Rapidly deteriorating renal function with membranoproliferative glomerulonephritis Type 1 associated with hepatitis C treated successfully with steroids and antiviral therapy: a case report and review of literature.

INTRODUCTION

The hepatitis C virus (HCV) infection is associated with several renal diseases including mixed essential cryoglobulinemia, membranoproliferative glomerulonephritis (MPGN) and less frequently membranous nephropathy and crescentic glomerulonephritis. We present a case of HCV-associated cryoglobulin-negative, MPGN Type 1 with features of early crescents and rapidly deteriorating renal function requiring urgent treatment.

CASE

A 35-year-old male was admitted with history of arthralgia and erythematous rash. His past medical history included being an intravenous drug abuser. Biochemistry test showed raised serum creatinine of 150 micromol/l. He had nephrotic range proteinuria of 6 g/day and a serum albumin of 23 g/l. Viral serology for hepatitis B and HIV was negative but confirmed evidence of HCV infection with genotype 3A and viral load of 151,014 copies. He had a renal biopsy and histology demonstrated features of crescentic MPGN Type 1. His renal function deteriorated rapidly with his serum creatinine rising to 300 micromol/l over 2 days. We commenced treatment with intravenous methylprednisolone, 500 mg once daily (o.d.) for 3 days, followed by oral prednisolone 40 mg o.d. Concurrently, pegylated Interferon- (IFN) I+/- was commenced. After a 2-week treatment, his renal function showed remarkable recovery with creatinine reduced to 140 micromol/l. After 3 months, ribavirin was added when his renal function remained stable. He had tolerated his treatment without any major side effects. At 6 months follow-up clinic, his renal function was normal with serum creatinine of 69 micromol/l, 24-h urinary protein had dropped to 0.35 g/day, serum albumin increased to 38 g/l and HCV PCR was negative.

DISCUSSION

The current treatment strategy of HCV-associated renal diseases includes targeting viral trigger HCV with interferon and ribavirin. Both IFN-I+/- and ribavirin have their limitation and adverse effects. In a clinical scenario where there is evidence of rapidly deteriorating renal function with crescentic glomerulonephritis, cautious use of immunosuppressive therapy may well be essential in the acute stage to halt the progression of kidney damage. Literature review of the treatment strategy for MPGN Type 1, cryoglobulin-negative with early features of crescents associated with HCV showed that there was no report or guideline available.

CONCLUSIONS

To our knowledge, this is the first case in the literature of rapidly progressing MPGN Type 1 associated with HCV and nephrotic syndrome treated successfully with antiviral drugs and steroids concurrently. Our case highlights an important treatment strategy and may be beneficial to nephrologists facing this clinical scenario in the future. However, a randomized controlled trial is required to evaluate the efficacy of this treatment combination before it can be a standard treatment.