Multicenter Study on Hepatitis C Virus–Related Cryoglobulinemic Glomerulonephritis

Roccatello, Dario; Fornasieri, A; Giachino, Osvaldo; Rossi, Daniela; Beltrame, Alessandra; Banfi, Giovanni; Confalonieri, R.; Tarantino, A; Pasquali, Sonia; Amoroso, Antonio; Savoldi, Silvana; Colombo, Valeriana; Manno, Carlo; Ponzetto, Antonio; Moriconi, L; Pani, Antonello; Rustichelli, Roberto; Belgiojoso, G. Barbiano di; Comotti, Chiara; Quarenghi, Maria Ida

doi:10.1053/j.ajkd.2006.09.015

Cited by 199 publications

(170 citation statements)

References 33 publications

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“…Nephrotic syndrome (21%) and nephritic syndrome (14%) are less common. 54 Upto 14% patients with develop chronic renal failure after a mean follow up of six years. 55 Pulmonary and gastrointestinal involvement are less common.…”

Section: Renal Involvementmentioning

confidence: 99%

Hepatotropic Viral Infection Associated Systemic Vasculitides—Hepatitis B Virus Associated Polyarteritis Nodosa and Hepatitis C Virus Associated Cryoglobulinemic Vasculitis

Sharma

2013

Journal of Clinical and Experimental Hepatology

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Two hepatotropic viruses have been shown to have causal relationship with systemic vasculitis-hepatitis B with classical polyarteritis nodosa and hepatitis C with cryoglobulinemic vasculitis. The present paper provides an updated overview on the clinical presentations and management of these vasculitides.HBV associated PAN patients have higher weight loss, peripheral neuropathy, mononeuritis multiplex, abdominal pain, gastrointestinal manifestations requiring surgery, cardiomyopathy, orchitis, hypertension, and/or elevated transaminase levels. Microaneurysms are also more common in mesenteric artery. Skin manifestations, however are less common. These patients also have a severe disease as suggested by higher five factor score and higher BVAS. Though relapses are less common, mortality is higher in patients with HBV PAN as compared to non HBV PAN. Plasmapheresis has a role in treatment in clearing off immune complexes.The common clinical manifestations of HCV associated cryoglobulinemic vasculitis are skin lesions, peripheral neuropathy, glomerulonephritis, arthritis, and sicca symptoms. Though combination therapy comprising of pegylated interferon a and ribavirin is the first line of management, immunotherapy is needed for severe or life threatening manifestations. Recent randomized trials have shown the efficacy of rituximab in such situations. ( J CLIN EXP HEPATOL 2013;3:204-212)

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Section: Renal Involvementmentioning

confidence: 99%

Hepatotropic Viral Infection Associated Systemic Vasculitides—Hepatitis B Virus Associated Polyarteritis Nodosa and Hepatitis C Virus Associated Cryoglobulinemic Vasculitis

Sharma

2013

Journal of Clinical and Experimental Hepatology

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“…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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“…26 Various other forms of renal disorders like minimal change nephropathy (MGN), IgA nephropathy, focal segmental glomerulosclerosis ( FSGS) have been described in subsequent studies. [27][28][29] A very few studies a r e available regarding HCV prevalence in general population in our country. According to a study 30 conducted by ICDDRB at Kamlapur, Dhaka, 1997 participants ( general population) were screened for anti-HCV.…”

Section: Discussionmentioning

confidence: 99%

Seroprevalence of Anti-HCV Antibody in Patients with Chronic Kidney Disease before Starting Dialysis Therapy

Rabbi

Fatema

Alam³

2017

J Enam Med Col

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Multicenter Study on Hepatitis C Virus–Related Cryoglobulinemic Glomerulonephritis

Cited by 199 publications

References 33 publications

Hepatotropic Viral Infection Associated Systemic Vasculitides—Hepatitis B Virus Associated Polyarteritis Nodosa and Hepatitis C Virus Associated Cryoglobulinemic Vasculitis

Hepatotropic Viral Infection Associated Systemic Vasculitides—Hepatitis B Virus Associated Polyarteritis Nodosa and Hepatitis C Virus Associated Cryoglobulinemic Vasculitis

Emerging Paradigms in the Renal Pathology of Viral Diseases

Seroprevalence of Anti-HCV Antibody in Patients with Chronic Kidney Disease before Starting Dialysis Therapy

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