icon-    folder.gif   Conference Reports for NATAP  
  17th CROI
Conference on Retroviruses
and Opportunistic Infections
San Francisco CA
February 16-19, 2010
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Determinants of Incident Chronic Kidney Disease in a Cohort of HIV-infected Patients with Free Access to Care
  Reported by Jules Levin
CROI 2010 Feb 16-19 SF
Anuradha Ganesan*1,2, E Krantz1,3, K Huppler Hullsiek1,3, M Ross4, M Riddle5, M Landrum1,6, T Lalani1,7, A Weintrob1,8, B Agan1, N Crum-Cianflone1,9, and the IDCRP HIV Working Group 1Uniformed Svcs Univ of the Hlth Sci, Bethesda, MD, US; 2Natl Naval Med Ctr, Bethesda, MD, US; 3Univ of Minnesota, Minneapolis, US; 4Mt Sinai Sch of Med, New York, NY, US; 5Naval Med Res Ctr, Silver Spring, MD, US; 6San Antonio Military Med Ctr, TX, US; 7Naval Med Ctr Portsmouth, VA, US; 8Walter Reed Army Med Ctr, Washington, DC, US; and 9Naval Med Ctr San Diego, CA, US

In the US, estimates of chronic kidney disease (CKD) in HIV-infected patients are mostly derived from urban clinics, settings where socio-economic factors may influence progression to CKD. We evaluated the incidence and risk factors of CKD among participants enrolled in the US Military HIV Natural History Study, a prospective cohort characterized by free access to healthcare and minimal illicit drug use.
Methods: The Modification of Diet in Renal Disease Equation was used to estimate the glomerular filtration rate (eGFR). Incident CKD was defined as a GFR <60 ml/min/1.73 m2 for at least 90 days among those negative for CKD at baseline (BL; HIV diagnosis). Rates are expressed per 1000 person-years (PY). BL risk factors (age, race, sex, year of HIV diagnosis, hypertension (HTN), CD4 cell count) were assessed with Cox proportional hazards models. Rates and hazard ratios (HR) are reported with 95% confidence intervals.
Results: Between 1986 and 2008, 4044 subjects contributed a median of 6.5 yrs (IQR 3.7-10.9) of follow-up. 2109 subjects had documented HIV positive and negative dates within a 3 year window. At BL median age was 29 yrs (IQR 24-34), 92% were male, 45% African-American (AA) and 44% European-American (EA), with a median CD4 count of 506 (IQR 360-671). Overall CKD incidence rate (n=90) was 2.8/1000 PY (2.3-3.5). Incidence was similar for AA 2.5 (1.8-3.5) and EA 3.2 (2.3-4.3).
At CKD diagnosis, median age was 39 yrs (IQR 36-50),median CD4 count was 119 (IQR 11-408), and median time from HIV diagnosis to onset of CKD was 5.8 yrs (IQR 4.3-9.6). In a multivariate model, age [Referent (Ref) < 35; Age ≥35, HR 2.6 (1.7-4.0)], female sex [HR 2.2 (1.2-4.1)], year of diagnosis [Ref 1996 or later; pre-1996, HR 6.0 (2.4-15.2)], and BL CD4 count [Ref CD4 ≥ 500; CD4 350-499, HR 2.4 (1.3-4.6); CD4 201-349, HR 4.3 (2.3-8.1); CD4 <=200, HR 7.0 (3.1-16.0)] were significant, whereas race was not [Ref EA; AA, HR 0.7 (0.5-1.1)], while the association with HTN was marginal [HR 2.1 (0.9- 4.6)].
Conclusion: The incidence of CKD in our cohort was lower than previously reported and an association with AA ethnicity was not observed. Unique features of our cohort such as younger age, early diagnosis, unrestricted access to healthcare, and minimal drug use may in part explain the observed differences. The extent of immunologic dysfunction (reflected by the CD4 cell count) at the time of HIV diagnosis is a strong determinant of the future risk of CKD, emphasizing the need for early diagnosis and treatment to prevent CKD.


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