Rapidly progressive glomerulonephritis laboratory findings: Difference between revisions

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==Laboratory Findings==
==Laboratory Findings==
===Blood Work-Up===
===Blood Work-Up===
* Complete blood count (CBC) differential and platelet count
* [[Complete blood count]] (CBC)


* Serum electrolytes
* Serum [[Electrolyte|electrolytes]]


* Creatinine and blood urea nitrogen (BUN)
* [[Creatinine]] and [[blood urea nitrogen]]


* Lactate dehydrogenase (LDH)
* [[Lactate dehydrogenase]] (LDH)


* Creatine phosphokinase (CPK)
* [[Creatine phosphokinase]] (CPK)


* Liver function tests
* [[Liver function tests]]


* Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
* [[Erythrocyte sedimentation rate]] and [[C-reactive protein]] (CRP)


* Antinuclear antibody (ANA)
* [[Anti-nuclear antibody|Antinuclear antibody]] (ANA)


* Anti-GBM antibodies
* [[Anti-glomerular basement membrane antibody|Anti-GBM antibodies]]


* ANCA
* [[ANCA]]


* Cryoglobulins
* [[Cryoglobulins]]


* HBV and HCV titers
* [[Hepatitis B virus|HBV]] and [[Hepatitis C|HCV]] titers


* Complement C3 and C4 levels
* [[Complement]] C3 and C4 levels


* Serum protein electrophoresis
* Serum [[protein electrophoresis]]


Anemia is common among patient with RPGN, mostly due to renally impaired production of erythropoietin or GI bleeding. Eosinophilia may be seen in a subset of patients with Churg-Strauss disease.
[[Anemia]] is common among patient with RPGN, mostly due to renally impaired production of [[erythropoietin]] or [[Gastrointestinal bleeding|GI bleeding]]. [[Eosinophilia]] may be seen in a subset of patients with [[Churg-Strauss syndrome|Churg-Strauss disease]].


Patients with RPGN may show formation of immune complexes and cryoglobulins. Complement C3 levels is usually low in immune-complex mediated RPGN. The presence of ANCA and anti-GBM is variable; their presence is important for classification of disease and further management planning. Anti-GBM levels is However, anti-GBM antibody level is not prognostic and is not associated with disease activity.<ref name="pmid9744974">{{cite journal| author=Hricik DE, Chung-Park M, Sedor JR| title=Glomerulonephritis. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 13 | pages= 888-99 | pmid=9744974 | doi=10.1056/NEJM199809243391306 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9744974 }} </ref> On the contrary, literature regarding ANCA-associated glomerulonephritis suggests that levels of ANCA is associated with disease activity and may be used as an index for such purposes.<ref name="pmid2857806">{{cite journal| author=van der Woude FJ, Rasmussen N, Lobatto S, Wiik A, Permin H, van Es LA et al.| title=Autoantibodies against neutrophils and monocytes: tool for diagnosis and marker of disease activity in Wegener's granulomatosis. | journal=Lancet | year= 1985 | volume= 1 | issue= 8426 | pages= 425-9 | pmid=2857806 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2857806 }} </ref><ref name="pmid2684074">{{cite journal| author=Tervaert JW, van der Woude FJ, Fauci AS, Ambrus JL, Velosa J, Keane WF et al.| title=Association between active Wegener's granulomatosis and anticytoplasmic antibodies. | journal=Arch Intern Med | year= 1989 | volume= 149 | issue= 11 | pages= 2461-5 | pmid=2684074 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2684074 }} </ref><ref name="pmid2221646">{{cite journal| author=Falk RJ, Hogan S, Carey TS, Jennette JC| title=Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network. | journal=Ann Intern Med | year= 1990 | volume= 113 | issue= 9 | pages= 656-63 | pmid=2221646 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2221646 }} </ref>
Patients with RPGN may show formation of [[immune complexes]] and [[cryoglobulins]]. [[Complement|Complement C3]] levels is usually low in immune-complex mediated RPGN. The presence of [[ANCA]] and [[Anti-GBM antibody|anti-GBM]] is variable; their presence is important for classification of disease and further management planning. Anti-GBM levels is However, anti-GBM antibody level is not prognostic and is not associated with disease activity.<ref name="pmid9744974">{{cite journal| author=Hricik DE, Chung-Park M, Sedor JR| title=Glomerulonephritis. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 13 | pages= 888-99 | pmid=9744974 | doi=10.1056/NEJM199809243391306 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9744974 }} </ref>  


ESR and CRP may be elevated and are correlated with the level of inflammation and thus activity of the disease.
On the contrary, literature regarding [[ANCA]]-associated [[glomerulonephritis]] suggests that levels of [[ANCA]] is associated with disease activity and may be used as an index for such purposes.<ref name="pmid2857806">{{cite journal| author=van der Woude FJ, Rasmussen N, Lobatto S, Wiik A, Permin H, van Es LA et al.| title=Autoantibodies against neutrophils and monocytes: tool for diagnosis and marker of disease activity in Wegener's granulomatosis. | journal=Lancet | year= 1985 | volume= 1 | issue= 8426 | pages= 425-9 | pmid=2857806 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2857806 }} </ref><ref name="pmid2684074">{{cite journal| author=Tervaert JW, van der Woude FJ, Fauci AS, Ambrus JL, Velosa J, Keane WF et al.| title=Association between active Wegener's granulomatosis and anticytoplasmic antibodies. | journal=Arch Intern Med | year= 1989 | volume= 149 | issue= 11 | pages= 2461-5 | pmid=2684074 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2684074 }} </ref><ref name="pmid2221646">{{cite journal| author=Falk RJ, Hogan S, Carey TS, Jennette JC| title=Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network. | journal=Ann Intern Med | year= 1990 | volume= 113 | issue= 9 | pages= 656-63 | pmid=2221646 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2221646 }} </ref>
 
[[ESR]] and [[CRP]] may be elevated and are correlated with the level of inflammation and thus activity of the disease.


===Urine Work-Up===
===Urine Work-Up===
*Urinalysis
*[[Urinalysis]]
*Urinary protein electrophoresis
*Urinary [[protein electrophoresis]]
 
*Patients with RPGN do not usually have a full-blown picture of [[nephrotic syndrome]]; Nephrotic syndrome only occurs in less than 30% of cases.<ref name="pmid9744974">{{cite journal| author=Hricik DE, Chung-Park M, Sedor JR| title=Glomerulonephritis. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 13 | pages= 888-99 | pmid=9744974 | doi=10.1056/NEJM199809243391306 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9744974 }} </ref>  
Patients with RPGN do not usually have a full-blown picture of nephrotic syndrome; Nephrotic syndrome only occurs in less than 30% of cases.<ref name="pmid9744974">{{cite journal| author=Hricik DE, Chung-Park M, Sedor JR| title=Glomerulonephritis. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 13 | pages= 888-99 | pmid=9744974 | doi=10.1056/NEJM199809243391306 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9744974 }} </ref> Proteinuria, if present, is usually mild to moderate. Hematuria of glomerular type with dysmorphic red blood cells is usually present on urinalysis and associated with red cell casts. Mild to moderate leukocyturia may be seen and other casts, such as epithelial cell leukocyte, or fatty casts. Urinary findings in RPGN are important features that not only favor diagnostic work-up, but also follow-up and therapeutic effectiveness.  
*[[Proteinuria]], if present, is usually mild to moderate. [[Hematuria]] of glomerular type with [[dysmorphic]] [[Red blood cell|red blood cells]] is usually present on [[urinalysis]] and associated with red cell casts.  
 
*Mild to moderate [[leukocyturia]] may be seen and other [[casts]], such as epithelial cell [[leukocyte]], or fatty casts. Urinary findings in RPGN are important features that not only favor diagnostic work-up, but also follow-up and therapeutic effectiveness.
===Kidney Ultrasound===
Kidney ultrasound is usually done during diagnostic biopsy. Due to its rapid progression, renal biopsy usually shows normal-sized kidneys. Although the test is not diagnostic, its non-invastive nature and the necessity to rule out other etiologies of renal impairment are both in favor of performing a renal ultrasound. 
 
===Kidney Biopsy===
An ultrasound or CT-guided kidney biopsy is the only gold standard to diagnose RPGN and determine prognosis of the disease. The pathological hallmark of RPGN is presence of epithelial crescents in the Bowman’s capsule with or without endocapillary proliferation.<ref name="pmid7360526">{{cite journal| author=Cunningham RJ, Gilfoil M, Cavallo T, Brouhard BH, Travis LB, Berger M et al.| title=Rapidly progressive glomerulonephritis in children: a report of thirteen cases and a review of the literature. | journal=Pediatr Res | year= 1980 | volume= 14 | issue= 2 | pages= 128-32 | pmid=7360526 | doi=10.1203/00006450-198002000-00012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7360526 }} </ref> The extent of fibrous crescents along the glomerulus are considered a poor prognostic element.
 
 
==References==
==References==



Revision as of 15:15, 1 June 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Laboratory Findings

Blood Work-Up

Anemia is common among patient with RPGN, mostly due to renally impaired production of erythropoietin or GI bleeding. Eosinophilia may be seen in a subset of patients with Churg-Strauss disease.

Patients with RPGN may show formation of immune complexes and cryoglobulins. Complement C3 levels is usually low in immune-complex mediated RPGN. The presence of ANCA and anti-GBM is variable; their presence is important for classification of disease and further management planning. Anti-GBM levels is However, anti-GBM antibody level is not prognostic and is not associated with disease activity.[1]

On the contrary, literature regarding ANCA-associated glomerulonephritis suggests that levels of ANCA is associated with disease activity and may be used as an index for such purposes.[2][3][4]

ESR and CRP may be elevated and are correlated with the level of inflammation and thus activity of the disease.

Urine Work-Up

References

  1. 1.0 1.1 Hricik DE, Chung-Park M, Sedor JR (1998). "Glomerulonephritis". N Engl J Med. 339 (13): 888–99. doi:10.1056/NEJM199809243391306. PMID 9744974.
  2. van der Woude FJ, Rasmussen N, Lobatto S, Wiik A, Permin H, van Es LA; et al. (1985). "Autoantibodies against neutrophils and monocytes: tool for diagnosis and marker of disease activity in Wegener's granulomatosis". Lancet. 1 (8426): 425–9. PMID 2857806.
  3. Tervaert JW, van der Woude FJ, Fauci AS, Ambrus JL, Velosa J, Keane WF; et al. (1989). "Association between active Wegener's granulomatosis and anticytoplasmic antibodies". Arch Intern Med. 149 (11): 2461–5. PMID 2684074.
  4. Falk RJ, Hogan S, Carey TS, Jennette JC (1990). "Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network". Ann Intern Med. 113 (9): 656–63. PMID 2221646.

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