HIV-associated Renal Disease Research Articles

Renal diseases in HIV-infected patients: pathogenesis, diagnosis, and treatment.

There are several HIV-associated renal disease, the pathogenesis of which is intimately related to the viral infection. Patients' demographic characteristics and clinical syndrome analysis may provide clinical clues to the individual renal disease, but in cases where a precise diagnosis is necessary, a renal biopsy is the only definitive way to establish the diagnosis. The explosion of knowledge regarding the molecular biology of the HIV life cycle and its mechanisms of infection has provided us not only with insights into the causes of the renal diseases, but has allowed nephrologists to advance, in the course of a decade, from therapeutic nihilism to the ability to provide treatment for the early and later stages of several of these diseases. It is hoped that with better understanding of the pathogenesis of the spectrum of kidney diseases encountered in HIV-infected patients, and the initiation and completion of properly designed and controlled therapeutic trials, patients quality and length of life will be enhanced.

HIV-associated renal disease in London hospitals

We report experience from London hospitals which further illustrates the heterogeneous nature of HIV-associated nephropathy (HIVAN). Nineteen HIV-positive patients underwent renal biopsy from 1992 to 1994. Fourteen were male, five female. Eleven were Afro-Caribbean, 7 Caucasian and 1 Asian. Eleven patients had classical HIVAN with proteinuria, rapidly progressive renal failure and features of focal and segmental glomerulosclerosis (FSGS) on renal biopsy, and three of these had associated tubulo-interstitial nephritis (TIN). One further patient had TIN and tubular changes suggestive of HIVAN but no glomeruli were present in the biopsy. Other biopsy findings were of focal proliferative glomerulonephritis and TIN (1 patient), pauci-immune crescentic glomerulonephritis and TIN (1 patient), membranous nephropathy (1 patient), membranoproliferative nephropathy (1 patient) and haemolytic uraemic syndrome (2 patients). Of 11 patients with FSGS, seven died with median survival of 8 months (range 23 days-46 months) and five are still alive after median follow-up of 18 months (range 10-22 months). Of patients with glomerular disease other than FSGS, five died, with median survival of 3 months (range 1-27 months) and two have survived (10 and 27 months, respectively). Thirteen patients had renal failure, 10 of whom had FSGS. In 10 cases renal failure was acute and in two was the presenting feature of HIV infection. Thirteen patients underwent renal replacement therapy. Four received haemodialysis, and all died within one month. Nine patients received CAPD. Two were able to discontinue dialysis. Of the remaining seven, five died with median survival of 8 months (range 1.3-40 months) and two are alive 1 and 10 months after beginning dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

HIV-associated immune-mediated renal disease

Although focal glomerulosclerosis is the most common renal disease, other proliferative glomerulonephritides are encountered in HIV-infected patients. We studied four HIV-infected patients with renal insufficiency, proteinuria, and proliferative glomerulonephritis, consistent with immune-mediated disease, to investigate the role of the virus and immune complexes in the pathogenesis of the nephropathy. Circulating immune complexes (CICs) and HIV-reactive antibodies were measured and characterized in each patient. Renal biopsy tissue was acid eluted, and the eluate analyzed. DNA extracted from biopsies was subjected to the polymerase chain reaction (PCR) to detect HIV genome. CICs were detected in each patient: an IgA-p24 HIV antigen complex and an IgG antibody-gp 120 HIV antigen complex in two patients; two patients had an IgG-p24 HIV antigen complex. Identical complexes were eluted from renal tissue in the first three patients; p24 HIV antigen, and complement from the fourth. The eluted antibodies reacted with the HIV antigens from the isolated CICs. Direct immunofluorescence for viral antigen in the eluted glomerular tissue revealed HIV antigens; PCR confirmed the presence of gag genome in all four biopsies. We conclude both circulating and in-situ HIV antigen-specific immune complexes may be associated with glomerulonephritis in HIV infected patients. Viral incorporation into renal tissue may be important in the pathogenesis of HIV-associated renal disease.