Hepatitis C virus-associated glomerulonephritis

Stehman‐Breen, Catherine; Willson, Richard A.; Alpers, Charles E.; Gretch, David R.; Johnson, Richard J.

doi:10.1097/00041552-199505000-00015

Cited by 55 publications

(29 citation statements)

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“…This hypothesis was generated based on observations that hepatitis C is associated with some forms of glomerular disease [7][8][9][10][11] , that the co-existence of hepatitis C appears to increase the progression of CKD 14 , that viral particles or antigenicity is found in glomeruli and tubules of kidney biopsies 16,17 , and that CKD is very prevalent in areas with particularly high rates of hepatitis C infection 22 . Our results demonstrated no increased risk of having or developing CKD in patients who are hepatitis C positive in cross-sectional and longitudinal analyses after controlling for multiple other known risk factors for CKD.…”

Section: Discussionmentioning

confidence: 99%

Association of Hepatitis C Virus Infection With Prevalence and Development of Kidney Disease

Moe

Pampalone

Ofner

et al. 2008

American Journal of Kidney Diseases

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Section: Discussionmentioning

confidence: 99%

Association of Hepatitis C Virus Infection With Prevalence and Development of Kidney Disease

Moe

Pampalone

Ofner

et al. 2008

American Journal of Kidney Diseases

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“…Other forms of glomerular injury have been documented as well (21,22,24 -27). Both individual case reports and small series have reported membranous glomerulonephritis (MGN) in HCV-infected patients (21,27,28). The clinical features and pathology in these cases do not distinguish those patients from those with idiopathic or other secondary forms of MGN.…”

Section: Hepatitis C Virus-associated Glomerulonephritismentioning

confidence: 99%

Emerging Paradigms in the Renal Pathology of Viral Diseases

Alpers¹,

Kowalewska²

2007

Clinical Journal of the American Society of Nephrology

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This review considers recent information that illuminates pathogenetic mechanisms that involve three of the major viral infections that cause renal injury in the form of HIV-associated nephropathy, polyoma virus nephropathy, and hepatitis C virus-associated glomerulonephritis.Clin J Am Soc Nephrol 2: S6 -S12, 2007. doi: 10.2215/CJN.00280107 HIV-Associated NephropathyA nephropathy that is associated with HIV infection was identified soon after the epidemic of HIV/AIDS first became recognized in the early 1980s. HIV-associated nephropathy (HIVAN) is a combined glomerular and tubular injury that is characterized by a collapsing glomerulopathy (CG) with collapse of glomerular capillary structures and a striking hyperplasia of podocytes, microcystic transformation of renal tubules, and concomitant and likely nonspecific interstitial inflammation and fibrosis consequent to the glomerular and tubular injuries (Figure 1). From a pathology standpoint, three major areas of investigation have led to a deeper understanding of this lesion.The first of these addresses the issue of whether HIVAN is a direct consequence of viral infection of the renal parenchyma or is a secondary consequence of systemic infection. Cohen et al.(1) first reported the presence of HIV RNA in podocytes as revealed by in situ hybridization (ISH) in 1989, a finding that was supported by microdissection studies of Kimmel et al. (2). These studies were difficult to validate because of the failure of others to replicate these findings using conventional techniques of ISH, the inability to demonstrate the presence of viral peptides in renal parenchymal cells by immunohistochemistry, and the inability to demonstrate appropriate receptors for viral entry into cells, namely CD4 and the chemokine receptors CXCR4 or CCR5, on renal parenchymal cells (3). This created a conundrum in that a mechanism for viral entry into renal cells could not be defined. Some but not all of the difficulties were resolved by a more sophisticated form of ISH, which is based on a technique that detects forms of viral DNA that are characteristic of replicating virus (4 -6). With these techniques, it was possible to substantiate the findings of Cohen et al. and convincingly demonstrate HIV infection of podocytes and tubular epithelial cells.A second key development concomitant with the demonstration of HIV infection of human renal epithelial cells was the development of murine models of HIVAN. The best studied of these involves the Tg26 mouse: Mice are made transgenic for a nearly whole-length HIV virus but with a deletion of HIV gag and pol genes to render the virus nonreplicative (7). Studies of these mice, largely by the group of Klotman and their collaborators, have established that expression of HIV genes, presumably modeling the events of renal HIV infection, is sufficient to produce a renal injury in the mouse that is similar to HIVAN in humans. Studies in which kidneys from transgenic mice were transplanted into wild-type controls demonstrated that renal expression of HIV gene...

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“…18,19 Hepatitis C virus (HCV) infection is associated primarily with MPGN, but fibrillary glomerulonephritis also is seen. [20][21][22][23] In addition, HCV is associated with diabetes; however, the impact of diabetes on renal function of HCV-positive patients with ESLD and liver transplant recipients is yet to be determined. 13,24 Conversely, in patients already showing type 2 diabetes, more rapid renal function loss is seen in HCV-infected compared with uninfected patients.…”

Section: Renal Disease In the Setting Of Cirrhosis: Primary Renal Dismentioning

confidence: 99%

Pathophysiology of renal disease associated with liver disorders: Implications for liver transplantation. Part I

Davis

Gonwa

Wilkinson

2002

Liver Transplantation

117

131

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Hepatitis C virus-associated glomerulonephritis

Cited by 55 publications

References 0 publications

Association of Hepatitis C Virus Infection With Prevalence and Development of Kidney Disease

Association of Hepatitis C Virus Infection With Prevalence and Development of Kidney Disease

Emerging Paradigms in the Renal Pathology of Viral Diseases

Pathophysiology of renal disease associated with liver disorders: Implications for liver transplantation. Part I

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