PubMed · 3827640
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N A Mukhin. 1987. [Does glomerulonephritis exist?].. https://pubmed.ncbi.nlm.nih.gov/3827640/
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Almost all forms of glomerulonephritis affecting the native kidney may recur in the transplanted kidney. However, in a large majority of patients, recurrent glomerulonephritis has only a minimal impact on graft function and survival; less than 5% of all graft losses are the result of recurrence. Kidney transplantations provide an attractive experimental model for investigating the pathophysiological mechanisms in diseases, such as diabetes, in which the recurrence of glomerulonephritis is frequent, and segmental glomerular sclerosis in which glomerulonephritis is severe.
Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and is associated with a variety of extrahepatic manifestations, including cryoglobulinemia and glomerulonephritis. Epidemiologic evidence suggests that HCV infection may be a major risk factor for both cryoglobulinemic and type I membranoproliferative glomerulonephritis (MPGN). Clinical symptoms and laboratory data may or may not reflect the presence of chronic liver disease. Most patients have evidence of hypocomplementemia, circulating rheumatoid factors, and cryoglobulinemia. The pathogenesis of HCV-associated MPGN is probably a result of glomerular deposition of circulating HCV and anti-HCV antibodies. Treatment with interferon-alpha has been shown to improve proteinuria, suppress viremia, and stabilize renal function. However, patients often relapse after therapy is stopped. The optimal therapy remains to be defined but may involve different dosage regimens of interferon-alpha or the combination of several antiviral agents.