Membranoproliferative Glomerulonephritis and Hepatitis C Virus Infection
Author(s) -
Ana Gonzalo,
Rafael Bárcena,
F Mampaso,
Antonio Zea,
J. Ortuño
Publication year - 1993
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000187259
Subject(s) - membranoproliferative glomerulonephritis , medicine , glomerulonephritis , hepatitis c virus , virology , immunology , mesangial proliferative glomerulonephritis , hepatitis c , cryoglobulinemia , virus , kidney
Ana Gonzalo, MD, Servicio de Nefrología, Hospital Ramón y Cajal, Carretera de Colmenar, Km. 9,100, E-28034 Madrid (Spain) Fig. 1. Glomerulus showing increased number of mesangial cells and matrix. HE. × 400. remained raised at 100 U/1 and a liver biopsy showed active chronic hepatitis. A severe mononuclear cell infiltrate was observed in the portal tracts with rupture of the limiting plate (piecemeal necrosis). Ground glass he-patocytes were absent and liver architecture was conserved. Three months later, proteinuria and microhematuria persisted unchanged and a renal biopsy was performed. It contained five glomeruli, all of them showing diffuse mesangial cell proliferation and an increased mesangial matrix. Accentuation of the glomerular lobular pattern as well as peripheral mesangial cell interposition was also observed (fig. 1). Presence of Dear Sir, Membranoproliferative glomerulonephritis (MPGN) with subendothelial deposits (type I) is a well-defined clinicopathological entity [1] which although it may be associated with several conditions [2], is usually idio-pathic. Many cases of GN related to chronic hepatitis B virus (HBV) infection have been classified as MPGN and the etiologic role of HBV in MPGN has been considered. Rollino et al. [3] have recently described the association of hepatitis C virus (HCV) infection and membranous nephropathy, stressing the importance of systematic research of HCV antibodies in order to identify one more causal factor of this nephropathy. We present a patient with HCV infection and type I MPGN. A 28-year-old previously non transfused woman, consulted her physician in September 1990 because of asthenia, anorexia and weight loss during the preceding month. She did not have arthralgias, Raynaud’s phenomenon or cutaneous lesions. On physical examination blood pressure was 130/80 mm Hg, the liver was not palpable and she did not have edema. Analytical studies disclosed serum creatinine 0.7 mg/dl, proteinuria 19 mg/ kg/day and urine red blood cells 375,000/ min with hyaline and hyaline-granular casts. Alanine aminotransferase (ALT) was 649 U/ 1, total serum bilirubin 0.9 mg/dl, serum albumin 32 g/l and total protein 62 g/l. Serum IgG and IgA levels were in the normal range (1,070 and 113 mg/dl, respectively) and IgM was 348 mg/dl (normal 70-280 mg/dl). Serum complement
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