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1.
Nefrologia ; 35(2): 197-206, 2015.
Artículo en Inglés, Español | MEDLINE | ID: mdl-26300514

RESUMEN

BACKGROUND: Renin-angiotensin system inhibitors (ACEI/ARB-II), diuretics and NSAIDs, a combination known as "Triple Whammy", can result in decreased glomerular filtration rate (GFR) and acute kidney injury (AKI). Objectives: To describe the incidence of AKI for each drug type and their combinations. To define the profile of patients admitted for drug-related AKI secondary to Triple Whammy drugs (AKITW), with an assessment of costs and mortality. METHODS: A retrospective observational 15-month study developed in three stages: - First: a cross-sectional stage to identify and describe hospitalizations due to AKITW. - Second: a follow-up stage of an outpatient cohort consuming these drugs (15,307 subjects). - Third: a cohort stage to assess costs and mortality, which compared 62 hospitalized patients with AKITW and 62 without AKI, paired by medical specialty, sex, age and comorbidity according to their Clinical Risk Groups. RESULTS: There were 85 hospitalization episodes due to AKITW, and 78% of patients were over the age of 70. The incidence of AKITW in the population was 3.40 cases/1000 users/year (95% CI: 2.59-4.45). By categories, these were: NSAIDs + diuretics 8.99 (95% CI: 3.16-25.3); Triple Whammy 8.82 (95% CI: 4.4-17.3); ACEI/ARB-II + diuretics 6.87 (95% CI: 4.81-9.82); and monotherapy with diuretics 3.31 (95% CI: 1.39-7.85). Mean hospital stay was 7.6 days (SD 6.4), and mean avoidable costs were estimated at €214,604/100,000 inhabitants/year. Mortality during hospitalization and at 12 months was 11.3% and 38.7% respectively, and there were no significant differences when compared with the control group. CONCLUSIONS: Treatment with ACEI, ARB-II, diuretics and/or NSAIDs shows a high incidence of hospitalization episodes due to AKI; diuretics as monotherapy or dual and triple combination therapy cause the highest incidence. AKITW involves high health care costs and avoidable mortality.


Asunto(s)
Lesión Renal Aguda/tratamiento farmacológico , Bloqueadores del Receptor Tipo 1 de Angiotensina II/efectos adversos , Inhibidores de la Enzima Convertidora de Angiotensina/efectos adversos , Antiinflamatorios no Esteroideos/efectos adversos , Diuréticos/efectos adversos , Lesión Renal Aguda/economía , Lesión Renal Aguda/mortalidad , Adulto , Anciano , Anciano de 80 o más Años , Bloqueadores del Receptor Tipo 1 de Angiotensina II/farmacocinética , Inhibidores de la Enzima Convertidora de Angiotensina/farmacocinética , Antiinflamatorios no Esteroideos/farmacocinética , Estudios Transversales , Diuréticos/farmacocinética , Sinergismo Farmacológico , Femenino , Costos de Hospital , Hospitalización/estadística & datos numéricos , Humanos , Masculino , Persona de Mediana Edad , Sistema Renina-Angiotensina/efectos de los fármacos , Estudios Retrospectivos , España
2.
Clin Nephrol ; 81(3): 203-9, 2014 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-23006341

RESUMEN

Intolerance to fava beans in subjects with glucose-6-phosphate-dehydrogenase deficiency (favism) may lead to severe hemolytic crises and decreased renal function. Renal biopsy findings exploring the molecular mechanisms of renal damage in favism have not been previously reported. We report a case of favism-associated acute kidney injury in which renal biopsy showed acute tubular necrosis and massive iron deposits in tubular cells. Interestingly, iron deposit areas were characterized by the presence of oxidative stress markers (NADPH-p22 phox and heme-oxigenase-1) and macrophages expressing the hemoglobin scavenger receptor CD163. In addition, iron deposits, NADPH-p22 phox, hemeoxigenase- 1 and CD163 positive cells were observed in some glomeruli. These results identify both glomerular and tubular involvement in favism-associated acute kidney injury and suggest novel therapeutic targets to prevent or accelerate recovery from acute kidney injury.


Asunto(s)
Lesión Renal Aguda/etiología , Favismo/complicaciones , Glomérulos Renales/química , Túbulos Renales/química , Lesión Renal Aguda/diagnóstico , Lesión Renal Aguda/metabolismo , Lesión Renal Aguda/terapia , Antígenos CD/análisis , Antígenos de Diferenciación Mielomonocítica/análisis , Biomarcadores/análisis , Biopsia , Favismo/diagnóstico , Hemo-Oxigenasa 1/análisis , Humanos , Inmunohistoquímica , Glomérulos Renales/patología , Necrosis Tubular Aguda/etiología , Necrosis Tubular Aguda/metabolismo , Túbulos Renales/patología , Macrófagos/química , Masculino , Persona de Mediana Edad , NADPH Oxidasas/análisis , Receptores de Superficie Celular/análisis , Diálisis Renal , Factores de Tiempo , Resultado del Tratamiento
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