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Hepatitis C Virus RNA as an EarlyIndicator of Hepatitis C Virus Associated Glomerulonephritis

Accessible online at: www.karger.com/journals/nef Dear Sir, The mechanisms of onset of glomerulonephritis after hepatitis C virus (HCV) infection (HCVGN) are not well understood [1, 2]. We thought that the mechanisms of HCVGN might be similar to those in experiments involving models of serum sickness. We hypothesized that HCV forms an immune complex which triggers HCVGN. An interesting case supports this hypothesis. We have followed a 72-year-old male who was diagnosed as having HCV hepatitis and cholelithiasis in 1996. The hepatic function had been stable with glutamic-oxaloacetic and glutamic-pyruvic transaminase levels of about 70 IU. HCV RNA (by RT PCR) was 140 K copy/ml (KC/ml) (normal 1.0 KC/ml or less), and the HCV antibody level was high (11.5), as evaluated by a third-generation RIA assay. Serum creatinine was 1 mg/ dl, and urinalysis was normal. In August 1998, edema of the lower legs developed when the urinary protein concentration was 6 g/day and the serum total protein level 5 g/ dl, and the patient was diagnosed as having nephrotic syndrome. Other laboratory values were C3 59 mg/dl, C4 35 mg/dl, and CH50 10 U, cryoglobulin and rheumatoid factor were negative. As the urinary protein concentration increased, the HCV RNA level decreased to 1.9 KC/ml, and HCV RNA became negative within 1 month. The hepatic function was normal. During this period the renal failure progressed with development of pleural fluid, abdominal fluid, and an increase in the creatinine concentration to 2.5 mg/ml. Methylprednisolone pulse therapy with heparin and prednisolone were started. Within 3 weeks the nephrotic syndrome disappeared with a urinary protein levels of 0.28 g/day and a creatinine concentration of 1.1 mg/ml. HCV RNA at this time was 170 KC/ml. Two months after onset of HCVGN, the hepatic condition was stable. The patient was then treated with prednisolone 10 mg/day, and HCV RNA increased temporarily to 1,200 KC/ml and glutamicoxaloacetic and glutamic-pyruvic transaminases to 104 and 144 IU, respectively. However, 4 months later HCV RNA was 120 KC/ml, and liver function test results were close to normal. Renal biopsy was not done. Changes of HCV RNA and the clinical course of nephrotic syndrome in this noncryoglobulinemic patient suggest that HCV forms a circulating immune complex and participates in the kidneys to cause nephritis. The increase in HCV RNA levels after glucocorticoid therapy probably resulted from suppressed antibody synthesis. A fall in HCV RNA may be useful as an early indicator of HCVGN. References