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    "titulo" => "Acute renal failure and proximal renal tubular dysfuntion in a patient with acquired immunodeficiency syndrome treated with tenofovir"
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        "resumen" => "Tenofovir es un nuevo inhibidor de la transcriptasa inversa con buena actividad frente a cepas resistentes del virus de inmunodeficiencia humana (HIV), de estructura similar a adefovir y cidofovir. Con éstos se ha descrito la aparición de un defecto en el transporte de sustancias en el túbulo proximal. Los estudios in vitro y las primeras referencias clínicas sobre tenofovir indicaban que presentaba poca toxicidad a nivel renal, y que su toxicidad a nivel mitocondrial era escasa. No obstante se han descrito recientemente casos de disfunción tubular proximal e insuficiencia renal relacionados con el uso de este fármaco. Además tenofovir puede aumentar las concentraciones plasmáticas de didanosina, aumentando la toxicidad mitocondrial de ésta, y los inhibidores de la proteasa pueden provocar una acumulación de tenofovir en las células tubulares renales, pudiendo desarrollarse una tubulopatía proximal. Presentamos una paciente HIV positiva que había presentado complicaciones con el tratamiento con didanosina, que desarrolla un cuadro de insuficiencia renal aguda y tubulopatía proximal (glucosuria normoglucémica, acidosis metabólica hiperclorémica) tras el tratamiento con tenofovir. Aunque la nefrotoxicidad de este fármaco parece ser menos frecuente que con otros análogos de nucleósidos, la utilización de tenofovir en pacientes con disfunción renal subyacente, durante largos períodos de tiempo, o asociados a didanosina y/o inhibidores de la proteasa, podría asociarse a ésta toxicidad. Si se utiliza tenofovir en estos pacientes deben monitorizarse la aparición de signos de tubulopatía, además de vigilar la función renal y la aparición de signos de toxicidad mitocondrial, suspendiendo su utilización para evitar la progresión a insuficiencia renal avanzada."
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        "resumen" => "Tenofovir, a new nucleotide reverse transcriptase inhibitor that has good antiviral activity against drug-resistant strains of HIV, is structurally similar to cidofovir and adefovir and seems to be less nephrotoxic. Nephrotoxicity of cidofovir and adefovir is well established and they have been associated with increase for acute renal insufficiency due to tubular toxicity, possibly induced via mitochondrial deplection. Tenofovir has little mithocondrial toxicity in in vitro assays and early clinical studies. However some cases of renal tubular dysfuntion and renal failure related to tenofovir treatment have been published recently. Increased plasma concentrations of didanosine were observed after the adition of tenofovir and protease inhibitors can interact with the renal transport of organic anions leading to proximal tubular intracellular accumulation of tenofovir, yield Fanconi syndrome-type tubulopathy. We present a case in wich acute renal failure and proximal tubular dysfunction developed after therapy with tenofovir in a patiente with HIV who had suffered from complications of didanosine treatment. Although nephrotoxicity certainly occurs much less frequently with tenofovir that it does with other nuclotide analogues, use of tenofovir by patients with underlying renal disfuntion, for longer durations and/or associated with didanosine or lopinavir-ritonavir, might be associated with renal toxicity. Patients receiving tenofovir must be monitored for sings of tubulopathy with simple tests such us glycosuria, phosphaturia, proteinuria, phosphoremia and renal function, as well as assessment for signs of mithocondrial toxicity when a nucleoside analogue is being administered, and therapy should be stopped to avoid the risk of definitive renal failure."
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