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Acute Glomerulonephritis Differential Diagnoses

  • Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Aug 03, 2015
 
 

Diagnostic Considerations

The following four renal syndromes commonly mimic the early stage of acute glomerulonephritis (GN):

  • Anaphylactoid purpura with nephritis
  • Chronic GN with an acute exacerbation
  • Idiopathic hematuria
  • Familial nephritis

Postinfectious GN must be differentiated from the following conditions:

  • Immunoglobulin A (IgA) nephritis - The latent period between infection and onset of nephritis is 1-2 days; alternatively, nephritis may be concomitant with upper respiratory tract infection (ie, “synpharyngitic nephritis,” in contrast to the “postpharyngitic nephritis” seen in poststreptococcal GN [PSGN], which occurs 1-3 weeks later).
  • Membranoproliferative GN (MPGN), types I and II - This is a chronic disease, but it can manifest with an acute nephritic picture with hypocomplementemia; failure of acute nephritis to resolve should prompt consideration of this possibility.
  • Lupus nephritis - Gross hematuria is unusual in lupus nephritis.
  • GN of chronic infection - This can manifest as acute nephritis. Unlike PSGN, in which the infection may have resolved by the time nephritis occurs, patients with nephritis of chronic infection have an active infection at the time nephritis becomes evident. Circulating immune complexes play an important role in the pathogenesis of acute GN in these diseases.
  • Vasculitis - Nephritis of methicillin-resistant Staphylococcus aureus (MRSA) may be associated with vasculitic lesions of the lower extremities.
  • Predominantly nonglomerular diseases - Thrombotic thrombocytopenic purpura (TTP), hemolytic-uremic syndrome (HUS), atheroembolic renal disease, and acute hypersensitivity interstitial nephritis may present with features of acute nephritic syndrome and should be differentiated.

Go to Emergent Management of Acute Glomerulonephritis and Acute Poststreptococcal Glomerulonephritis for complete information on these topics.

Other problems to be considered include the following:

  • Bacterial, viral, and fungal etiologies
  • Chronic GN
  • Idiopathic hematuria
  • IgA nephropathy
  • Irradiation of Wilms tumor
  • Trauma

Differential Diagnoses

 
 
Contributor Information and Disclosures
Author

Malvinder S Parmar, MB, MS FRCP(C), FACP, FASN, Associate Professor, Department of Internal Medicine, Northern Ontario School of Medicine; Assistant Professor, Department of Medicine, University of Ottawa Faculty of Medicine; Consulting Physician, Timmins and District Hospital, Ontario, Canada

Malvinder S Parmar, MB, MS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ajay K Singh, MB, MRCP, MBA Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Chike Magnus Nzerue, MD, FACP Professor of Medicine, Associate Dean for Clinical Affairs, Meharry Medical College

Chike Magnus Nzerue, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

References
  1. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis. Clin Nephrol. 2010 Mar. 73(3):173-9. [Medline].

  2. Oda T, Yoshizawa N, Yamakami K, Sakurai Y, Takechi H, Yamamoto K, et al. The role of nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with streptococcal infection. J Biomed Biotechnol. 2012. 2012:417675. [Medline]. [Full Text].

  3. Nasr SH, Markowitz GS, Stokes MB, et al. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore). 2008 Jan. 87(1):21-32. [Medline].

  4. Safadi R, Almog Y, Dranitzki-Elhalel M, Rosenmann E, Tur-Kaspa R. Glomerulonephritis associated with acute hepatitis B. Am J Gastroenterol. 1996 Jan. 91(1):138-9. [Medline].

  5. Aggarwal A, Kumar D, Kumar R. Acute glomerulonephritis in hepatitis A virus infection: a rare presentation. Trop Doct. 2009 Jul. 39(3):186-7. [Medline].

  6. Tang J, Liu N, Zhuang S. Role of epidermal growth factor receptor in acute and chronic kidney injury. Kidney Int. 2013 Jan 16. [Medline].

  7. Sasaki K, Anderson E, Shankland SJ, Nicosia RF. Diffuse Proliferative Glomerulonephritis Associated With Cetuximab, an Epidermal Growth Factor Receptor Inhibitor. Am J Kidney Dis. 2013 Mar 6. [Medline].

  8. Anochie I, Eke F, Okpere A. Childhood acute glomerulonephritis in Port Harcourt, Rivers State, Nigeria. Niger J Med. 2009 Apr-Jun. 18(2):162-7. [Medline].

  9. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009 May. 24(5):1021-6. [Medline].

  10. Becquet O, Pasche J, Gatti H, et al. Acute post-streptococcal glomerulonephritis in children of French Polynesia: a 3-year retrospective study. Pediatr Nephrol. 2010 Feb. 25(2):275-80. [Medline].

  11. Murakami CA, Attia D, Carter-Monroe N, Lucas GM, Estrella MM, Fine DM, et al. The clinical characteristics and pathological patterns of postinfectious glomerulonephritis in HIV-infected patients. PLoS One. 2014. 9(10):e108398. [Medline]. [Full Text].

  12. Chen S, Chen H, Liu Z, Zhang H, Hu W, Tang Z, et al. Pathological spectrums and renal prognosis of severe lupus patients with rapidly progressive glomerulonephritis. Rheumatol Int. 2015 Apr. 35 (4):709-17. [Medline].

  13. Nebuloni M, Barbiano di Belgiojoso G, Genderini A, et al. Glomerular lesions in HIV-positive patients: a 20-year biopsy experience from Northern Italy. Clin Nephrol. 2009 Jul. 72(1):38-45. [Medline].

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Light microscopy (hematoxylin and eosin stain X 25): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light microscopy (periodic acid-Schiff stain X 40): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Immunofluorescence (X25): Fine granular deposits of immunoglobulin G (IgG) along the basement membrane and mesangium, with "starry sky" appearance. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Ultrastructure (electron microscopy): Photograph showing proliferation of endothelial cells and mesangial cells and leukocyte infiltrate associated with presence of large, subepithelial, electron-dense deposits (ie, "hump") (see arrow). Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
 
 
 
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