Brief Communication: Glomerulonephritis in Patients with Hepatitis C Cirrhosis Undergoing Liver Transplantation

McGuire, Brendan M.; Julian, Bruce A.; Bynon, John S.; Cook, William J.; King, Scott A.; Curtis, John J.; Accortt, Neil A.; Eckhoff, Devin E.

doi:10.7326/0003-4819-144-10-200605160-00007

Cited by 153 publications

(97 citation statements)

References 12 publications

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“…Furthermore, a recent study of patients who underwent protocol renal biopsy at the time of liver transplantation for HCVassociated liver failure found that most of these patients (25 of 30 patients) had an immune complex-mediated glomerulonephritis, which was often clinically unsuspected (33). This points to a potential major contributing cause of renal failure that may occur after transplant in these patients and suggests that the patient group with clinically evident HCV-associated glomerular injury may be akin to the tip of an iceberg.…”

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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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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“…Liver recipients are among the most likely to develop renal insufficiency after transplantation. Curtis's University of Alabama at Birmingham group performed protocol kidney biopsies in 30 patients who had hepatitis C and normal renal function and underwent liver transplantation (53). Twenty-five (83%) had significant preexisting glomerular pathology.…”

Section: Alternatives To An Incomplete Paradigmmentioning

confidence: 99%

Chronic Calcineurin Inhibitor Nephrotoxicity

Gaston

2009

Clinical Journal of the American Society of Nephrology

113

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Use of the calcineurin inhibitors (CNI) cyclosporine and tacrolimus has revolutionized solid organ transplantation. For more than 30 yr, the transplant community has dealt with nephrotoxicity attributed to these agents. Acute renal vasoconstriction (as described by many investigators, including John Curtis and colleagues) is the unequivocal consequence of their use; chronic CNI nephropathy, although indistinct in terms of histology and pathophysiology, has become accepted as a major cause of late kidney allograft failure. This article examines clinical, laboratory, and histologic findings that evolved into a paradigm that was never fully consistent with observed outcomes and new evidence that may offer an alternative interpretation for adverse events that are attributed to CNI nephrotoxicity in kidney transplant recipients.

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“…We suggest that a native kidney biopsy should be performed whenever possible to assist in the diagnosis of renal failure and gauge the risk for development of recurrent disease (8 -10). Liver transplant recipients, in particular, seem to have a high frequency of glomerular abnormalities without significant clinical or biochemical evidence of renal dysfunction (11,12).…”

Section: Discussionmentioning

confidence: 99%

Increasing Referral for Renal Transplant Evaluation in Recipients of Nonrenal Solid-Organ Transplants

Chandrakantan

Mattos

Naftel

et al. 2006

Clinical Journal of the American Society of Nephrology

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The use of cyclosporine and tacrolimus therapy in nonrenal (heart, heart/lung, lung, and liver) transplantation has resulted in improved patient and graft survival. Nephrotoxicity is one of the major side effects of tacrolimus and cyclosporine therapy and may lead to ESRD. The trend of referral of nonrenal solid-organ transplant recipients for kidney transplant evaluation at a large multiorgan transplant center was examined. Records of all patients who were referred for renal transplantation at the University of Alabama between January 1, 1993, and June 30, 2004, were reviewed. Eighty (0.96%) of 8318 individuals had previously undergone a nonrenal solid-organ transplant and were included in the study. The majority (72%) of patients had their nonrenal transplants performed at the University of Alabama. Twenty-two patients had their nonrenal transplant performed elsewhere and had fewer data available for analysis. From the period 1993-1996 to 2001-2004, an 11-fold increase in the absolute number of referrals of patients with nonrenal transplants was noted. Of patients who were referred for transplant evaluation, 25 became recipients of kidney transplants with a predominance of living-donor transplants. Referral for kidney transplant evaluation among nonrenal solid-organ transplant recipients is increasing and will exacerbate the existing shortage of deceased-donor kidneys that are available for transplantation. There was a trend for liver transplant recipients compared with other solid-organ recipients to develop ESRD at a greater rate.

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Brief Communication: Glomerulonephritis in Patients with Hepatitis C Cirrhosis Undergoing Liver Transplantation

Abstract: Immune-complex glomerulonephritis was common in patients with end-stage HCV-induced cirrhosis and was often clinically silent. Its potential to cause renal failure after liver transplantation may be underappreciated.

Cited by 153 publications

References 12 publications

Emerging Paradigms in the Renal Pathology of Viral Diseases

Emerging Paradigms in the Renal Pathology of Viral Diseases

Chronic Calcineurin Inhibitor Nephrotoxicity

Increasing Referral for Renal Transplant Evaluation in Recipients of Nonrenal Solid-Organ Transplants

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