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Glomerular filtration rate change during chronic hepatitis C treatment with Sofosbuvir/Ledipasvir in HCV/HIV Coinfected patients treated with Tenofovir and a boosted protease inhibitor: an observational prospective study

INTRODUCTION: Concomitant use of ledipasvir and boosted protease inhibitors (PIs) may increase the risk of tenofovir (TDF) nephrotoxicity, since both these drugs increase TDF levels. Our aim was to evaluate glomerular filtration rate (eGFR) evolution during HCV treatment with sofosbuvir/ledipasvir (...

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Detalles Bibliográficos
Autores principales: Soeiro, Cristina Aurora São Pedro, Gonçalves, Celina Andreia Melo, Marques, Marta Sofia Correia, Méndez, Maria Josefina Vazquez, Tavares, Ana Paula Ribeiro Almeida, Horta, Ana Maria Lacerda Morgado Fernandes de Carvalho de Aboim, Sarmento-Castro, Rui Manuel do Rosário
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090809/
https://www.ncbi.nlm.nih.gov/pubmed/30075765
http://dx.doi.org/10.1186/s12879-018-3278-3
Descripción
Sumario:INTRODUCTION: Concomitant use of ledipasvir and boosted protease inhibitors (PIs) may increase the risk of tenofovir (TDF) nephrotoxicity, since both these drugs increase TDF levels. Our aim was to evaluate glomerular filtration rate (eGFR) evolution during HCV treatment with sofosbuvir/ledipasvir (SOF/LDV) in HCV/HIV coinfected patients, according to their antiretroviral treatment (ARV). METHODS: Observational prospective study of HCV/HIV coinfected patients treated with SOF/LDV. eGFR evolution was evaluated during and 12 weeks after HCV treatment. Patients were categorized in three groups based on ARV regimen: non TDF, non-boosted TDF and TDF + boosted PI. RESULTS: We included 273 patients: 145 were receiving a non-TDF regimen, 78 a non-boosted TDF scheme and 50 were receiving TDF + boosted PI. We observed a statistically significant decrease in eGFR during treatment in all groups (non TDF p = 0.03, 95%CI [0.23–3.86], non-boosted TDF p < 0.01, 95%CI [3.36–7.44], TDF + PI p = 0.01, 95%CI [1.09–7.53]). The decrease was more pronounced in those receiving unboosted TDF (− 5.40 ml/min/1.73m(2)), but differences in eGFR decrease between the three groups were small and not statistically different (p = 0.06). eGFR decrease was greater in patients treated for 24 weeks (p = 0.009) and in cirrhotic patients (p = 0.036). At the end of follow up a recovery of eGFR was observed in all groups. CONCLUSION: We observed a significant decrease in eGFR during treatment in all study groups, that was small and reversible after SOF/LDV discontinuation. TDF was not associated with an increase in renal toxicity.