Abstract

Infection with human immunodeficiency virus type 1 (HIV-1) is associated with a variety of well-known renal diseases like IgA nephropathy, membranous nephropathy, and haemolytic uraemic syndrome [1]. HIV-associated nephropathy (HIVAN) is now being recognized as a distinct clinico-pathological entity that presents with proteinuria in the nephrotic range and impairment of renal function [1]. Untreated, HIVAN caries a poor prognosis and invariably leads to endstage renal failure within months. The most striking finding on renal biopsy is collapsing focal glomerulosclerosis, but all renal compartments are essentially affected [1]. HIVAN is predominantly seen in black patients and has become a major cause for end-stage renal disease (ESRD) in this patient group. Treatment of HIVAN has included the use of steroids, ACEinhibition and anti-retroviral drugs but the optimal treatment is not known [1]. Corticosteroids and ACEinhibition probably slow down the progression to ESRD especially in cases with mild to moderate renal impairment. An animal model of mice transgenic for an HIV-1 gene construct suggested a direct pathogenic effect of HIV on renal cells [2]. Aggressive reduction of the viral load by a combination of anti-retroviral drugs, also known as highly active anti-retroviral therapy (HAART), is now considered standard therapy for HIV-1 infection. Anecdotal data suggest that marked improvement of renal function may occur after starting HAART [3]. Preliminary reports showed a better renal survival for patients with HIVAN treated with HAART [4,5]. Prospective randomized clinical trials comparing different treatment regimes for HIVAN have not been performed. Based on present data, HAART combined with ACE-inhibition may be the optimal treatment for HIVAN. In this report we describe three patients with HIVAN, who presented with rapidly progressive renal insufficiency and were not treated previously for their HIV-1 infection. Marked and prolonged improvement of renal function was established after starting HAART and ACE-inhibition.

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