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Viruses and Diseases of the Kidneys

Jeffrey S. Berns^*, and Arthur H. Cohen

^* The Renal-Electrolyte and Hypertension Division, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; and the Department of Pathology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, California

Address correspondence to: Dr. Jeffrey S. Berns, Renal-Electrolyte and Hypertension Division, Hospital of the University of Pennsylvania, 3400 Spruce St., 1 Founders Pavilion, Philadelphia, PA. Phone: 215-615-1677; Fax: 215-615-1688; bernsj{at}uphs.upenn.edu

Virus-induced kidney diseases are common, are increasing in frequency, have different mechanisms of injury, and are intensely studied because of the morbidity and mortality that are associated with them, yet these diseases are less familiar to clinical nephrologists than many other renal disorders. This supplement of CJASN, the result of two symposia at the 2006 annual meeting of the American Society of Nephrology in which investigators with considerable and varied interest in viruses and diseases of the kidneys discussed their work, is intended to increase the understanding among clinical nephrologists of this interesting group of disorders.

Faulhaber and Nelson describe manners of injury to the kidneys that result from the development of adaptive immune responses once viral infection is established. Cell-mediated immunity coupled with extracellular factors of the immune system, such as complement and lysozyme, are effective defenses to viral infection. However, once this immune response is initiated, several injuries to renal parenchyma may result, regardless of the outcome for the invading virus. These involve various receptors; the best characterized are the Toll-like receptors, which recognize viral RNA and activate immune responses that may trigger deleterious bystander organ damage. In addition, B lymphocytes, mononuclear phagocytes, and T lymphocytes may result in direct or indirect renal injury in several viral diseases in native kidneys and transplants.

Alpers and Kowalewska tackle a broad range of issues related to pathogenic mechanisms and pathologic features of HIV-associated nephropathy (HIVAN), polyoma virus nephropathy, and hepatitis C virus–associated glomerulonephritis. They critically review evidence for mechanisms for HIV entry into renal epithelium and indicate that this issue is still unresolved. They present evidence for immune mechanisms in patients with polyoma virus nephropathy. They also address the important consideration of glomerular disease in hepatitis C virus, especially but not limited to membranoproliferative glomerulonephritis; the pathogenic sequence of injury in this setting is critically assessed, and difficulties in determining actual mechanisms are explored.

Bruggeman discusses mechanisms of viral replication and molecular events in cells that are infected with viruses that are pathogenic to the kidneys. These include HIV, cytomegalovirus, polyomavirus (BK), and parvovirus B19. This article provides interesting information concerning strategies that viruses use to replicate in the host cells, integrate themselves into the genetic machinery, avoid antiviral measures of the cell, and modulate cell functions.

Wyatt and Klotman trace the history of the HIV epidemic and consider the effect of this infection and its treatment on the kidneys. They discuss HIVAN and its pathogenesis and progression to ESRD and the development of ESRD from other disorders in HIV-infected patients. It is expected that, despite and because of the effect of antiretroviral therapy, a global epidemic of HIV-related renal disease is likely in the future. The patients live longer because AIDS-related deaths are decreasing, allowing other diseases to develop in these patients. Furthermore, because some antiretroviral agents are nephrotoxic, they also contribute to kidney diseases in some treated individuals.

The role of genetic susceptibility to viral infection, most notably HIV and HIVAN, are addressed by Kiryluk et al. They consider genetic variations in the virus as well as in the patient. This is especially important in the case of HIVAN, which, throughout the world, is almost exclusively a disease of individuals of black race. Furthermore, of those who have HIVAN, approximately 25% report a family member with ESRD. The authors also report on studies of the roles of the various HIV proteins in the pathogenesis of HIVAN.

Polyoma viral infection of renal transplants, a major problem with immunosuppressive therapy that has been introduced in the past decade or so, now affects approximately 8% of recipients and likely contributes to decreased longevity of the grafts. Bohl and Brennan examine strategies to identify and prevent this infection. They discuss in detail pertinent aspects of epidemiology, virology, pathology, and therapy.

Finally, Waldman and Kopp consider in detail the association of parvovirus B19 with human renal glomerular diseases. The authors reviewed the considerable literature on this subject involving both native kidneys and transplants. Although some reports have documented reasonably convincing evidence linking B19 infection to collapsing glomerulopathy, the authors maintain a skeptical approach to such data.

We are pleased to edit this exciting collection of articles that review major issues in viral diseases and renal injury and are sure that the reader will find them stimulating, informative, and complete.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Berns, J. S. Articles by Cohen, A. H. Search for Related Content PubMed PubMed Citation Articles by Berns, J. S. Articles by Cohen, A. H.