Alvestrand A, Bergström J
Lancet. 1984 Jan 28;1(8370):195-7. doi: 10.1016/s0140-6736(84)92115-9.
Glomerular hyperfiltration induced by various stimuli (protein ingestion, amino-acid infusion, glucagon infusion, diabetes mellitus) is postulated to be associated with increased secretion by the liver of a hormone that increases glomerular filtration rate. In severe liver failure deficient secretion of this hormone is presumed to cause or contribute to the development of the hepatorenal syndrome. There is evidence that increased hepatic uptake of aminoacids is a factor triggering secretion of this hormone. The hypothesis, which is based on earlier published studies in laboratory animals and in man, accords well with clinical observations. This hypothesis may explain how glomeruli respond to metabolic stimuli and raises the possibility of therapeutic intervention in the glomerular hyperfiltration of diabetes and chronic renal failure.
由各种刺激（蛋白质摄入、氨基酸输注、胰高血糖素输注、糖尿病）引起的肾小球高滤过被认为与肝脏分泌一种增加肾小球滤过率的激素增多有关。在严重肝功能衰竭时，推测这种激素分泌不足会导致肝肾综合征的发生或促使其发展。有证据表明肝脏对氨基酸摄取增加是触发这种激素分泌的一个因素。该假说基于早期在实验动物和人类中发表的研究，与临床观察结果非常吻合。这一假说或许可以解释肾小球如何对代谢刺激作出反应，并增加了对糖尿病和慢性肾衰竭患者肾小球高滤过进行治疗干预的可能性。
