%0 Journal Article
%T De Novo Fibrillary Glomerulonephritis (FGN) in a Renal Transplant with Chronic Hepatitis C
%A Edward J. Filippone
%A Christine Chmielewski
%A Rakesh Gulati
%A Eric Newman
%A John L. Farber
%J Case Reports in Transplantation
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/978481
%X Chronic hepatitis C viremia (HepC) has been associated with numerous renal manifestations both in native kidneys and in the setting of renal transplantation. Glomerulonephritis (GN) of the renal allograft in the setting of HepC most commonly manifests as type 1 membranoproliferative GN (MPGN), either representing recurrence of the original disease or arising de novo. Other GNs were reported after transplantation in the patient with HepC including membranous nephropathy and thrombotic microangiopathy, as well as an enhanced susceptibility to transplant glomerulopathy. We describe the first case of de novo fibrillary GN in a renal transplant patient with HepC where the primary renal disease was biopsy proven type 1 MPGN. We discuss this relationship in detail. 1. Introduction Chronic hepatitis C (HepC) affects 170 million persons worldwide and is a leading cause of cirrhosis and hepatocellular carcinoma. Renal disease is a prominent extrahepatic complication of£¿£¿HepC, typically manifesting as membranoproliferative glomerulonephritis (MPGN) in the setting of cryoglobulinemia (cryo) [1]. In addition, HepC remains a major concern after renal transplantation, affecting both patient and graft survival [2]. A strong association is documented with development of posttransplant diabetes mellitus, de novo glomerulonephritis, and possibly transplant glomerulopathy. Here we report a patient with HepC and biopsy proven MPGN, who progressed to end-stage, and after 2 years on dialysis received a deceased donor renal transplant. Eight years later, in the setting of proteinuria and declining renal function, transplant biopsy revealed de novo FGN. 2. Case Report A 56-year-old Caucasian male with HepC presented in 1994 with an elevated serum creatinine and nephrotic-range proteinuria. He had a history of hypertension, nephrolithiasis, and diverticulitss. Renal biopsy revealed type 1 MPGN. Symptomatic cryoglobulinemic vasculitis (cryoV) developed, which was treated in 1995 with plasmapheresis, intravenous cyclophosphamide, and steroids. Renal function progressively deteriorated necessitating dialysis in 1996. Treatment with interferon was curtailed, owing to severe psychiatric symptoms, and the patient remained viremic and on dialysis. A deceased donor renal transplant was performed in April 2003. An early Banff 1A rejection was treated with a course of IV methylprednisolone with resolution. Immunosuppressive therapy included cyclosporine and sirolimus. A biopsy in June 2003 showed no signs of rejection. In July 2003 cryoV reappeared with asthenia, severe arthralgias,
%U http://www.hindawi.com/journals/crit/2013/978481/