Renal manifestations of hepatitis C virus infection

Johnson, Richard J.; Willson, Richard A.; Yamabe, Hideaki; Couser, William G.; Alpers, Charles E.; Wener, Mark H.; Davis, Connie L.; Gretch, David R.

doi:10.1038/ki.1994.393

Cited by 146 publications

(90 citation statements)

References 106 publications

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“…Infective endocarditis, HIV, and HBV and HBC infections are associated with renal pathologic patterns similar to those previously described in heroin users (123)(124)(125)(126)(127)(128)(129)(130)(131)(132)(133)(134)(135)(136)(137). Because reports of heroin-associated nephropathy predated the surveillance of HCV and HIV infection with serologic and virologic tools, it is conceivable that some of the various histologic findings might have been related to the spectrum of viral illnesses that are encountered in injection drug users (3).…”

Section: Historical Perspective Of Renal Disease and Heroin Usesupporting

confidence: 56%

“…Since the rise in heroin abuse in the United States, there also has been an increased incidence of HIV and HCV infection and their associated renal diseases (126,151,152) (Figure 1). There has been a consistent decline in the number of reported cases of heroin nephropathy since 1992, and the incidence of ESRD has increased 53.6% from 306,000 from 1991 to 1995 to 470,000 from 1998 to 2002 (153,154).…”

Section: Epidemiology Of Heroin-associated Nephropathymentioning

confidence: 99%

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Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased, the incidence of "heroin nephropathy" has declined. Because reports of heroin nephropathy predated the surveillance of hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities may be more associated with the development of nephropathy in heroin users than the drug's pharmacologic properties. Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.

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Section: Historical Perspective Of Renal Disease and Heroin Usesupporting

confidence: 56%

Section: Epidemiology Of Heroin-associated Nephropathymentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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“…Both subendothelial and subepithelial immune complexes can be identified by electron microscopy, typically without distinctive substructure. In both forms of HCV-associated MPGN, mesangial and capillary wall deposition of IgM, IgG, and C3 are frequently but not invariably demonstrated (19,22,24). Other forms of glomerular injury have been documented as well (21,22,24 -27).…”

Section: Hepatitis C Virus-associated Glomerulonephritismentioning

confidence: 98%

“…MPGN typically presents many years, often decades, after initial infection with HCV. The majority of cases, but not all, have concomitant clinical features of mixed cryoglobulinemia, and the biopsy appearance of glomerular injury may reflect this noteworthy association (23,24). In the MPGN that is associated with cryoglobulinemia, termed cryoglobulinemic glomerulonephritis by some, there may be a marked infiltration of glomerular capillaries by leukocytes, typically with a large component of monocytes.…”

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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“…MCGN commonly presents as a nephrotic syndrome but in 16%-30% of patients the initial presentation is with acute nephritis. The disease can be subdivided into types I and II, with its idiopathic forms mostly seen in children and young adults with cases presenting at a younger age in type II (15 years ±11 It has recently been realised that a significant proportion of cases of type I MCGN previously labelled as idiopathic in fact occur in association with chronic hepatitis C infection 20 of which 20%-25% will present with acute nephritis. 21 There is geographical variation in this association and while hepatitis C associated renal disease appears particularly common in Japan (where the infection is found in up to 60% of cases of membranoproliferative glomerulonephritis) and Italy, it is less common in the USA (10%-20% of cases of membranoproliferative glomerulonephritis) and has been seen relatively little in France.…”

Section: Mesangiocapillary Glomerulonephritis; Also Known As Membranomentioning

confidence: 99%

Acute glomerulonephritis

IZAGUIRRE¹

Rheumatology and Immunology Therapy

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Renal manifestations of hepatitis C virus infection

Cited by 146 publications

References 106 publications

Chronic Nephropathies of Cocaine and Heroin Abuse

Chronic Nephropathies of Cocaine and Heroin Abuse

Emerging Paradigms in the Renal Pathology of Viral Diseases

Acute glomerulonephritis

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