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202 CRYOGLOBULINEMIA RELATED TO HEPATITIS C PRESENTING AS POLYARTERITIS NODOSA: TREATMENT CONSIDERATIONS
  1. R. B. Canada,
  2. B. M. Wall
  1. Memphis, TN.

Abstract

Introduction Symptomatic polyarteritis nodosa (PAN) and cryoglobulinemic glomerulonephritis associated with hepatitis C (HCV) were histologically confirmed in a patient who initially presented with findings of acute cholecystitis and subsequently developed acute renal failure. Therapeutic challenges for these life-threatening complications of HCV are presented.

Case Report 53 year old male with hypertension, diabetes, COPD, chronic untreated HCV, and non-nephrotic range proteinuria required cholecystectomy for presumed cholecystitis. Gallstones were not present, and histological examination demonstrated small artery vasculitis, consistent with PAN. He was readmitted 2 months later with hypertensive encephalopathy, marked volume overload, and acute renal failure (serum creatinine, 3.1 mg/dL with baseline of 1.2 mg/dL). Urinalysis revealed nephrotic range proteinuria and new onset microhematuria. Serological studies were positive for rheumatoid factor, cryoglobulins, and low C4 (normal C3). The patient was negative for hepatitis B surface antigen, ANCA, FANA, and anti-GBM antibody. Kidney biopsy demonstrated HCV-associated cryoglobulinemic glomerulonephritis, superimposed on diabetic glomerulosclerosis. A risk/benefit analysis was undertaken in order to recommend treatment. Because of the patient's severe vasculitis, it was decided to treat with immunosuppressives (pulse methylprednisolone followed by oral steroids and monthly intravenous cyclophosphamide for 6 months). Since the patient had no arthritis or skin lesions, and repeat tests for serum cryoglobulins were negative, plasmapharesis was not performed. During treatment, mental status, blood pressure control, and volume status markedly improved. Microhematuria resolved, proteinuria decreased, and serum creatinine stabilized, ˜ 2 mg/dL. He experienced no detriment to liver function and subsequently underwent treatment for HCV with interferon and ribavirin.

Conclusion This case demonstrates one diagnostic and therapeutic strategy for a patient who presented with multiple manifestations of HCV. Although taking some risk in worsening the HCV infection, we were able to improve the renal function of a patient with severe HCV-associated vasculitis using aggressive treatment with immunosuppressives. We were then able to treat the HCV itself using standard therapy.

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