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Chronic Kidney Disease Incidence and Progression to ESRD in HIV-infected Individuals: A Tale of 2 Races
Gregory Lucas*, B Lau, M Atta, D Fine, J Keruly, and R Moore
Johns Hopkins Univ, Baltimore, MD, US
Background: Among HIV-infected individuals, African
Americans are at substantially higher risk of end-stage renal disease (ESRD)
than white individuals. However, little is known about racial differences in
the incidence and progression of chronic kidney disease (CKD) that underlie
ESRD disparities. Our objective was to assess racial differences in HIV-associated
CKD incidence, glomerular filtration rate (GFR) slope, and progression to ESRD
in subjects with CKD.
Methods: Data were analyzed from 3332 (78%) African
American and 927 (22%) white participants in the Johns Hopkins HIV Cohort, who
contributed 18,778 person-years of follow-up between 1990 and 2004. GFR was
estimated by modification of diet in renal disease (MDRD) equation; CKD was
defined as GFR <60 mL/min/L·73 m2 for >3 months; ESRD was
defined as initiation of renal replacement therapy. GFR slopes were estimated
with a random-effects linear model. Factors associated incident CKD in the
overall cohort and with progression to ESRD among those with CKD were assessed
separately in Cox proportional hazards models.
Results: Of the 284 individuals who developed CKD (7%
of cohort), 100 progressed to ESRD. African American subjects were at increased
risk for incident CKD compared to white participants (hazard ratio [HR] 1.9,
95% confidence interval [CI] 1.2 to 2.8). However, once commenced, CKD
progression to ESRD was markedly higher in African American than white
participants (HR 17.7, 95%CI 2.5 to 127.0). Correspondingly, high-grade
proteinuria was more common in African American than white subjects with CKD
(45% and 4%, respectively, p <0.001), and GFR decline following CKD
diagnosis was 6-fold more rapid in the former than the latter group (p <0.001).
Compared to white subjects with CKD, African American subjects with CKD were
significantly more likely to progress to ESRD irrespective of whether they had
a kidney biopsy demonstrating HIV-associated nephropathy (HIVAN) (HR 45, 95%CI
6 to 343, p <0.001), a biopsy showing non-HIVAN histopathology (HR
14, 95%CI 2 to 109, p =0.009), or did not have a kidney biopsy performed
(HR 16, 95%CI 2 to 117, p =0.006).
Conclusions: Our results suggest that black–white
disparities in HIV-related ESRD are explained predominantly by a more
aggressive CKD natural history in blacks, and less by racial differences in CKD
incidence. Significantly faster progression of CKD to ESRD occurs in blacks
than whites even when non-HIVAN histopathology is identified in the former.
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