Therapy with interferon-alpha plus ribavirin for membranoproliferative glomerulonephritis induced by hepatitis C virus.

We describe a treatment made with interferon-alpha (IFN-alpha) plus ribavirin of two patients with membranoproliferative glomerulonephritis (MPGN) induced by hepatitis C virus (HCV): case # 1 was a 22-yr-old woman with leg and facial edema, hypertension and proteinuria, whose liver biopsy revealed chronic active hepatitis; and case # 2 was a 42-yr-old man with anasarca, hypertension and proteinuria, whose liver biopsy indicated cirrhosis. Both had anti-HCV, HCV-RNA and cryoglobulins. IFN-alpha (3 million units (MU), 3 times/week) and ribavirin (1 g/day) were administered for 12 months. The drugs were well tolerated by both patients. Serum alanine aminotransferase (ALT) levels normalized and HCV-RNA became negative. Cryoglobulins disappeared and an improvement in renal disease was seen after 6 months of therapy. However, after 9 months, case # 2 presented ALT elevation, and proteinuria was detected. Two years after the end of therapy, both patients were negative in repeated HCV-RNA and cryoglobulin tests. Case # 1 was asymptomatic, with normal liver and renal tests, and case # 2 had normal blood pressure, with mild edema of the ankles. Based on the evolution of these two cases, the association of IFN-alpha and ribavirin may be a therapeutic option for patients with MPGN related to HCV.

Hepatitis B-associated nephrotic syndrome in Jamaican children.

Between December 1984 and November 1996, 171 children under 12 years old presented to the University Hospital of the West Indies with nephrotic syndrome. Hepatitis B surface antigen (HBsAg) was found in ten (6%) of these children, eight of whom had membranous nephropathy (MN), and one each had mesangial proliferative glomerulonephritis (MesN) and minimal change nephrotic syndrome (MCNS). Only those children with MesN and MCNS were steroid-sensitive. The HBsAg-positive status was identified incidentally on screening. At a mean follow-up of 34 months, seven of ten children had experienced complete or partial remission and three had persistent nephrotic syndrome, although none was in renal failure. Six of the ten had biochemical hepatitis. All the children were still HBsAg-positive. Hepatitis B virus (HBV) is a factor contributory to nephrotic syndrome in Jamaican children. As diagnostic clinical markers for HBV-associated nephropathy are usually absent, all children presenting with nephrotic syndrome should be screened for HBsAg. A policy should be implemented in Jamaica for screening pregnant women and at-risk groups for HBsAg, as well as for immunising susceptible neonates, in order to reduce the incidence of HBV-associated pathology.

Human T-cell lymphotropic virus-1-associated renal disease in Jamaican children.

This report documents the clinicopathological features in two Jamaican children who presented with infective dermatitis, glomerulonephritis, renal failure and human T-cell lymphotropic virus (HTLV-1) seropositivity. Severe hypertension with hypertensive encephalopathy was the most impressive clinical feature. Histological findings from renal biopsy specimens in both cases revealed significant glomerulosclerosis with fibrosis, chronic inflammatory cell infiltrates in the interstitium, and arteriolar hypertensive changes. Membranoproliferative glomerulonephritis (MPGN) was demonstrable in case 1 and marked focal glomerulosclerosis in case 2. Case 1 developed end stage renal failure and died within 3 years of diagnosis. Case 2 remains hypertensive and in chronic renal failure. Although a causal relationship between HTLV-1 infection and renal disease cannot be proven by these two cases, it appears that renal involvement in children with HTLV-1 infection is severe, with the potential for chronic renal failure and malignant hypertension. HTLV-1 nephropathy should be suspected in children with infective dermatitis and renal disease.

[Hepatitis C virus and resulting diseases]. / El virus C de la hepatitis y las enfermedades que produce.

In 1989, the main agent causing non A non B hepatitis was identified as a RNA virus of the flavivirus family, with several serotypes, and was denominated virus C. At the present moment, the knowledge about the infection features and diseases that it causes has expanded thanks to the availability of reliable laboratory techniques to detect the antibody and the virus. The prevalence of infection and the frequency of serotypes varies in different regions of the world. Chile is a country with a low prevalence. The detection of infected blood in blood banks has reduced the spreading of the disease. Other means of infection such as the use of intravenous drugs, hemodialysis and transplantation have acquired greater importance. Sexual, maternal and familial transmission is exceptional. Infected people develop an acute hepatitis, generally asymptomatic. Eighty percent remain with a chronic hepatic disease, that can be mild or progressive, evolving to cirrhosis or hepatic carcinoma. Chronic hepatitis, closely resembling an autoimmune disease, can be caused by the virus. Alcohol intake increases viral activity causing severe hepatic diseases, refractory to treatments. Several non hepatic diseases are associated to hepatitis C virus infection such as essential mixed cryoglobulinemia, mesangiocapillary glomerulonephritis, porphyria cutanea tarda, dysglobulinemias and probably type 2 diabetes mellitus. The only available treatment is interferon, that is successful in a minority of patients, frequently causing a transient improvement. The use of Ribaravine associated to interferon improve the effectiveness of therapy. Liver transplantation is the only therapy for severe hepatic disease. The use of new antiviral drugs should improve the prognosis of the disease.

Prevalence of hepatitis C virus antibodies in primary glomerulonephritis in Brazil.

The association between hepatitis B virus and membranous glomerulonephritis and membranoproliferative glomerulonephritis (MPGN) was first described in 1971. Recently, a similar association between hepatitis C virus (HCV) and glomerulonephritis (GN) has been reported. We investigated the prevalence of hepatitis C serum antibodies (anti-HCV) in patients with primary GN followed up at our Nephrology Outpatient Clinic between March 1993 and November 1995. The diagnosis of primary GN was established after excluding the presence of connective tissue disease, diabetes, infectious disease, and malignancy. Anti-HCV antibodies were detected by a second-generation enzyme immunosorbent assay and HCV RNA by polymerase chain reaction. Of 81 patients with primary GN, 24 had membranous glomerulonephritis, 17 MPGN, 15 minimal-change disease, 12 focal-segmental glomerulosclerosis, 9 diffuse proliferative GN, and 4 IgA nephropathy. Anti-HCV were detected in 2 cases (2.5%), both were HCV RNA positive and had a polyclonal mixed cryoglobulinemia (IgM-IgG). These 2 cases both came from the group of 17 patients with MPGN. Biochemical investigation in these patients revealed persistent elevation of serum aminotransferase activity, and a liver biopsy specimen in 1 of them showed evidence of chronic active hepatitis. We conclude that in our setting the prevalence of anti-HCV among patients with primary GN is low, being higher (11.8%) only if we consider the patients with MPGN as the reference group. Further studies are necessary to clarify this association and to determine appropriate therapy for these patients.