Rodrigo R, Thielemann L, Olea M, Muñoz P, Cereceda M, Orellana M
Programa de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas, Santiago, Chile.
Arch Med Res. 1998 Autumn;29(3):209-18.
Ethanol may alter the homeostasis of water and electrolytes before the occurrence of liver damage able to explain these disorders. How the kidney may become involved in water diuresis or sodium and potassium retention has not been well elucidated. During the last decade, an increasing body of evidence has guided interest toward the relevance of the biochemical basis of ethanol-induced injury to the kidney. Multiple functional abnormalities of renal tubules may be associated with ethanol-induced changes in membrane composition and lipid peroxidation of these epithelial cells. Ethanol interferes with the carrier function by decreasing (Na+K)-ATPase activity, but this activity is enhanced by chronic exposure. Recently, it was reported that ethanol oxidation by the kidney is favored in chronic ethanol-treated rats, thereby suggesting a pathogenic role for acetaldehyde in the nephrotoxic effect of ethanol ingestion. Also, increased reactive oxygen species, partly generated from acetaldehyde oxidation, may contribute to the occurrence of oxidative stress. The pathophysiology of renal regulation of water and electrolytes of alcoholic disease is analyzed on the basis of recent advances in our knowledge concerning the biochemical effects of ethanol on the kidney.
在能够解释这些紊乱的肝损伤出现之前,乙醇可能会改变水和电解质的稳态。肾脏如何参与水利尿或钠钾潴留尚未得到充分阐明。在过去十年中,越来越多的证据引导人们关注乙醇诱导的肾损伤的生化基础的相关性。肾小管的多种功能异常可能与乙醇诱导的这些上皮细胞膜成分变化和脂质过氧化有关。乙醇通过降低(Na + K)-ATP酶活性来干扰载体功能,但长期暴露会增强这种活性。最近,有报道称在慢性乙醇处理的大鼠中,肾脏对乙醇的氧化作用增强,从而提示乙醛在乙醇摄入的肾毒性作用中具有致病作用。此外,部分由乙醛氧化产生的活性氧增加可能导致氧化应激的发生。基于我们对乙醇对肾脏生化作用的最新认识进展,分析了酒精性疾病中水和电解质肾脏调节的病理生理学。