" | [[Glomerular deposition disease|Glomerular Deposition Diseases]] 
![[Light chain nephropathy|Light Chain Deposition Disease]]<ref name="pmid21511832">{{cite journal |vauthors=Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N |title=Early reduction of serum-free light chains associates with renal recovery in myeloma kidney |journal=J. Am. Soc. Nephrol. |volume=22 |issue=6 |pages=1129–36 |date=June 2011 |pmid=21511832 |pmc=3103732 |doi=10.1681/ASN.2010080857 |url=}}</ref>
|
* Occurs in the setting of high tumor burden
| -
|<nowiki>-</nowiki>
| +
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>+</nowiki>
| -
|
* Light-chain deposits
|
|
* Thick [[glomerular basement membrane]]
* Granular deposits on electron microscopy
|
|
* Sub-[[Epithelial cells|epithelial]] [[immune complex]] depositis with 'spike and dome' appearance
* Detection of light chain deposits using anti–light chain antibody
|<nowiki>-</nowiki>
|-
|-
| rowspan="7" align="center" style="background:#4479BA; color: #FFFFFF;" + |Proliferative
![[Amyloidosis|Renal Amyloidosis]]<ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid23979488">{{cite journal |vauthors=Gillmore JD, Hawkins PN |title=Pathophysiology and treatment of systemic amyloidosis |journal=Nat Rev Nephrol |volume=9 |issue=10 |pages=574–86 |date=October 2013 |pmid=23979488 |doi=10.1038/nrneph.2013.171 |url=}}</ref><ref name="pmid26155101">{{cite journal |vauthors=Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA |title=Primary systemic amyloidosis as a real diagnostic challenge - case study |journal=Cent Eur J Immunol |volume=39 |issue=1 |pages=61–6 |date=2014 |pmid=26155101 |pmc=4439975 |doi=10.5114/ceji.2014.42126 |url=}}</ref><ref name="pmid16409147">{{cite journal |vauthors=Pepys MB |title=Amyloidosis |journal=Annu. Rev. Med. |volume=57 |issue= |pages=223–41 |date=2006 |pmid=16409147 |doi=10.1146/annurev.med.57.121304.131243 |url=}}</ref>
![[IgA nephropathy]]
|
|
* [[Idiopathic]]
* For the secondary causes of amloidosis:
* [[Viral infections]]  
* [[Tuberculosis]]
* [[Familial mediterranean fever|Familial Mediterranean fever]]
* [[Rheumatoid arthritis]]  
* [[Multiple myeloma]]  
|
|
* Young children
* [[Dyspnea]]
* History of [[mucosal]] [[infections]] (e.g. [[gastroenteritis]]) and [[upper respiratory tract infection]]
* [[Lethargy]]
* 2-3 days after [[infection]] (synpharyngitic)
* Weight loss
|<nowiki>+/-</nowiki>
 
|<nowiki>+</nowiki>
* [[Hemorrhagic diathesis|Bleeding tendency]]
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| -
| +
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| -
|
|
* Crescent formation
* Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
|
* Nodular deposit
|
|
* [[Mesangial cell|Mesangial]] proliferation
* AA amyloidosis type: negative for immunoglobulins and complement
|<nowiki>-</nowiki>
* AL amyloidosis type: Positive for lambda or kappa light chains
|-
|-
! rowspan="5" |[[Rapidly progressive glomerulonephritis]]
!Fibrillary-Immunotactoid Glomerulopathy<ref name="pmid1996564">{{cite journal |vauthors=Korbet SM, Schwartz MM, Lewis EJ |title=Immunotactoid glomerulopathy |journal=Am. J. Kidney Dis. |volume=17 |issue=3 |pages=247–57 |date=March 1991 |pmid=1996564 |doi= |url=}}</ref>
|
|
* [[Goodpasture syndrome]]
* [[Malignancy]]  
|
* [[Monoclonal gammopathy]]
* Young adults
* [[Autoimmunity|Autoimmune]] disease
| -
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| -
| -
|
* Diffuse sclerosing glomerulonephritis
* Diffuse proliferative glomerulonephritis
* Membranoproliferative glomerulonephritis
* Mesangioproliferative/sclerosing disease
* Membranous glomerulonephritis
|
* Large fibrillar deposits in the mesangium randomly
* Glomerular capillary walls different from amloidosis
* No staining with Congo red or thioflavine-T or with antibodies to a specific type
|
* Positive for immunoglobulin G (IgG), C3
* [[Light chain|Kappa]] and lambda (ie, polyclonal) light chains
|-
![[Fabry's disease|Fabry's Disease]]<ref name="pmid12068025">{{cite journal |vauthors=Alroy J, Sabnis S, Kopp JB |title=Renal pathology in Fabry disease |journal=J. Am. Soc. Nephrol. |volume=13 Suppl 2 |issue= |pages=S134–8 |date=June 2002 |pmid=12068025 |doi= |url=}}</ref><ref name="pmid9918480">{{cite journal |author=Meikle PJ, Hopwood JJ, Clague AE, Carey WF |title=Prevalence of lysosomal storage disorders |journal=[[JAMA : the Journal of the American Medical Association]] |volume=281 |issue=3 |pages=249–54 |year=1999 |month=January |pmid=9918480 |doi= |url=}}</ref><ref name="pmid11889412">{{cite journal |author=Branton MH, Schiffmann R, Sabnis SG, ''et al.'' |title=Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course |journal=[[Medicine]] |volume=81 |issue=2 |pages=122–38 |year=2002 |month=March |pmid=11889412 |doi= |url=}}</ref>
|
* [[Family history]] suggestive of the disorder
|
* [[Anhidrosis]] or decreased sweating
* [[Fatigue (medical)|Fatigue]]
* [[Angiokeratoma|Angiokeratomas]]
* Burning pain of the extremities
* Corneal opacities.
* [[Dysphagia]]
* [[Abdominal pain]]
* [[Steatorrhea]]
* [[Delayed puberty]]
* [[Raynaud's phenomenon]]
* [[Hearing loss]]
* [[Telangiectasis]]
* [[Ataxia]]
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
| -
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
* Glycolipid accumulation
|
|
*  Diffuse thickening of the [[glomerular basement membrane]] with absence of sub-[[Epithelial cells|epithelial]] and sub-[[endothelial]] deposits 
* Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
|<nowiki>+ (Linear)</nowiki>
* Inclusions, composed of concentric layers (onion skin appearance)
|<nowiki>-</nowiki>
|-
|-
! rowspan="4" style="background:#4479BA; color: #FFFFFF;" align="center" + |Basement Membrane Syndrome
! colspan="2" |[[Alport syndrome|Alport's Syndrome]]<ref name="pmid111374282">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid84141532">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid8414153">{{cite journal| author=Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN et al.| title=Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds. | journal=Nephrol Dial Transplant | year= 1993 | volume= 8 | issue= 8 | pages= 690-5 | pmid=8414153 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8414153 }}</ref><ref name="pmid11137428">{{cite journal| author=McCarthy PA, Maino DM| title=Alport syndrome: a review. | journal=Clin Eye Vis Care | year= 2000 | volume= 12 | issue= 3-4 | pages= 139-150 | pmid=11137428 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11137428 }}</ref><ref name="pmid7819734">{{cite journal| author=Amari F, Segawa K, Ando F| title=Lens coloboma and Alport-like glomerulonephritis. | journal=Eur J Ophthalmol | year= 1994 | volume= 4 | issue= 3 | pages= 181-3 | pmid=7819734 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7819734 }}</ref><ref name="pmid6871140">{{cite journal| author=Govan JA| title=Ocular manifestations of Alport's syndrome: a hereditary disorder of basement membranes? | journal=Br J Ophthalmol | year= 1983 | volume= 67 | issue= 8 | pages= 493-503 | pmid=6871140 | doi= | pmc=PMC1040106 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6871140 }}</ref>
|
|
* [[Poststreptococcal glomerulonephritis|Post infectious glomerulonephritis]]
* Positive family history
|
|'''Auditary:'''
* [[Streptococcal infections|Streptococcal]] [[skin]] [[infections]]  
*Early [[Tinnitus]]
* [[Streptococcus|Streptococcal]] [[pharyngitis]]
*[[Vertigo]]
* 2-3 weeks after [[infection]]
*High-frequency progressive bilateral [[Hearing impairment|hearing loss]]
|<nowiki>+/-</nowiki>
 
|<nowiki>+</nowiki>
'''Occular problems:'''
|<nowiki>+</nowiki>
* Refractory Error
|<nowiki>+</nowiki>
 
|<nowiki>+</nowiki>
*Arcus
|<nowiki>+</nowiki>
*[[Glaucoma]]
*Band Keratopathy
*[[Lenticonus]]
*[[Weill-Marchesani syndrome|Spherophakia]]
*[[Cataract|Cataracts]]  
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
|<nowiki>+</nowiki>
| -
|
* Early stage: unremarkable
 
* Late stages: [[glomerulosclerosis]], [[interstitial fibrosis]], and interstitial [[foam cells]] (due to prolonged [[proteinuria]]).
|
|
* Hypercellular and [[inflamed]] [[glomeruli]]
* Within [[glomerular basement membrane]] ([[GBM]]): longitudinal splitting of the lamina densa
|
|
* Sub-[[epithelial]] [[immune complex]] deposits
* Absence of staining of the alpha-3, alpha-4, and alpha-5 (IV) chains in the [[glomerular basement membrane]]
| + (Granular)
* Minimal binding to a glomerulus in indirect [[immunofluorescence]] microscopy with [[Anti-glomerular basement membrane antibody|anti-glomerular basement membrane]] antibodies
|-
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
|-
! colspan="2" |[[Thin basement membrane disease|Thin Basement Membrane Disease]]<ref name="pmid12969134">{{cite journal |author=Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY |title=Thin basement membrane nephropathy |journal=Kidney Int. |volume=64 |issue=4 |pages=1169–78 |year=2003 |month=October |pmid=12969134 |doi=10.1046/j.1523-1755.2003.00234.x}}</ref><ref name="pmid17726307">{{cite journal |author=Hou P, Chen Y, Ding J, Li G, Zhang H |title=A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy |journal=Am. J. Nephrol. |volume=27 |issue=5 |pages=538–44 |year=2007 |pmid=17726307 |doi=10.1159/000107666 |url=http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000107666}}</ref>
|
|
* [[Granulomatosis with polyangiitis|Granulomatosis with polyangitis]] ([[Wegener's granulomatosis|Wegner's granulomatosis]])
* Positive [[family history]]
|
 
* [[Necrotizing]] [[granulomas]] ([[Nasopharynx]], [[lungs]], [[kidneys]])
* Gross [[hematuria]] following [[upper respiratory tract infection]]
* [[Conjunctivitis]]
* Ulceration of the [[cornea]]
* [[Episcleritis]]
* [[Peripheral neuropathy]]
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| -
| +
| -/+
| -
|<nowiki>-/+</nowiki>
| -
| -/+
| -
| -
| -
|Diffuse thinning of the [[Glomerular basement membrane|glomerular basement membranes]] (GBM)
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|-
! colspan="2" |[[Nail-patella syndrome|Nail-Patella Syndrome]]<ref name="pmid28941488">{{cite journal |vauthors=Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB |title=AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy |journal=Am. J. Kidney Dis. |volume=70 |issue=4 |pages=e19–e20 |date=October 2017 |pmid=28941488 |doi=10.1053/j.ajkd.2017.08.001 |url=}}</ref><ref name="pmid1960197">{{cite journal |vauthors=Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T |title=Nail patella syndrome: a review of 44 orthopaedic patients |journal=J Pediatr Orthop |volume=11 |issue=6 |pages=737–42 |date=1991 |pmid=1960197 |doi= |url=}}</ref>
|
* Positive family history
|
* Poorly developed [[fingernails]], toe nails, and patellae (kneecaps).
* [[Elbow]] deformities
* Abnormally shaped [[pelvis]] bone ([[hip]] bone)
* [[Knee]] may be small, deformed or absent
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
| + ([[C-ANCA]])
| +
|<nowiki>-</nowiki>
| -
|<nowiki>-</nowiki>
| -
| -
| -
| -
| -
| -
|
* Mostly unremarkable changes
* Secondary FSGS
* Late stages:
 
** Global glomerulosclerosis,
** Tubulointerstitial fibrosis
|
* [[Glomerular basement membrane|Glomerular basement membranes (GBMs)]]: Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
* Similar collagen fibrils can be seen in mesangial matrix.
* Podocytes: Segmental effacement of foot processes.
|
* [[Immunofluorescence]] studies are typically negative.
 
* Nonspecific [[IgM]] and C3 deposition may be seen in sclerotic glomeruli.
|-
! rowspan="6" style="background:#4479BA; color: #FFFFFF;" align="center" + | Glomerular-Vascular Syndromes 
! colspan="2" |[[Hypertensive nephropathy|Hypertensive Nephrosclerosis]]<ref name="pmid24327566">{{cite journal |vauthors=Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF |title=Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race |journal=Nephrol. Dial. Transplant. |volume=29 |issue=7 |pages=1399–409 |date=July 2014 |pmid=24327566 |pmc=4071048 |doi=10.1093/ndt/gft480 |url=}}</ref>
|Chronic [[hypertension]]
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* [[Hypertensive retinopathy|Hypertensive retinal]] changes.
|<nowiki>- (pauci-immune)</nowiki>
 
* High [[jugular venous pressure]]
 
* [[Rales]] from [[pulmonary edema]] on auscultation
* .Signs of [[left ventricular hypertrophy]]
 
* [[Left ventricle|Left ventricular]] heave
* Shifting of apex towards the left
 
* [[S3]] and [[gallop rhythm]]
* Loud S2
 
* [[Ascites]]
 
* [[Paralysis]] from [[stroke]] secondary to [[hypertension]]
 
* Inferior limb [[edema]]
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| -
| +/-
| -
| colspan="3" |
* Interstitial [[fibrosis]] and atrophy
* Medial thickening and intimal fibrosis of medium-sized and larger vessels
* Arteriolar thickening, and hyalinosis
* Chronic stages:
** Global sclerosis
** Focal segmental [[sclerosis]]
|-
|-
! colspan="2" |[[Cholesterol emboli syndrome|Cholesterol Emboli]]<ref name="pmid27012950">{{cite journal |vauthors=Lusco MA, Najafian B, Alpers CE, Fogo AB |title=AJKD Atlas of Renal Pathology: Cholesterol Emboli |journal=Am. J. Kidney Dis. |volume=67 |issue=4 |pages=e23–4 |date=April 2016 |pmid=27012950 |doi=10.1053/j.ajkd.2016.02.034 |url=}}</ref>
|
|
* [[Churg-Strauss syndrome|Churg Strauss syndrome]]
* [[Atherosclerotic]] [[cardiovascular disease]]
* [[Anticoagulation therapy]]
* [[Cardiopulmonary]] [[resuscitation]]
* [[Hypertension]]
* [[Aortic aneurysm]]
* [[Hypercholesterolemia]]
* Smoking history
* Male sex
* Age over 55 years
* [[Vascular]] procedures
* Invasive [[angiography]]
* [[Aortic aneurysm]] rupture or surgery
* [[Vascular]] surgery
|
|
* [[Necrotizing]] [[granulomas]] ([[Lungs]] and [[kidneys]])
* Depends on the organ involved
* [[Asthma]]
|<nowiki>+/-</nowiki>
* [[Peripheral neuropathy]]
|<nowiki>+/-</nowiki>
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
| -
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
| -
|<nowiki>+</nowiki>
|
|<nowiki>+</nowiki>
* Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of [[cholesterol]] crystals
|<nowiki>-</nowiki>
* Acute lesions:
|<nowiki>-</nowiki>
** Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions 
|<nowiki>+</nowiki>
* Chronic lesions:
** Cholesterol clefts are surrounded by intimal fibrosis
** Vessel recanalization of chronic lesions can occur.
* Global and segmental sclerosis of glomeruli may be present.
|
|
+ ([[C-ANCA]])
* Extensive foot process effacement can be seen
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* Not specific changes
|<nowiki>- (pauci-immune)</nowiki>
|-
|<nowiki>-</nowiki>
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Disease
! style="background:#4479BA; color: #FFFFFF;" align="center" + |History
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Systemic symptoms
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hemeturia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Proteinuria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hypertension
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Pitting edema
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Oliguria
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephrotic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Nephritic features
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Hyperlipidemia and hypercholesterolemia
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Auto-antibodies,
Complements
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Light microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Electron microscope
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Immunoflourescence pattern
|-
|-
! colspan="2" |[[Sickle-cell disease|Sickle Cell Disease]]<ref name="pmid12028473">{{cite journal |vauthors=Wesson DE |title=The initiation and progression of sickle cell nephropathy |journal=Kidney Int. |volume=61 |issue=6 |pages=2277–86 |date=June 2002 |pmid=12028473 |doi=10.1046/j.1523-1755.2002.00363.x |url=}}</ref>
|
|
* [[Microscopic polyangiitis]]
* Positive family history
|
|
* [[Necrotizing]] [[vasculitis]] (no [[granuloma]])
* [[Pain and nociception|Pain]] and/or [[bone pain]]
* [[Dactylitis]]
* [[Blurry vision]]
* [[Priapism|Persistent and painful erection]]
* [[Numbness]]
* [[Tingling]]
* Motor skill loss
* [[Aphasia|Speech deficits]]
* [[Gait disturbance]]
* Leg [[ulceration]]
* [[Jaundice]]
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
| +/-
| -
| -
| -
| -
| -
| -
| colspan="3" |
* [[Glomerulus|Glomerular]] hypertrophy
* [[Hemosiderin]] deposits
* Focal areas of hemorrhage or necrosis
* Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and [[papillary]] infarcts
 
* Glomerular enlargement and focal segmental glomerulosclerosis ([[Focal segmental glomerulosclerosis|FSGS]])
|-
! colspan="2" |[[Thrombotic microangiopathies|Thrombotic Microangiopathies]]<ref name="pmid27884283">{{cite journal |vauthors=Lusco MA, Fogo AB, Najafian B, Alpers CE |title=AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy |journal=Am. J. Kidney Dis. |volume=68 |issue=6 |pages=e33–e34 |date=December 2016 |pmid=27884283 |doi=10.1053/j.ajkd.2016.10.006 |url=}}</ref>
| colspan="2" |'''''Click for more information on [[Thrombotic microangiopathies|Thrombotic Microangiopathies]].'''''
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +/-
| +/-
| +/-
| -
| -
| -
|
|
+ ([[P-ANCA]])
* Acute stage:
|<nowiki>-</nowiki>
** Inravasculr fibrin thrombi
|<nowiki>-</nowiki>
* Chronic stage:
** Endocapillary hypercellularity.
** Intimal proliferation of [[Arteriole|arterioles]]
|
* Swollen glomerular endothelial cells with loss of [[Fenestration|fenestrations]]
* Chronic stage: interposed cells with new [[GBM]] matrix material deposition.
|
|
* Hypercellular and [[inflamed]] [[glomeruli]] (Crescent formation)
* [[Thrombus|Thrombi]] stain positive for [[fibrinogen]]
|<nowiki>- (pauci-immune)</nowiki>
|<nowiki>-</nowiki>
|-
|-
![[Membranoproliferative glomerulonephritis]]
! colspan="2" |[[Antiphospholipid syndrome|Antiphospholipid Antibody Syndrome]] <ref name="pmid24684307">{{cite journal| author=Jayakody Arachchillage D, Greaves M| title=The chequered history of the antiphospholipid syndrome. | journal=Br J Haematol | year= 2014 | volume= 165 | issue= 5 | pages= 609-17 | pmid=24684307 | doi=10.1111/bjh.12848 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24684307  }}</ref><ref name="pmid246843072">{{cite journal| author=Jayakody Arachchillage D, Greaves M| title=The chequered history of the antiphospholipid syndrome. | journal=Br J Haematol | year= 2014 | volume= 165 | issue= 5 | pages= 609-17 | pmid=24684307 | doi=10.1111/bjh.12848 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24684307  }}</ref><ref name="pmid18714484">{{cite journal| author=Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C et al.| title=[Primary antiphospholipid syndrome]. | journal=Oftalmologia | year= 2008 | volume= 52 | issue= 1 | pages= 13-7 | pmid=18714484 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18714484  }}</ref>
|
|
* [[Idiopathic]]
* [[Thrombosis]]
* [[Hepatitis B]] and [[Hepatitis C|C]] (Type 1)
* [[Miscarriage]] 
* C3 nepritic factor (Type2)
* History of [[nephropathy]]
* History of [[Hematology|hematologic]] abnormalities
* Nonthrombotic neurologic symptoms, such as [[migraine]] headaches
* [[Pulmonary hypertension]]
|
|
* [[Hematuria]]
*[[Fatigue]]
* [[Oliguria]]
*[[Fever]]
* [[Periorbital edema]]
*[[Weight loss]]
* [[Hypertension]]
 
*[[Venous thrombosis]]
*[[Arterial thrombosis]]  
*[[Thrombocytopenia]]
*Recurrent fetal loss     
| +
|<nowiki>+/-</nowiki>
|<nowiki>+/-</nowiki>
|<nowiki>+</nowiki>
| +
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
| +/-
|<nowiki>+</nowiki>
| -
|<nowiki>-</nowiki>
| -
|<nowiki>+</nowiki>
| -
|<nowiki>-</nowiki>
|
|<nowiki>-</nowiki>
* Acute stage:
|<nowiki>-</nowiki>
** Inravasculr fibrin [[Thrombus|thrombi]]
|<nowiki>+</nowiki>
* Chronic stage:
** [[Endocapillary proliferative glomerulonephritis|Endocapillary]] hypercellularity.
** Intimal proliferation of [[Arteriole|arterioles]]
|
|
* Thick [[glomerular basement membrane]] (Tram-track appearance)
* Swollen glomerular endothelial cells with loss of fenestrations
* Chronic stage: interposed cells with new GBM matrix material deposition.
|
|
* [[Mesangial cell|Mesangial]] proliferation and [[Leukocytes|leukocyte]] infiltration
* [[Thrombus|Thrombi]] stain positive for [[fibrinogen]]
|<nowiki>+ (Granular)</nowiki>
|}
|}
<small>
'''Some infectious diseases such as [[HIV]], [[Hepatitis B virus|HBV]], [[Hepatitis C|HCV]], [[syphilis]], [[leprosy]], [[malaria]], and [[schistosomiasis]] may cause glomerular diseases.'''
==Images==
[http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 1.jpg|This is a low-power photomicrograph of a saggital section of end stage chronic glomerulonephritis (GN). Note the marked thinning of the cortex (arrow).
Image:Glomerulonephritis case 2.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (arrows) and glomeruli with thick basement membranes.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 3.jpg|This is a higher-power photomicrograph of hyalinized glomeruli (1) and glomeruli with thickened basement membranes (2).
Image:Glomerulonephritis case 4.jpg|This is a photomicrograph of interstitial and vascular lesions in end stage renal disease.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 5.jpg|This is an immunofluorescent photomicrograph of granular membranous immunofluorescence (immune complex disease). The antibody used for these studies was specific for IgG.
Image:Glomerulonephritis case 6.jpg|This is an electron micrograph of subepithelial granular electron dense deposits (arrows) which correspond to the granular immunofluorescence seen in the previous image.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 7.jpg|This is a photomicrograph of a glomerulus from another case with acute poststreptococcal glomerulonephritis. In this case the immune complex glomerular disease is ongoing with necrosis and accumulation of neutrophils in the glomerulus.
Image:Glomerulonephritis case 8.jpg|This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.
</gallery>
</div>
<div align="left">
<gallery heights="175" widths="175">
Image:Glomerulonephritis case 9.jpg|This electron micrograph demonstrates scattered subepithelial dense deposits (arrows) and a polymorphonuclear leukocyte in the lumen.
Image:Glomerulonephritis case 10.jpg|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.
</gallery>
</div>
===Microscopic Pathology===
[http://www.peir.net Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<div align="left">
<gallery heights="175" widths="175">
image:Acute GN 1.jpg|Glomerulonephritis: Micro H&E med mag; an excellent example of AGN with many neutrophils
image:Acute GN 2.jpg|Acute Glomerulonephritis: Micro H&E high mag; an  excellent example of acute exudative glomerulonephritis.
</gallery>
</div>
<br>
===Glomerulonephritis Videos===
====Rapidly progressive glomerulonephritis====
{{#ev:youtube|CqSyj4cVZPE}}
====Chronic glomerulonephritis====
{{#ev:youtube|eA1vYarRAWo}}
===Images:===
*[http://www.pathologyatlas.ro/Crescentic%20Glomerulonephritis.html Crescentic GN]
*[http://www.pathologyatlas.ro/Chronic%20Glomerulonephritis1.html Chronic GN]


==References==
==References==
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[[Category:Disease]]
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[[Category:Inflammations]]
[[Category:Kidney diseases]]
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Latest revision as of 21:53, 29 July 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2], Syed Hassan A. Kazmi BSc, MD [3]

This page contains general information about Glomerular disease.
For more information on specific types, please visit the pages on:

Nephritic syndrome
Nephrotic syndrome
Fabry's disease
Post-streptococcal glomerulonephritis
Lupus nephritis
Antiglomerular basement membrane disease
(Goodpasture's syndrome)
Cryoglobulinemia
Henoch-Schönlein purpura
Amyloidosis
Pulmonary-renal syndromes (vasculitis)
Thin basement membrane disease
Alport's Syndrome
anti-GBM Disease
Hypertensive nephrosclerosis
Subacute bacterial endocarditis


Overview

Glomerular disease is a condition that affects the glomerulus. It consists of different diseases with different clinical courses and treatment options. Glomerular disease can be isolated hematuria, isolated proteinuria; acute or chronic glomerulonephritis, and nephrotic or nephritic features of glomerulonephritis. The end stage of all of these diseases will be glomerulosclerosis which is characterized by fibrosis of the glomerulus, and end-stage renal disease.

Classification

Glomerular dieseases can be classified into several clinical and pathological syndromes as below:

Syndrome Disease
Acute nephritic syndromes
Nephrotic syndrome
Glomerular Deposition Diseases
Pulmonary-Renal Syndromes:
Basement Membrane Syndromes
Glomerular-Vascular Syndromes
Infectious Disease–Associated Syndromes

Also, glomerular diseases can be classified based on their clinical and urinary pattern in to below types:

Mild nephritc:

This category include mild nephritic sediment that is associated with less than half involvement of glomeruli.

Severe nephritic:

More severe clinical features such as edema, heavy proteinuria, hypertension, and/or renal failure may occur.

Nephrotic:

This syndrome is associated with heavy proteinuria and lipiduria.

Glomerular diseases also may classified by their presentation as below:

Glomerular hematuria:

1- Isolated hematuria

2- Glomerulonephritis (nephritic syndrome)

Proteinuria:

1-Isolated non-nephrotic proteinuria 

2- Nephrotic syndrome

Rapidly progressive glomerulonephritis

Glomerulonephritis

Glomerulonephritis which is inflammation of the glomeruli can be classified based on pathogenic type into three subtypes:

  • Anti-GBM disease: Linear deposit
    1. Goodpasture syndrome (renal and lung involvement)
    2. Renal involvement alone
    3. Lung involvement alone

Glomerulonephritis (nephritic syndrome) also may be classified based on disease course into acute or chronic nephritic syndrome; primary vs secondary causes; or systemic vs renal limited disease. For more information about nephritic syndrome classifications click here.

Differential Diagnosis

The various types of glomerular diseases should be differentiated from each other based on associations, presence of pitting edema, hematuria, hypertension, hemoptysis, oliguria, peri-orbital edema, hyperlipidemia, type of antibodies, light and electron microscopic features. The following table differentiates between various types of glumerular diseases:

Glomerular diseases Disease History and Symtoms Laboratory Findings Pathology
History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Acute Nephritic Syndromes Poststreptococcal Glomerulonephritis[1][2][3] +/- + +/- +/- +/- +/- +/- +/-
  • Immune complex GN
  • Granular deposit
Renal disease due to Subacute Bacterial Endocarditis, or cardiac shunt (Atrioventricular)[4][5] +/- + +/- +/- +/- +/- +/- +/-
  • Crescentic GN is the most common pathological features
  • Mesangial deposits,
  • Subendothelial deposits
  • Subepithelial "humps," in minority of cases
  • Pauci-immune GN
Lupus Nephritis[6]
  • History of SLE features
+/- + +/- +/- +/- +/- +/- +/-
  • Differs based on the disease classification
  • Differs based on the disease classification
  • Differs based on the disease classification, mostly immune complex GN
  • Granular deposit
Antiglomerular Basement Membrane Disease (Goodpasture's syndrome)[7][8]
  • Young adults
+ + + + + + - - Diffuse thickening of the glomerular basement membrane with absence of sub-epithelial and sub-endothelial deposits 
  • Immune complex GN
  • Linear deposit
IgA Nephropathy[9][10] + +/- + +/- + - + -
  • Immune complex deposition
  • Crescent formation
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
ANCA Small-Vessel Vasculitis[11][12] Granulomatosis with Polyangiitis (Wegener's)[13][14][15]
  • Middle age male
+ + + +/- + - + -
  •  Pauci-immune GN
Microscopic Polyangiitis[16] +/- + + + + + + -
  •  Pauci-immune GN
Churg-Strauss Syndrome[17] +/- + + + + + + -
  •  Pauci-immune GN
Membranoproliferative Glomerulonephritis[18][19] + + + +/- + + - - -
  • Immune complex GN
  • Granular deposite
Henoch-Schönlein purpura [20] + + + +/- + + - - -
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Diffuse mesangial IgA deposits often associated with mesangial hypercellularity
  • Immune complex GN, granular deposite
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Cryoglobulinemia[21] Patients having cryoglobulinemia may have positive history of: Pulmonary symptoms:
  • Cough

Cutaneous symptoms:

Gastrointestinal symptoms:

  • Abdominal pain

General symptoms:

+/- + +/- + +/- +/- +/- +/- +/-
  • Prominent IgM and C3
Nephrotic Syndrome Minimal Change Disease[22][23] - + - + +/- + - +
  • Normal
-
Focal Segmental Glomerulosclerosis[24][25][26] - + - + +/- + - + -
Membranous Glomerulonephritis[27][28] - + - + +/- + - + Immune complex deposition Immune complex GN, granular deposite
Diabetic Nephropathy[29][30][31][32][33][34][35][36][37][38] For more information on diabetes click here. - + - + +/- + - +
  • Diffuse mesangial matrix expansion (nodular glomerulosclerosis)
  • Increased mesangial hypercellularity
  • Prominent glomerular basement membranes
  • Thick basement membrane without any deposit
  • Nodular glomerulosclerosis
-
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
 Glomerular Deposition Diseases  Light Chain Deposition Disease[39]
  • Occurs in the setting of high tumor burden
- - + - + +/- + - + -
  • Light-chain deposits
  • Granular deposits on electron microscopy
  • Detection of light chain deposits using anti–light chain antibody
Renal Amyloidosis[40][41][42][43] - + - + +/- + - + -
  • Diffuse glomerular deposition of amorphous hyaline material (nodular pattern), in mesangium (weakly staining with periodic acid-Schiff (PAS)
  • Nodular deposit
  • AA amyloidosis type: negative for immunoglobulins and complement
  • AL amyloidosis type: Positive for lambda or kappa light chains
Fibrillary-Immunotactoid Glomerulopathy[44] - +/- + +/- +/- +/- + +/- +/- -
  • Diffuse sclerosing glomerulonephritis
  • Diffuse proliferative glomerulonephritis
  • Membranoproliferative glomerulonephritis
  • Mesangioproliferative/sclerosing disease
  • Membranous glomerulonephritis
  • Large fibrillar deposits in the mesangium randomly
  • Glomerular capillary walls different from amloidosis
  • No staining with Congo red or thioflavine-T or with antibodies to a specific type
  • Positive for immunoglobulin G (IgG), C3
  • Kappa and lambda (ie, polyclonal) light chains
Fabry's Disease[45][46][47] - + - + +/- + - + -
  • Vacuolization of visceral glomerular epithelial cells (podocytes) and distal tubular epithelial cells
  • Glycolipid accumulation
  • Myeloid or zebra bodies: Gb3 deposition within enlarged secondary lysosomes as lamellated membrane structures
  • Inclusions, composed of concentric layers (onion skin appearance)
-
Basement Membrane Syndrome Alport's Syndrome[48][49][50][51][52][53]
  • Positive family history
Auditary:

Occular problems:

  • Refractory Error
- + - + +/- + - + -
  • Early stage: unremarkable
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Thin Basement Membrane Disease[54][55] - - + -/+ - -/+ - -/+ - - - Diffuse thinning of the glomerular basement membranes (GBM) -
Nail-Patella Syndrome[56][57]
  • Positive family history
  • Poorly developed fingernails, toe nails, and patellae (kneecaps).
  • Elbow deformities
  • Abnormally shaped pelvis bone (hip bone)
  • Knee may be small, deformed or absent
+ + - - - - - - -
  • Mostly unremarkable changes
  • Secondary FSGS
  • Late stages:
    • Global glomerulosclerosis,
    • Tubulointerstitial fibrosis
  • Glomerular basement membranes (GBMs): Focal or diffuse irregular thickening with electron-lucent areas (moth-eaten appearance) containing type III collagen bundles.
  • Similar collagen fibrils can be seen in mesangial matrix.
  • Podocytes: Segmental effacement of foot processes.
  • Nonspecific IgM and C3 deposition may be seen in sclerotic glomeruli.
 Glomerular-Vascular Syndromes  Hypertensive Nephrosclerosis[58] Chronic hypertension +/- +/- + +/- +/- +/- - +/- -
  • Interstitial fibrosis and atrophy
  • Medial thickening and intimal fibrosis of medium-sized and larger vessels
  • Arteriolar thickening, and hyalinosis
  • Chronic stages:
Cholesterol Emboli[59]
  • Depends on the organ involved
+/- +/- + +/- +/- +/- - +/- -
  • Atheroemboli are seen in interlobular and arcuate arteries, as lance-shaped clefts, due to dissolution of cholesterol crystals
  • Acute lesions:
    • Atheroemboli are surrounded by red blood cells, fibrin, and leukocytes, with multinucleated giant cell reactions
  • Chronic lesions:
    • Cholesterol clefts are surrounded by intimal fibrosis
    • Vessel recanalization of chronic lesions can occur.
  • Global and segmental sclerosis of glomeruli may be present.
  • Extensive foot process effacement can be seen
  • Not specific changes
Disease History Systemic symptoms Hemeturia Proteinuria Hypertension Pitting edema Oliguria Nephrotic features Nephritic features Hyperlipidemia and hypercholesterolemia Auto-antibodies,

Complements

Light microscope Electron microscope Immunoflourescence pattern
Sickle Cell Disease[60]
  • Positive family history
+/- +/- +/- - - - - - -
  • Glomerular hypertrophy
  • Hemosiderin deposits
  • Focal areas of hemorrhage or necrosis
  • Chronic stage: interstitial inflammation, edema, fibrosis, tubular atrophy, and papillary infarcts
  • Glomerular enlargement and focal segmental glomerulosclerosis (FSGS)
Thrombotic Microangiopathies[61] Click for more information on Thrombotic Microangiopathies. + +/- + +/- +/- +/- - - -
  • Acute stage:
    • Inravasculr fibrin thrombi
  • Chronic stage:
    • Endocapillary hypercellularity.
    • Intimal proliferation of arterioles
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.
Antiphospholipid Antibody Syndrome [62][63][64] + +/- + +/- +/- +/- - - -
  • Swollen glomerular endothelial cells with loss of fenestrations
  • Chronic stage: interposed cells with new GBM matrix material deposition.


Some infectious diseases such as HIV, HBV, HCV, syphilis, leprosy, malaria, and schistosomiasis may cause glomerular diseases.

Images

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology


Microscopic Pathology

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology


Glomerulonephritis Videos

Rapidly progressive glomerulonephritis

{{#ev:youtube|CqSyj4cVZPE}}


Chronic glomerulonephritis

{{#ev:youtube|eA1vYarRAWo}}

Images:

References

  1. GERMUTH FG (1953). "A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type". J Exp Med. 97 (2): 257–82. PMC 2136196. PMID 13022878.
  2. Germuth FG, Senterfit LB, Dreesman GR (1972). "Immune complex disease. V. The nature of the circulating complexes associated with glomerular alterations in the chronic BSA-rabbit system". Johns Hopkins Med J. 130 (6): 344–57. PMID 5031005.
  3. Radhakrishnan J, Cattran DC (2012). "The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient". Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
  4. Neugarten J, Baldwin DS (August 1984). "Glomerulonephritis in bacterial endocarditis". Am. J. Med. 77 (2): 297–304. PMID 6380288.
  5. Arze RS, Rashid H, Morley R, Ward MK, Kerr DN (January 1983). "Shunt nephritis: report of two cases and review of the literature". Clin. Nephrol. 19 (1): 48–53. PMID 6831779.
  6. Weening JJ, D'Agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, Balow JE, Bruijn JA, Cook T, Ferrario F, Fogo AB, Ginzler EM, Hebert L, Hill G, Hill P, Jennette JC, Kong NC, Lesavre P, Lockshin M, Looi LM, Makino H, Moura LA, Nagata M (February 2004). "The classification of glomerulonephritis in systemic lupus erythematosus revisited". Kidney Int. 65 (2): 521–30. doi:10.1111/j.1523-1755.2004.00443.x. PMID 14717922.
  7. Bolton WK (November 1996). "Goodpasture's syndrome". Kidney Int. 50 (5): 1753–66. PMID 8914046.
  8. Mathew TH, Hobbs JB, Kalowski S, Sutherland PW, Kincaid-Smith P (February 1975). "Goodpasture's syndrome: normal renal diagnostic findings". Ann. Intern. Med. 82 (2): 215–8. PMID 1090223.
  9. Suzuki H, Kiryluk K, Novak J, Moldoveanu Z, Herr AB, Renfrow MB, Wyatt RJ, Scolari F, Mestecky J, Gharavi AG, Julian BA (October 2011). "The pathophysiology of IgA nephropathy". J. Am. Soc. Nephrol. 22 (10): 1795–803. doi:10.1681/ASN.2011050464. PMC 3892742. PMID 21949093.
  10. Wyatt RJ, Julian BA (June 2013). "IgA nephropathy". N. Engl. J. Med. 368 (25): 2402–14. doi:10.1056/NEJMra1206793. PMID 23782179.
  11. Higgins RM, Goldsmith DJ, Connolly J, Scoble JE, Hendry BM, Ackrill P, Venning MC (January 1996). "Vasculitis and rapidly progressive glomerulonephritis in the elderly". Postgrad Med J. 72 (843): 41–4. PMC 2398323. PMID 8746284.
  12. Jennette JC (March 2003). "Rapidly progressive crescentic glomerulonephritis". Kidney Int. 63 (3): 1164–77. doi:10.1046/j.1523-1755.2003.00843.x. PMID 12631105.
  13. Renaudineau Y, Le Meur Y (October 2008). "Renal involvement in Wegener's granulomatosis". Clin Rev Allergy Immunol. 35 (1–2): 22–9. doi:10.1007/s12016-007-8066-6. PMID 18172777.
  14. Weiss MA, Crissman JD (October 1984). "Renal biopsy findings in Wegener's granulomatosis: segmental necrotizing glomerulonephritis with glomerular thrombosis". Hum. Pathol. 15 (10): 943–56. PMID 6384024.
  15. Pagnoux C (March 2008). "[Wegener's granulomatosis and microscopic polyangiitis]". Rev Prat (in French). 58 (5): 522–32. PMID 18524109.
  16. Chung SA, Seo P (August 2010). "Microscopic polyangiitis". Rheum. Dis. Clin. North Am. 36 (3): 545–58. doi:10.1016/j.rdc.2010.04.003. PMC 2917831. PMID 20688249.
  17. Sinico RA, Di Toma L, Maggiore U, Tosoni C, Bottero P, Sabadini E, Giammarresi G, Tumiati B, Gregorini G, Pesci A, Monti S, Balestrieri G, Garini G, Vecchio F, Buzio C (May 2006). "Renal involvement in Churg-Strauss syndrome". Am. J. Kidney Dis. 47 (5): 770–9. doi:10.1053/j.ajkd.2006.01.026. PMID 16632015.
  18. Alchi B, Jayne D (August 2010). "Membranoproliferative glomerulonephritis". Pediatr. Nephrol. 25 (8): 1409–18. doi:10.1007/s00467-009-1322-7. PMC 2887509. PMID 19908070.
  19. Davis AE, Schneeberger EE, Grupe WE, McCluskey RT (May 1978). "Membranoproliferative glomerulonephritis (MPGN type I) and dense deposit disease (DDD) in children". Clin. Nephrol. 9 (5): 184–93. PMID 657595.
  20. Jennette JC, Falk RJ (July 1994). "The pathology of vasculitis involving the kidney". Am. J. Kidney Dis. 24 (1): 130–41. PMID 8023818.
  21. Fogo AB, Lusco MA, Najafian B, Alpers CE (February 2016). "AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis". Am. J. Kidney Dis. 67 (2): e5–7. doi:10.1053/j.ajkd.2015.12.007. PMID 26802335.
  22. Saha TC, Singh H (November 2006). "Minimal change disease: a review". South. Med. J. 99 (11): 1264–70. doi:10.1097/01.smj.0000243183.87381.c2. PMID 17195422.
  23. Saleem MA, Kobayashi Y (2016). "Cell biology and genetics of minimal change disease". F1000Res. 5. doi:10.12688/f1000research.7300.1. PMC 4821284. PMID 27092244.
  24. Rosenberg AZ, Kopp JB (March 2017). "Focal Segmental Glomerulosclerosis". Clin J Am Soc Nephrol. 12 (3): 502–517. doi:10.2215/CJN.05960616. PMC 5338705. PMID 28242845.
  25. Jefferson JA, Shankland SJ (September 2014). "The pathogenesis of focal segmental glomerulosclerosis". Adv Chronic Kidney Dis. 21 (5): 408–16. doi:10.1053/j.ackd.2014.05.009. PMC 4149756. PMID 25168829.
  26. Gephardt GN, Tubbs RR, Popowniak KL, McMahon JT (October 1986). "Focal and segmental glomerulosclerosis. Immunohistologic study of 20 renal biopsy specimens". Arch. Pathol. Lab. Med. 110 (10): 902–5. PMID 2429634.
  27. Lai WL, Yeh TH, Chen PM, Chan CK, Chiang WC, Chen YM, Wu KD, Tsai TJ (February 2015). "Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment". J. Formos. Med. Assoc. 114 (2): 102–11. doi:10.1016/j.jfma.2014.11.002. PMID 25558821.
  28. Wasserstein AG (April 1997). "Membranous glomerulonephritis". J. Am. Soc. Nephrol. 8 (4): 664–74. PMID 10495797.
  29. Drummond K, Mauer M, International Diabetic Nephropathy Study Group (2002). "The early natural history of nephropathy in type 1 diabetes: II. Early renal structural changes in type 1 diabetes". Diabetes. 51 (5): 1580–7. PMID 11978659.
  30. Hørlyck A, Gundersen HJ, Osterby R (1986). "The cortical distribution pattern of diabetic glomerulopathy". Diabetologia. 29 (3): 146–50. PMID 3699305.
  31. Alpers CE, Hudkins KL (2011). "Mouse models of diabetic nephropathy". Curr Opin Nephrol Hypertens. 20 (3): 278–84. doi:10.1097/MNH.0b013e3283451901. PMC 3658822. PMID 21422926.
  32. Kimmelstiel P, Wilson C (1936). "Intercapillary Lesions in the Glomeruli of the Kidney". Am J Pathol. 12 (1): 83–98.7. PMC 1911022. PMID 19970254.
  33. Alpers CE, Biava CG (1989). "Idiopathic lobular glomerulonephritis (nodular mesangial sclerosis): a distinct diagnostic entity". Clin Nephrol. 32 (2): 68–74. PMID 2766585.
  34. Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M (2007). "Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy". Diabetes. 56 (8): 2155–60. doi:10.2337/db07-0019. PMID 17536064.
  35. Najafian B, Crosson JT, Kim Y, Mauer M (2006). "Glomerulotubular junction abnormalities are associated with proteinuria in type 1 diabetes". J Am Soc Nephrol. 17 (4 Suppl 2): S53–60. doi:10.1681/ASN.2005121342. PMID 16565248.
  36. Najafian B, Kim Y, Crosson JT, Mauer M (2003). "Atubular glomeruli and glomerulotubular junction abnormalities in diabetic nephropathy". J Am Soc Nephrol. 14 (4): 908–17. PMID 12660325.
  37. Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  38. Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  39. Hutchison CA, Cockwell P, Stringer S, Bradwell A, Cook M, Gertz MA, Dispenzieri A, Winters JL, Kumar S, Rajkumar SV, Kyle RA, Leung N (June 2011). "Early reduction of serum-free light chains associates with renal recovery in myeloma kidney". J. Am. Soc. Nephrol. 22 (6): 1129–36. doi:10.1681/ASN.2010080857. PMC 3103732. PMID 21511832.
  40. Baker KR, Rice L (2012). "The amyloidoses: clinical features, diagnosis and treatment". Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
  41. Gillmore JD, Hawkins PN (October 2013). "Pathophysiology and treatment of systemic amyloidosis". Nat Rev Nephrol. 9 (10): 574–86. doi:10.1038/nrneph.2013.171. PMID 23979488.
  42. Jerzykowska S, Cymerys M, Gil LA, Balcerzak A, Pupek-Musialik D, Komarnicki MA (2014). "Primary systemic amyloidosis as a real diagnostic challenge - case study". Cent Eur J Immunol. 39 (1): 61–6. doi:10.5114/ceji.2014.42126. PMC 4439975. PMID 26155101.
  43. Pepys MB (2006). "Amyloidosis". Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
  44. Korbet SM, Schwartz MM, Lewis EJ (March 1991). "Immunotactoid glomerulopathy". Am. J. Kidney Dis. 17 (3): 247–57. PMID 1996564.
  45. Alroy J, Sabnis S, Kopp JB (June 2002). "Renal pathology in Fabry disease". J. Am. Soc. Nephrol. 13 Suppl 2: S134–8. PMID 12068025.
  46. Meikle PJ, Hopwood JJ, Clague AE, Carey WF (1999). "Prevalence of lysosomal storage disorders". JAMA : the Journal of the American Medical Association. 281 (3): 249–54. PMID 9918480. Unknown parameter |month= ignored (help)
  47. Branton MH, Schiffmann R, Sabnis SG; et al. (2002). "Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course". Medicine. 81 (2): 122–38. PMID 11889412. Unknown parameter |month= ignored (help)
  48. McCarthy PA, Maino DM (2000). "Alport syndrome: a review". Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  49. Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). "Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds". Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  50. Chugh KS, Sakhuja V, Agarwal A, Jha V, Joshi K, Datta BN; et al. (1993). "Hereditary nephritis (Alport's syndrome)--clinical profile and inheritance in 28 kindreds". Nephrol Dial Transplant. 8 (8): 690–5. PMID 8414153.
  51. McCarthy PA, Maino DM (2000). "Alport syndrome: a review". Clin Eye Vis Care. 12 (3–4): 139–150. PMID 11137428.
  52. Amari F, Segawa K, Ando F (1994). "Lens coloboma and Alport-like glomerulonephritis". Eur J Ophthalmol. 4 (3): 181–3. PMID 7819734.
  53. Govan JA (1983). "Ocular manifestations of Alport's syndrome: a hereditary disorder of basement membranes?". Br J Ophthalmol. 67 (8): 493–503. PMC 1040106. PMID 6871140.
  54. Savige J, Rana K, Tonna S, Buzza M, Dagher H, Wang YY (2003). "Thin basement membrane nephropathy". Kidney Int. 64 (4): 1169–78. doi:10.1046/j.1523-1755.2003.00234.x. PMID 12969134. Unknown parameter |month= ignored (help)
  55. Hou P, Chen Y, Ding J, Li G, Zhang H (2007). "A novel mutation of COL4A3 presents a different contribution to Alport syndrome and thin basement membrane nephropathy". Am. J. Nephrol. 27 (5): 538–44. doi:10.1159/000107666. PMID 17726307.
  56. Najafian B, Smith K, Lusco MA, Alpers CE, Fogo AB (October 2017). "AJKD Atlas of Renal Pathology: Nail-Patella Syndrome-Associated Nephropathy". Am. J. Kidney Dis. 70 (4): e19–e20. doi:10.1053/j.ajkd.2017.08.001. PMID 28941488.
  57. Guidera KJ, Satterwhite Y, Ogden JA, Pugh L, Ganey T (1991). "Nail patella syndrome: a review of 44 orthopaedic patients". J Pediatr Orthop. 11 (6): 737–42. PMID 1960197.
  58. Hughson MD, Puelles VG, Hoy WE, Douglas-Denton RN, Mott SA, Bertram JF (July 2014). "Hypertension, glomerular hypertrophy and nephrosclerosis: the effect of race". Nephrol. Dial. Transplant. 29 (7): 1399–409. doi:10.1093/ndt/gft480. PMC 4071048. PMID 24327566.
  59. Lusco MA, Najafian B, Alpers CE, Fogo AB (April 2016). "AJKD Atlas of Renal Pathology: Cholesterol Emboli". Am. J. Kidney Dis. 67 (4): e23–4. doi:10.1053/j.ajkd.2016.02.034. PMID 27012950.
  60. Wesson DE (June 2002). "The initiation and progression of sickle cell nephropathy". Kidney Int. 61 (6): 2277–86. doi:10.1046/j.1523-1755.2002.00363.x. PMID 12028473.
  61. Lusco MA, Fogo AB, Najafian B, Alpers CE (December 2016). "AJKD Atlas of Renal Pathology: Thrombotic Microangiopathy". Am. J. Kidney Dis. 68 (6): e33–e34. doi:10.1053/j.ajkd.2016.10.006. PMID 27884283.
  62. Jayakody Arachchillage D, Greaves M (2014). "The chequered history of the antiphospholipid syndrome". Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  63. Jayakody Arachchillage D, Greaves M (2014). "The chequered history of the antiphospholipid syndrome". Br J Haematol. 165 (5): 609–17. doi:10.1111/bjh.12848. PMID 24684307.
  64. Popa A, Voinea L, Pop M, Stana D, Dascalu AM, Alexandrescu C; et al. (2008). "[Primary antiphospholipid syndrome]". Oftalmologia. 52 (1): 13–7. PMID 18714484.

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