RESUMEN
In this study we investigated the effects of N-hexacosanol on streptozotocin-induced rat diabetic nephropathy. Diabetes was induced in 8-week-old male Sprague-Dawley rats by administering an intraperitoneal injection of streptozotocin (50 mg/kg). The rats were divided into four groups and maintained for 8 weeks: control rats, diabetic rats without treatment with N-hexacosanol, and diabetic rats treated with N-hexacosanol (2 mg/kg and 8 mg/kg i.p. every day). Although N-hexacosanol failed to modify the diabetic status, increases in serum creatinine as well as in kidney weight were significantly reduced. The malonaldehyde and transforming growth factor beta-1 (TGF-beta1) concentrations as well as the protein kinase C (PKC) activities in the diabetic kidney were significantly higher than those of the control, which were decreased by treatment with N-hexacosanol. Histological examinations revealed that N-hexacosanol significantly ameliorated diabetic-induced tubulointerstitial pathological changes. Our data suggest that N-hexacosanol could prevent increases in the malonaldehyde and TGF-beta1 concentrations and PKC activities in the kidney, and ameliorate diabetic-induced nephropathy.
Asunto(s)
Nefropatías Diabéticas/inducido químicamente , Nefropatías Diabéticas/patología , Alcoholes Grasos/farmacología , Estreptozocina/farmacología , Animales , Nitrógeno de la Urea Sanguínea , Creatinina/metabolismo , Insulina/metabolismo , Masculino , Malondialdehído/metabolismo , Proteína Quinasa C/metabolismo , Ratas , Ratas Sprague-Dawley , Factor de Crecimiento Transformador beta1/metabolismoRESUMEN
We report a 71-year-old woman with autosomal dominant polycystic kidney disease (ADPKD), who presented with hepatic encephalopathy. She was diagnosed as having ADPKD at 61 years of age. Thereafter, her renal function gradually worsened and she was admitted to our hospital because of encephalopathy and end-stage renal failure. The main laboratory findings were as follows: BUN 77 mg/dl; creatinine 9.0 mg/d; ammonia 573 microg/dl. Hepatic encephalopathy was improved after hemodialysis and administration of lactulose. The liver demonstrated multiple cysts on computed tomography. Angiography demonstrated that the peripheral branch of the portal vein was stenotic and a spleno-renal shunt was detected. We considered that portal hypertension was caused by multiple liver cysts, and that hepatic encephalopathy was caused by the spleno-renal shunt. It is generally considered that severe hepatic complications are rare in ADPKD, but this case suggested the need to screen for the development of hepatic lesions in ADPKD.