New insight on crescentic glomerulonephritis
نویسندگان
چکیده
4þ haematuria, but urinary sediments showed few red blood cells (1-2-1/high-power fields). His renal function recovered concomitantly with improvement of haemolytic anaemia; thus, haemolysis might also have contributed to the development of his renal dysfunction. Indeed, haemolysisrelated renal dysfunction has occurred in patients with HCV infection [1]. Our patient showed cryoglobulinaemia, but cryoglobulin-related glomerulonephritis was unlikely because no immune-complexes were deposited in glomeruli. There are several reported cases of minimal-change nephropathy occurring in HCV-infected patients, but these patients were treated with interferon; thus, minimal-change nephropathy was thought to be caused by interferon-related immunological abnormalities, rather than directly by HCV infection [2,3]. Our patient had no history of interferon treatment. We could not identify the causes of our patient’s haematological abnormalities, thrombocytopenia and haemolytic anaemia, but these haematological abnormalities have been reported as HCV-related autoimmune disorders [4], indicating that HCV-related immune dysregulation might have caused his haematological abnormalities. Further, thrombocytopenia/haemolytic anaemia and nephrotic syndrome occurred simultaneously in our case; therefore, HCV-related immune dysregulation might also have contributed to the development of minimal-change nephropathy. A similar case, autoimmune haemolytic anaemia occurring prior to evident nephropathy in a chronic HCV-infected patient has been reported, but the nephropathy was an immune-complex type nephropathy: membranous nephropathy [5]. Therefore, the question remains as to whether our patient’s HCV infection was a root cause, a simple coincidence, or a precipitating factor of minimal-change nephropathy.
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