OBJECTIVE: to assess temporal changes in the incidence of human immunodeficiency virus-1-associated nephropathy (HIVAN), and the association with use of highly active antiretroviral therapy (HAART). METHODS: HIVAN incidence and risk factors were assessed in 3976 HIV-1-infected individuals followed in clinical cohort in Baltimore, Maryland, USA from 1989 to 2001. The incidence of HIVAN, defined by biopsy or a conservative uniformly applied clinical coding protocol, was expressed in terms of person-years, and Poisson regression was used for multivariate analysis. RESULTS: Ninety-four patients developed HIVAN over the course of the study for an incidence of 8.0 per 1000 person-years [95% confidence interval (CI), 6.5 to 9.8]. African American race and advanced immunosuppression were strongly associated with HIVAN risk. HIVAN incidence declined significantly in 1998-2001 compared with 1995-1997. Among patients with a prior diagnosis of AIDS, HIVAN incidence was 26.4, 14.4, and 6.8 per 1000 person-years in patients not receiving antiretroviral therapy, treated with nucleoside analogue therapy only, or treated with HAART, respectively (P < 0.001 for trend). In multivariate analysis, HIVAN risk was reduced 60% (95% CI, -30 to -80%) by use of HAART, and no patient developed HIVAN when HAART had been initiated prior to the development of AIDS. CONCLUSION: HAART was associated with a substantial reduction in HIVAN incidence. Additional follow-up will be needed to determine if renal damage in susceptible individuals is halted or merely slowed by HAART, particularly when control of viremia is incomplete or intermittent.
OBJECTIVE: to assess temporal changes in the incidence of human immunodeficiency virus-1-associated nephropathy (HIVAN), and the association with use of highly active antiretroviral therapy (HAART). METHODS: HIVAN incidence and risk factors were assessed in 3976 HIV-1-infected individuals followed in clinical cohort in Baltimore, Maryland, USA from 1989 to 2001. The incidence of HIVAN, defined by biopsy or a conservative uniformly applied clinical coding protocol, was expressed in terms of person-years, and Poisson regression was used for multivariate analysis. RESULTS: Ninety-four patients developed HIVAN over the course of the study for an incidence of 8.0 per 1000 person-years [95% confidence interval (CI), 6.5 to 9.8]. African American race and advanced immunosuppression were strongly associated with HIVAN risk. HIVAN incidence declined significantly in 1998-2001 compared with 1995-1997. Among patients with a prior diagnosis of AIDS, HIVAN incidence was 26.4, 14.4, and 6.8 per 1000 person-years in patients not receiving antiretroviral therapy, treated with nucleoside analogue therapy only, or treated with HAART, respectively (P < 0.001 for trend). In multivariate analysis, HIVAN risk was reduced 60% (95% CI, -30 to -80%) by use of HAART, and no patient developed HIVAN when HAART had been initiated prior to the development of AIDS. CONCLUSION: HAART was associated with a substantial reduction in HIVAN incidence. Additional follow-up will be needed to determine if renal damage in susceptible individuals is halted or merely slowed by HAART, particularly when control of viremia is incomplete or intermittent.
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