Rapidly progressive glomerulonephritis diagnostic study of choice: Difference between revisions

Jump to navigation Jump to search
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Rapidly progressive glomerulonephritis}}
{{Rapidly progressive glomerulonephritis}}
{{CMG}}; {{APM}} {{AE}} {{KW}}, {{ADS}}, {{AEL}}  
{{CMG}}; {{APM}} {{AE}} {{KW}}, {{ADS}},  
 
{{AEL}}  


==Overview==
==Overview==
Line 18: Line 20:
** Tubular necrosis may also be present.
** Tubular necrosis may also be present.
** Interstitial granulomas in the glomeruli indicate Wegener’s granulomatosis.
** Interstitial granulomas in the glomeruli indicate Wegener’s granulomatosis.
===Immunoflourescence===
=====Immunoflourescence=====
*In type I RPGN- diffuse and linear deposition of [[Immunoglobulin G|IgG]] along the [[GBM]].
*In type I RPGN- diffuse and linear deposition of [[Immunoglobulin G|IgG]] along the [[GBM]].
*In ttype II RPGN- diffuse and irregular deposition of IgG and C3 in the [[Mesangial cell|mesangial]] matrix.
*In ttype II RPGN- diffuse and irregular deposition of IgG and C3 in the [[Mesangial cell|mesangial]] matrix.
*In type III RPGN- no finding.
*In type III RPGN- no finding.
*
*'''Electron microscopy'''
Diabetic nephropathy and fibrillary glomerulonephritis can be easily distinguished from anti-GBM disease on both clinical and histopathologic grounds. Circulating anti-GBM antibodies are absent in both disorders, and crescents are not seen in diabetic nephropathy. The history of diabetes, the finding of diabetic glomerulosclerosis on light microscopy, and, in fibrillary glomerulonephritis, the presence of the characteristic fibrils on electron microscopy are also helpful.
*In type I and type III, no electron dense deposits are seen.
**In type II RPGN, subepithelial electron dense deposits indiacting the presence of [[Immune complex|immune complexes]] are seen.  


Serologic studies
===== Serologic studies =====
*[[ Complete blood cell count]] (CBC) with[[ differential]],
*[[ Complete blood cell count]] (CBC) with[[ differential]],
**[[ Anemia]] can be seen in patienst with [[renal failure]] or gastrointestinal tract bleeding.
**[[ Anemia]] can be seen in patienst with [[renal failure]] or gastrointestinal tract bleeding.
** [[Eosinophilia]] of 13% or greater suggest [[Churg-Strauss disease]].
** [[Eosinophilia]] greater than 13% suggest [[Churg-Strauss disease]].
* [[Serum electrolytes]]
* [[Serum electrolytes]]
* BUN([[blood urea nitrogen)]]
* BUN([[blood urea nitrogen)]]
Line 41: Line 44:
* C-reactive protein: levels are elevated and correspond with disease activity.
* C-reactive protein: levels are elevated and correspond with disease activity.
*[[ Antinuclear antibody]] (ANA).High ANA titer is present in systemic lupus erythematosus.
*[[ Antinuclear antibody]] (ANA).High ANA titer is present in systemic lupus erythematosus.
* ANCA with ELISA subtyping: More than 80% of patients with microscopic polyangiitis are ANCA-positive, and most of these demonstrate pANCA with MPO specificity. Of patients with granulomatosis with polyangiitis, 90% are ANCA-positive and most have cANCA with PR3 specificity, especially in pulmonary involvement. However, ANCA type and specificity is not pathognomonic for each of these clinical syndromes because some patients with granulomatosis with polyangiitisare pANCA-positive and some patients with microscopic polyangiitis are cANCA-positive. Simon and colleagues investigated the presence of anti-pentraxin 3 (PTX3)- autoantibodies (aAbs) in the sera of antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) patients and found that anti-PTX3 aAbs were present in nearly 40% of patients studied including in patients without detectable MPO and PR3 ANCA.
* Urine and serum protein electrophoresis,helpful in light-chain disease or multiple myeloma..


.
.

Revision as of 13:17, 24 July 2018

Rapidly progressive glomerulonephritis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Rapidly progressive glomerulonephritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray Findings

CT-scan Findings

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Rapidly progressive glomerulonephritis diagnostic study of choice On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Rapidly progressive glomerulonephritis diagnostic study of choice

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Rapidly progressive glomerulonephritis diagnostic study of choice

CDC on Rapidly progressive glomerulonephritis diagnostic study of choice

Rapidly progressive glomerulonephritis diagnostic study of choice in the news

Blogs on Rapidly progressive glomerulonephritis diagnostic study of choice

Directions to Hospitals Treating Rapidly progressive glomerulonephritis

Risk calculators and risk factors for Rapidly progressive glomerulonephritis diagnostic study of choice

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Krzysztof Wierzbicki M.D. [3], Amandeep Singh M.D.[4],

Ahmed Elsaiey, MBBCH [5]

Overview

Rapid diagnosis of rapidly progressive glomerulonephritis is very crucial to save kidneys function

Diagnostic study of choice:

Renal biopsy:

  • Renal biopsy will provide the most accurate reslt.
  • Renal biopsy will give accurate information about the extent of the disease and therapy can be planned accordingly.

results of Renal biopsy:

  • Light microscopy reveals
    • Diffuse inflammation in glomeruli with rupture and damage to glomerular basement membrane.
    • Crescents are present in the Bowmans space.
    • Renal vessels can show transmural vasculitis, with necrosis and lymphocyte infiltrates.
    • Tubular necrosis may also be present.
    • Interstitial granulomas in the glomeruli indicate Wegener’s granulomatosis.
Immunoflourescence
  • In type I RPGN- diffuse and linear deposition of IgG along the GBM.
  • In ttype II RPGN- diffuse and irregular deposition of IgG and C3 in the mesangial matrix.
  • In type III RPGN- no finding.
  • Electron microscopy
  • In type I and type III, no electron dense deposits are seen.
    • In type II RPGN, subepithelial electron dense deposits indiacting the presence of immune complexes are seen.
Serologic studies

.

References