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Detection of Chronic Renal Failure among HIV Patients within the EuroSIDA Study
Amanda Mocroft*1, O Kirk2, J Gatell3, P Reiss4, P Gargalianos-Kakolyris5, K Zilmer6, M Beniowski7, J P Viard8, S Staszewski9, J Lundgren2, and The EuroSIDA Study Group
1Univ Coll London, Royal Free Hosp, UK; 2Copenhagen HIV Prgm, Hvidovre, Denmark; 3Hosp Clin of Barcelona, Spain; 4Univ of Amsterdam, The Netherlands; 5Gen Hosp of Athens, Greece; 6West-Tallinn Central Hosp, Estonia; 7Szpital Specjalistyczny, Chorzow, Poland; 8Hosp Necker-Enfants Malades, Paris, France; and 9JW Goethe Univ Hosp, Frankfurt, Germany
Background: Chronic renal failure (CRF) in HIV may be due
to HIV-associated nephropathy or well-identified risk factors seen in HIV–
persons; the role of exposure to ART drugs is not well understood. Single
determinations of glomerular filtration rates (GFR)
using serum creatinine and the Cockcroft-Gault (CG) or modification of diet in renal disease (MDRD)
equations can be imprecise as many factors influence serum creatinine
in addition to renal function.
Methods: Baseline was defined as the first recorded GFR;
patients with 2 consecutive GFR ≤60 mL/minute/1.73 m2 were
defined as having CRF. Logistic regression was used to determine odds ratio
(OR) of having CRF at baseline. ART exposure (yes/no or cumulative exposure)
prior to baseline was included in multivariate models (adjusted for region of Europe, age, prior AIDS, CD4 nadir, viral load, and
hypertension).
Results: The median GFR at baseline (n = 4474; CG) was 94.4 (IQR 80.5 to
109.3) and 158 patients (3.5%) had CRF. Patients with CRF were older (median
61.9 vs 43.1 years), had lower CD4 nadir (80 vs 137), and were more likely to be diagnosed with AIDS
(44.3 vs 30.4%), diabetes (16.5 vs
4.3%), or hypertension (53.8 vs 26.4%), all p <0.001. They were also more likely to have
received potentially nephrotoxic drugs for opportunistic infections therapy
(26.0 vs 15.1%, p <0.001) and
combination ART (97.5 vs 91.0%, p =
0.013). Of those with CRF, 120 had been exposed to indinavir
(IDV) and 61 to tenofovir (TDF). In a multivariate
model any use of IDV (OR 2.50, 1.63 to 3.84) or TDF (1.87, 1.25 to 2.79) was
associated with increased odds of CRF, as was cumulative exposure to IDV (2.51
per year of exposure, 1.63 to 3.85) or TDF (2.19, 1.26 to 3.83). There was no
association with concomitant use of TDF and ritonavir
(RTV). Highly
consistent results were seen using the MDRD formula.
Conclusions: The prevalence of CRF, defined as a confirmed
low GFR, was <5%. Older age, presence of diabetes and hypertension were
associated with increased odds of CRF, as was lower CD4 nadir and prior AIDS.
The latter might be explained by use of nephrotoxic drugs to manage
opportunistic infections. Among the ART, only exposure (any/cumulative) to IDV
or TDF was associated with increased odds of CRF. We used a confirmed low GFR
to define CRF to increase the robustness of our analysis, although there are
several potential biases associated with this cross-sectional analysis. Future
analyses should focus on confirmed changes in GFR, thus requiring large numbers
of patients and serial GFR measurements.
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