eMedicine Specialties > Nephrology > Glomerular Diseases

Glomerulonephritis, Nonstreptococcal Associated With Infection

Author: James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
Coauthor(s): Quresh T Khairullah, MBBS, Consulting Staff, Department of Medicine, Division of Nephrology, St John's Hospital and Medical Center
Contributor Information and Disclosures

Updated: Dec 15, 2008

Introduction

Background

The classic association of glomerulonephritis (GN) with infection is poststreptococcal GN, usually developing after streptococcal pharyngitis (see Glomerulonephritis, Poststreptococcal). However, a number of glomerular diseases are associated with other bacterial, viral, fungal, and parasitic diseases.

Pathophysiology

Most glomerular diseases associated with infection are mediated by the immune complex. The classic example observed in poststreptococcal GN involves an antigen-antibody reaction, which may occur in the circulation or in the glomerulus. Deposition in the glomerulus results in activation of the complement cascade, which may involve either the classic or alternative pathway. The immune complexes may activate endogenous glomerular cells. The reduction of chemotactic factors results in the accumulation of leukocytes and platelets within the glomerulus and, consequently, the inflammatory response.

Several possible pathogenic events occur in viral diseases associated with glomerular injury. These may include the formation of circulating immune complexes involving viral antigens and antibodies, formation of circulating immune complexes induced by the release of antigens following virally induced cellular injury, formation of in situ antigen-antibody reactions or cell-mediated injury, and autoimmune reactions to glomerular structures induced by the virus.

In protozoal infections, such as malaria, antibodies are formed against malarial antigens. The circulating immune complexes activate complement and macrophages. The complexes are primarily deposited in subendothelial areas. A cell-mediated immune response may also occur.

Frequency

United States

The various causes of infection-related GN have different prevalence rates. In endocarditis, associated GN may occur in up to 20% of cases. Staphylococcus aureus has become a more common cause of GN than Streptococcus in developed countries. GN associated with hepatitis C is becoming a far more commonly recognized cause of GN.

International

Although specific numbers for incidence statistics are not available, in certain developing areas of the world, hepatitis B, HIV disease, malaria, and schistosomiasis are major causes of glomerulopathy.

Mortality/Morbidity

Depending on the etiology, the outcome of GN associated with infection can be quite variable.

  • In GN associated with bacterial endocarditis, renal function returns after treatment with antibiotics. The GN usually resolves after the infection has cleared, with renal function beginning to improve within 1-2 weeks, complement levels normalizing within 6 weeks, and hematuria normalizing in approximately 6 months.
  • The course of GNs associated with viral infection is more variable, although patients with HIV nephropathy commonly progress to end-stage renal disease.

Race

This condition is not limited to any particular race.

Sex

In most GNs associated with infection, no sexual predilection exists. However, HIV-associated GN is far more common in males.

Age

This type of GN can occur at any age.

Clinical

History

Presentation may vary from asymptomatic hematuria to a full-blown acute nephritic syndrome consisting of proteinuria, edema, hypertension, and renal failure.

  • Hematuria may be gross or microscopic.
  • Patients may have evidence of edema.
  • Patients may report fever, night sweats, and rigors.
  • Weight loss is a possible complaint.
  • Patients may report arthralgias.
  • Abdominal, chest, or back pain may be caused by a visceral abscess.
  • Patients may have history of shunt placement for hydrocephalus, or they may have a vascular graft that has become infected.
  • Patients with hepatitis B or C may have a history of intravenous drug abuse, needle stick injury, blood transfusions, or sexual promiscuity.
  • Patients with HIV infection may have history of intravenous drug abuse, hemophilia, history of blood transfusion from 1977-1985, unprotected sex with multiple partners, or tuberculosis.

Physical

  • Hypertension may be due to renal failure.
  • Edema due to nephrotic syndrome is unusual but can develop in as many as 30% of cases associated with shunt nephritis.
  • Rash may be maculopapular or purpuric.
  • Lymphadenopathy is a reported finding.
  • Patients may have hepatosplenomegaly.
  • Findings of subacute bacterial endocarditis (SBE) may include the following:
    • Heart murmur
    • Purpura
    • Roth spots
    • Janeway lesions

Causes

Infections with bacteria, viruses, protozoa, and helminths can cause postinfectious GN (PIGN).

  • Bacterial endocarditis: PIGN occurs more commonly in subacute rather than acute endocarditis. S aureus is now the most common pathogen recognized.
  • Shunt nephritis: This may be associated with ventriculovascular, ventriculoperitoneal, peritoneovascular, or vascular shunts.
  • Visceral abscesses: These may occur with abdominal, pulmonary, or retroperitoneal abscesses.
  • Syphilis
  • Hepatitis B
  • Hepatitis C
  • Human immunodeficiency virus
  • Cytomegalovirus
  • Parvovirus B19
  • Hantavirus
  • Malaria
  • Schistosomiasis
  • Leishmaniasis
  • Filariasis
  • Hydatid disease
  • Toxoplasmosis
  • Aspergillosis

More on Glomerulonephritis, Nonstreptococcal Associated With Infection

Overview: Glomerulonephritis, Nonstreptococcal Associated With Infection
Differential Diagnoses & Workup: Glomerulonephritis, Nonstreptococcal Associated With Infection
Treatment & Medication: Glomerulonephritis, Nonstreptococcal Associated With Infection
Follow-up: Glomerulonephritis, Nonstreptococcal Associated With Infection
References

References

  1. Appel G. Viral infections and the kidney: HIV, hepatitis B, and hepatitis C. Cleve Clin J Med. May 2007;74(5):353-60. [Medline].

  2. Atta MG, Gallant JE, Rahman MH, et al. Antiretroviral therapy in the treatment of HIV-associated nephropathy. Nephrol Dial Transplant. Oct 2006;21(10):2809-13. [Medline].

  3. Barsoum R. The changing face of schistosomal glomerulopathy. Kidney Int. Dec 2004;66(6):2472-84. [Medline].

  4. Chadban SJ, Atkins RC. Glomerulonephritis. Lancet. May 21-27 2005;365(9473):1797-806. [Medline].

  5. Conlon PJ, Jefferies F, Krigman HR, et al. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol. Feb 1998;49(2):96-101. [Medline].

  6. Haffner D, Schindera F, Aschoff A, et al. The clinical spectrum of shunt nephritis. Nephrol Dial Transplant. Jun 1997;12(6):1143-8. [Medline].

  7. Jefferson JA, Johnson RJ. Treatment of hepatitis C-associated glomerular disease. Semin Nephrol. May 2000;20(3):286-92. [Medline].

  8. Kamar N, Izopet J, Alric L, et al. Hepatitis C virus-related kidney disease: an overview. Clin Nephrol. Mar 2008;69(3):149-60. [Medline].

  9. Lu TC, Ross M. HIV-associated nephropathy: a brief review. Mt Sinai J Med. May 2005;72(3):193-9. [Medline].

  10. Sorger K. Postinfectious glomerulonephritis. Subtypes, clinico-pathological correlations, and follow-up studies. Veroff Pathol. 1986;125:1-105. [Medline].

  11. Tang S, Lai FM, Lui YH, et al. Lamivudine in hepatitis B-associated membranous nephropathy. Kidney Int. Oct 2005;68(4):1750-8. [Medline].

  12. Wyatt CM, Rosenstiel PE, Klotman PE. HIV-associated nephropathy. Contrib Nephrol. 2008;159:151-61. [Medline].

Further Reading

Keywords

glomerular diseases associated with infection, glomerular disease, infection-related glomerulonephritis, GN, postinfectious glomerulonephritis, PIGN, bacterial infection, viral infection, protozoal infection, helminth infection, bacterial endocarditis, shunt nephritis, visceral abscesses, syphilis, hepatitis B, hepatitis C, human immunodeficiency virus, HIV, cytomegalovirus, CMV, parvovirus B19, Hantavirus, malaria, schistosomiasis, leishmaniasis, filariasis, hydatid disease, toxoplasmosis, aspergillosis

Contributor Information and Disclosures

Author

James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Coauthor(s)

Quresh T Khairullah, MBBS, Consulting Staff, Department of Medicine, Division of Nephrology, St John's Hospital and Medical Center
Quresh T Khairullah, MBBS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

Medical Editor

Frank C Brosius III, MD, Nephrology Program Director, Department of Internal Medicine, Division of Nephrology, Professor of Internal Medicine and Physiology, University of Michigan School of Medicine
Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ajay K Singh, MB, MRCP, MBA, Associate Professor of Medicine, Director of Dialysis, Department of Medicine, Harvard Medical School; Clinical Chief of Renal Division, Brigham and Women's Hospital
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Roche Honoraria Consulting

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.