PubMed · 5302862
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P Fleischman. 1967. [Diffuse acute glomerulonephritis].. https://pubmed.ncbi.nlm.nih.gov/5302862/
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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.
Immunosuppressive treatment in glomerulonephritis (GN) is still controversial. Most of the secondary forms of glomerulonephritis have the histologic features of one of the primary types of glomerulonephritis. Eight histologic expressions of primary glomerulonephritis can be distinguished and ordered in terms of severity of symptoms and prognosis: endocapillary GN, minimal change GN, mesangioproliferative GN, membranous GN, focal-sclerosing GN, membranoproliferative GN, focal-necrotizing GN, and rapidly progressive GN. Agreement exists only to the extent that immunosuppression is not required in endocapillary glomerulonephritis, although it is recommended in the other extreme of rapidly progressive GN. Primarily, an indication for immunosuppression is given by the severity of symptoms with a urinary protein excretion > 3.5 g per day and/or serum creatinine > 150 mumol per liter. As for anti-GBM, the type of glomerulonephritis is more important than the severity of symptoms in guiding therapy, whereas for IgA nephropathy it is controversial whether the prospective prognosis of even inexorably deteriorating renal function justifies immunosuppression. Renal biopsy is required to identify the type of glomerulonephritis so as to establish the specific immunosuppressive concept with different intensity and duration of treatment. Immunosuppression can reduce urinary protein excretion and improve deterioration of renal function; however, the proportion of patients responding varies with and depends on the different forms of GN.