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ESRD Risk High Among HIV-positive Blacks


SAN FRANCISCO -- HIV-positive African-Americans have a six-fold higher risk for end-stage renal disease than whites with HIV, investigators here reported.

SAN FRANCISCO, Oct. 17 -- HIV-positive African-Americans have a six-fold higher risk for end-stage renal disease than whites with HIV, investigators here reported.

The risk was comparable to that of HIV-negative blacks with diabetes, reported Andy I. Choi, M.D., of the University of California at San Francisco, in the November issue of the Journal of the American Society of Nephrology.

"Our study demonstrated a striking and unexpected degree of ESRD among HIV-infected persons of black race," said Dr. Choi. "On the other hand, among white patients with HIV, rates of ESRD were far lower than among blacks and HIV did not confer an increased risk of ESRD. We can think of few other risk factors for ESRD that are modified to this extent by race."

Dr. Choi and colleagues looked at Veterans Administration data on a national sample of 2,015,891 veterans who had kidney function tests in 2000 or 2001 and who were followed for progression of end-stage disease over a median of 3.7 years.

There were a total of 15,586 cases of ESRD during 7,072,237 person-years of observation, 15,135 of whom were HIV-positive. Of this latter group. 8,115 patients (53.6%) were African-American.

A total of 208 HIV-infected patients were treated for ESRD during 53,196 person-years of follow-up. Most of the cases (86.1%) occurred among black patients.

"Among both white and black HIV-infected patients who developed ESRD during follow-up, AIDS nephropathy was the most common cause listed in the U.S. Renal Data System (USRDS) PATIENTS file," the authors wrote. "When HIV and diabetes both were present, diabetes was the most frequently listed cause of ESRD."

The authors found that among black patients the age- and sex-adjusted incidence of ESRD was higher among those with HIV, at 7.3/1,000 person years (95% confidence interval 6.0 to 8.6) than among those who did not have either HIV or diabetes (2.3/1,000 py 95% CI 2.2 to 2.5), but was lower than for those with diabetes alone (8.9/1,000 py 95% CI 8.5 to 9.3).

In contrast, the age- and sex-adjusted incidence of ESRD among whites was similar between those with HIV (0.9/1000 py, 95% CI 0.4 to 1.4) and those who did not have HIV or diabetes (1.0/1000 py, 95% CI 0.9 to 1.0), but much lower than among those with diabetes (3.9/1000 py, 95% CI 3.7 to 4.0).

When the authors conducted multivariate Cox proportional hazard analyses, they found that among black patients the hazard ratio for ESRD and HIV infection was 4.56 (95% CI, 3.44 to 6.05), and for ESRD and diabetes was 4.15 (95% CI 3.89 to 4.43).

But among white patients, diabetes was associated with a more than two-fold increased risk for ESRD, with a hazard ratio of 2.18 (95% CI, 2.07 to 2.29), but HIV was not (hazard ratio 0.76, 95% CI., 0.45 to 1.30).

There was a six-fold greater risk for ESRD among HIV-positive blacks compared with HIV-positive whites, the authors found (hazard ratio 5.97 (95% CI, 3.12 to 11.41), a difference that was attenuated but not eliminated by the presence of diabetes (hazard ratio 2.33, 95% CI, 1.02 to 5.35).

"The findings highlight the importance of efforts to improve the management of kidney disease among black patients with HIV infection," said Dr. Choi. "The pronounced race-dependence of HIV as a risk factor for ESRD also suggests that HIV may serve as a model for understanding racial differences in progression of kidney disease."

The authors noted that the study was limited by potential misclassification of diabetes, and it is not known whether the results could be generalizable to non-veteran populations or to women.

In addition, they were unable to adjust for proteinuria, blood pressure, the severity of comorbid conditions, access to treatment, or the intensity or regularity of follow-up care, and they could not determine whether differences in antiretroviral therapy could have contributed to the racial differences they saw.

Co-author Paul A. Volberding, M.D., has served as a consultant to Pfizer, GlaxoSmithKline, Bristol-Myers Squibb, Gilead, Boehringer Ingelheim, Merck, and Schering-Plough; has received honoraria from Gilead and Bristol-Myers Squibb; and owns stock or options (other than mutual funds) in Immune Response Corp. No other authors reported conflicts of interest.

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