Acute Poststreptococcal Glomerulonephritis Differential Diagnoses

  • Author: Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal); Chief Editor: Craig B Langman, MD   more...
 
Updated: Sep 21, 2011
 
 

Diagnostic Considerations

In the evaluation of a patient with acute glomerulonephritis, if evidence of a previous streptococcal infection is missing or inconclusive, then a search for another infectious cause appears appropriate.

See also Acute Glomerulonephritis and Emergent Management of Acute Glomerulonephritis.

Bacterial and viral infections

The syndrome of acute glomerulonephritis has been reported following many other bacterial illnesses (eg, Streptococcus pneumoniae, Staphylococcus aureus and S epidermidis, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species). In addition, certain viral illnesses have preceded the onset of fairly typical acute glomerulonephritis; among the most common are varicella-zoster virus (VZV), cytomegalovirus (CMV), and the Epstein-Barr virus (EBV).

IgA-associated glomerulonephritis

Immunoglobulin A (IgA)–associated glomerulonephritis may be confused with acute poststreptococcal glomerulonephritis.[4, 18, 42, 54] In the form of IgA nephropathy associated with a typical anaphylactoid purpura (ie, Henoch-Schönlein purpura nephritis), the characteristic rash and the associated symptoms of either abdominal pain or arthritis and/or arthralgia help in the differentiation; however, in atypical cases, marked similarity may be present.

All of the clinical manifestations of APSGN have been reported in persons with Henoch-Schönlein purpura nephritis, although significant hypertension and edema are found less commonly in individuals with Henoch-Schönlein purpura than in those with APSGN. In addition, evidence of a previous streptococcal illness is usually lacking in individuals with Henoch-Schönlein purpura nephritis, and complement values (C3 and/or C4) are usually normal.

Urticarial or purpuric rashes, abdominal complaints, and arthritis and/or arthralgia are found almost exclusively in persons with Henoch-Schönlein purpura.

Berger disease or IgA nephropathy usually presents as an episode of gross hematuria occurring during the early stages of a respiratory illness; no latent period occurs, and hypertension or edema is uncommon.

Recurrent episodes of gross hematuria, associated with respiratory illnesses, followed by persistent microscopic hematuria, are highly suggestive of IgA nephropathy. In contrast, acute poststreptococcal glomerulonephritis usually does not recur, and second episodes are rare.

MPGN

Mesangiocapillary or membranoproliferative glomerulonephritis (MPGN) may have a presentation that is virtually identical to that of poststreptococcal acute glomerulonephritis. The initial manifestations are often more serious in persons with MPGN than in those with IgA nephropathy; the renal function is reduced markedly (ie, large elevation of serum creatinine).

Evidence of preexisting streptococcal infection is absent, although cases of MPGN have been reported in which clear evidence of such an infection is present. In most cases, C3 levels are depressed persistently, longer than 6 weeks.

Urinary abnormalities persist past the time of expected resolution for acute poststreptococcal glomerulonephritis.

Crescentic glomerulonephritis

Crescentic glomerulonephritis is the term used to describe a histologic picture of severe proliferative glomerulonephritis. In persons with crescentic glomerulonephritis, in addition to inflammatory changes within the glomerular tuft, extensive proliferation exists within the Bowman space, leading to the formation of synechiae between the glomerular tuft and Bowman capsule.[42]

The clinical picture is generally referred to as rapidly progressive glomerulonephritis and may be secondary to numerous causes, including an immune-complex mediated poststreptococcal nephritis. The initial clinical picture is generally severe, and resolution appears delayed.

Other types of glomerulonephritis

Other forms of glomerulonephritis (eg, systemic lupus erythematosus nephritis, familial nephritis, chronic glomerulonephritis) may occasionally be confused with acute poststreptococcal glomerulonephritis when an acute exacerbation of the previously present nephropathy is present. In addition to the lack of expected complete resolution, other features suggest a condition other than acute poststreptococcal glomerulonephritis.

See Hemolytic Complement under Workup for the differential diagnosis of acute glomerulonephritis according to C3 levels.

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal)  Associate Professor of Pediatrics, Principal Specialist, Department of Pediatrics and Child Health, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa

Rajendra Bhimma, MB, ChB, MD, DCH (SA), FCP (Paeds)(SA), MMed (Natal) is a member of the following medical societies: American Association for the Advancement of Science, International Pediatric Transplant Association, International Society of Nephrology, South African Medical Association, South African Paediatric Association, and South African Transplant Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard Neiberger, MD, PhD  Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Adrian Spitzer, MD  Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, Children's Memorial Hospital

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Robert G Schacht, MD, Yang Sun Kim, MD, and Luther Travis, MD,to the development and writing of the source article.

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A schematic representation of the proposed mechanism for acute poststreptococcal glomerulonephritis (APSGN). C = Activated complement; Pl = Plasmin; NAPlr = Nephritis-associated plasmin receptor; SK = Streptokinase; CIC = Circulating immune complex.
 
 
 
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