RESUMO
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.
Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Síndrome da Imunodeficiência Adquirida/tratamento farmacológico , Inibidores da Protease de HIV/efeitos adversos , Indinavir/efeitos adversos , Necrose Papilar Renal/induzido quimicamente , Necrose Papilar Renal/diagnóstico , Tuberculose Urogenital/diagnóstico , Diagnóstico Diferencial , Taxa de Filtração GlomerularRESUMO
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