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Lucas, Gregory M.; Jing, Yuezhou; Sulkowski, Mark; Abraham, Alison G.; Estrella, Michelle M.; Atta, Mohamed G.; Fine, Derek M.; Klein, Marina B.; Silverberg, Michael J.; Gill, M. John; Moore, Richard D.; Gebo, Kelly A.; Sterling, Timothy R.; Butt, Adeel A.
The Journal of infectious diseases, 10/2013, Letnik: 208, Številka: 8Journal Article
Background. The role of active hepatitis C virus (HCV) replication in chronic kidney disease (CKD) risk has not been clarified. Methods. We compared CKD incidence in a large cohort of HIV-infected subjects who were HCV seronegative, HCV viremic (detectable HCV RNA), or HCV aviremic (HCV seropositive, undetectable HCV RNA). Stages 3 and 5 CKD were defined according to standard criteria. Progressive CKD was defined as a sustained 25% glomerular filtration rate (GFR) decrease from baseline to a GFR < 60 mL/min/1.73 m². We used Cox models to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). Results. A total of 52 602 HCV seronegative, 9508 HCV viremic, and 913 HCV aviremic subjects were included. Compared with HCV seronegative subjects, HCV viremic subjects were at increased risk for stage 3 CKD (adjusted HR 1.36 95% CI, 1.26, 1.46), stage 5 CKD (1.95 1.64, 2.31), and progressive CKD (1.31 1.19, 1.44), while HCV aviremic subjects were also at increased risk for stage 3 CKD (1.19 0.98, 1.45), stage 5 CKD (1.69 1.07, 2.65), and progressive CKD (1.31 1.02, 1.68). Conclusions. Compared with HIV-infected subjects who were HCV seronegative, both HCV viremic and HCV aviremic individuals were at increased risk for moderate and advanced CKD.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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