Renal function in HIV/HBV co‐infected and HBV mono‐infected patients on a long‐term treatment with tenofovir in real life setting. (February 2017)

• Record Type: Journal Article
• Authors: Milazzo, Laura; Gervasoni, Cristina; Falvella, Felicia Stefania; Cattaneo, Dario; Mazzali, Cristina; Ronzi, Paola; Binda, Francesca; Cheli, Stefania; Sollima, Salvatore; Antinori, Spinello
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 44:Number 2(2017:Feb.)
• Page Start: 191
• Page End: 196
• Publication Date: 2017-02
• Subjects: pharmacogenetics -- renal toxicity -- tenofovir; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.12691
• Languages: English
• ISSNs: 0305-1870

Abstract

Summary: The human immunodeficiency virus (HIV)/hepatitis B virus (HBV) co‐infection is likely to be associated with an increased risk of kidney disease, due to the additional factors that may affect renal function in the HIV population. We aimed to evaluate renal toxicity in HIV/HBV and HBV mono‐infected patients on long‐term therapy with tenofovir (TDF) and to explore the association of polymorphisms in ATP‐binding cassette ( ABCC ) 2, ABCC4, ABCC10 with the development of renal dysfunction. From September 2006 to November 2014, 44 HIV/HBV co‐infected and 34 HBV mono‐infected patients were commenced on TDF. Data of renal safety were retrospectively collected and analyzed. ABCC2, ABCC4 and ABCC10 genotypes were identified by real‐time PCR. Over 60 months of observation, there was a significant increase in mean creatinine levels from baseline ( P <.01) that was not significantly different between the two study groups. Moreover, a significant decline in estimated glomerular filtration rate (eGFR) was observed from baseline ( P <.01), and it was significantly greater in HBV mono‐infected than co‐infected patients ( P =.03). The distribution of ABCC2, ABCC4 and ABCC10 genotypes among a subgroup of 34 patients did not show significant association with eGFR decline <90 mL/min per 1.73 m 2 . Although our findings showed a statistically significant decrease in eGFR with long‐term use of TDF, its clinical impact seems to be modest. The role of genetic factors to identify patients at greater risk for developing tenofovir‐induced renal toxicity needs to be further investigated.