RESUMEN
This case reported to a patient with AIDS who presented persistent sterile leukocyturia and hematuria, lower back pain, bladder suffering symptoms, and renal papillary necrosis which were thought to be secondary to urinary tuberculosis but were demonstrated to be indinavir-associated side effects. The intention of this report is to remind medical professionals involved in the care of HIV+ patients of this possible association in order to avoid unnecessary investigation and to stress the need of careful periodical assessment of renal function and urinalysis in patients treated with indinavir.
Asunto(s)
Humanos , Masculino , Persona de Mediana Edad , Síndrome de Inmunodeficiencia Adquirida/tratamiento farmacológico , Inhibidores de la Proteasa del VIH/efectos adversos , Indinavir/efectos adversos , Necrosis Papilar Renal/inducido químicamente , Necrosis Papilar Renal/diagnóstico , Tuberculosis Urogenital/diagnóstico , Diagnóstico Diferencial , Tasa de Filtración GlomerularRESUMEN
Background. The effect of bromoethylamine (BEA) administration on lipid peroxidation and on the activieties of antioxidant enzymes was studied. Methods. Adult rats received BEA at 1.2 mmol/kg, a dose that produces renal papillary necrosis. Lipid peroxidation assessed by maximal rate in MDA formation, the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the levels of non-protein sulfhydryls (NPSH) were measured in renal cortex and papilla of control and BEA-treated animals. Results. After BEA treatment, an increment in lipid peroxidation in papilla and cortex was found after 1.5 and 24 hours of treatment. Catalase activity decreased in both regions, but earlier cortex. Conclusion. These data suggest some role of oxidative stress in the mechanism of BEAinduced papillary necrosis