Saracyn Marek, Zdanowski Robert, Brytan Marek, Kade Grzegorz, Nowak Zbigniew, Patera Janusz, Dyrla Przemysław, Gil Jerzy, Wańkowicz Zofia
Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, Warsaw, Poland.
Department of Regenerative Medicine, Military Institute of Hygiene and Epidemiology, Warsaw, Poland.
Med Sci Monit. 2015 May 22;21:1469-77. doi: 10.12659/MSM.893291.
Short-term administration of Galactosamine to experimental animals causes liver damage and acute liver failure (ALF), as well as acute renal failure in some cases. The aim of our study was to describe kidney disorders that developed in the course of galactosamine-induced liver failure.
Sprague-Dawley rats were randomly divided into 2 groups: a study group administered galactosamine intraperitoneally and a control group administered saline.
All the animals in the study group developed liver damage and failure within 48 h, with significant increase of alanine (p<0.001), aspartate aminotransferases (p<0.0001), bilirubin (p<0.004), and ammonia (p<0.005) and decrease of albumin (p<0.001) concentrations. Acute renal failure was observed in all test animals, with a significant increase in creatinine (p<0.001) and urea (p<0.001) concentrations and a decrease in creatinine clearance (p<0.0012). Moreover, osmotic clearance (p<0.001), daily natriuresis (p<0.003), and fractional sodium excretion (p<0.016) decreased significantly in this group of animals. The ratio of urine osmolality to serum osmolality did not change. Histopathology of the liver revealed massive necrosis of hepatocytes, whereas renal histopathology showed no changes.
Acute renal failure that developed in the course of galactosamine-induced ALF was of a functional nature, with the kidneys retaining the ability to concentrate urine and retain sodium, and there were no renal changes in the histopathological examination. It seems that the experimental model of ALF induced by galactosamine can be viewed as a model of hepatorenal syndrome that occurs in the course of acute damage and liver failure.
给实验动物短期注射半乳糖胺会导致肝损伤和急性肝衰竭（ALF），某些情况下还会引发急性肾衰竭。我们研究的目的是描述在半乳糖胺诱导的肝衰竭过程中出现的肾脏疾病。
将Sprague-Dawley大鼠随机分为两组：腹腔注射半乳糖胺的研究组和注射生理盐水的对照组。
研究组所有动物在48小时内均出现肝损伤和肝衰竭，丙氨酸（p<0.001）、天冬氨酸转氨酶（p<0.0001）、胆红素（p<0.004）和氨（p<0.005）浓度显著升高，白蛋白浓度降低（p<0.001）。所有受试动物均出现急性肾衰竭，肌酐（p<0.001）和尿素（p<0.001）浓度显著升高，肌酐清除率降低（p<0.0012）。此外，该组动物的渗透清除率（p<0.001）、每日尿钠排泄量（p<0.003）和钠排泄分数（p<0.016）显著降低。尿渗透压与血清渗透压之比未发生变化。肝脏组织病理学显示肝细胞大量坏死，而肾脏组织病理学未显示变化。
半乳糖胺诱导的ALF过程中出现的急性肾衰竭属于功能性，肾脏保留了浓缩尿液和保留钠的能力，组织病理学检查未发现肾脏病变。似乎半乳糖胺诱导的ALF实验模型可被视为急性损伤和肝衰竭过程中发生的肝肾综合征模型。
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