Zhou Chong, Byard Roger W
The University of Adelaide Medical School, Adelaide, SA 5005, Australia.
J Forensic Sci. 2012 Jan;57(1):126-8. doi: 10.1111/j.1556-4029.2011.01957.x. Epub 2011 Nov 10.
Subnuclear renal tubular epithelial cell vacuolization is a marker for diabetic ketoacidosis. Whether it is because of hyperglycemia or of ketoacidosis is unclear. To examine the effect of ketoacidosis on renal cells in isolation, five cases of lethal alcoholic ketoacidosis without hyperglycemia were examined (vitreous humor β-hydroxybutyrate: 6.42-8.75 mM, mean 7.66 mM; and glucose: 0.1-4.2 mM, mean 1.46 mM). Microscopic examination of the kidneys revealed basal vacuoles in three cases (60%). Seven control cases with acute alcohol toxicity without ketoacidosis (blood alcohol: 0.18-0.43%, mean 0.31%; and β-hydroxybutyrate: 0.12-0.42 mM, mean 0.21 mM) did not have these changes. In this study, basal epithelial vacuolization was found only in cases with significant ketoacidosis. Although the numbers are small, the finding of basal renal tubular epithelial vacuolization in normoglycemic cases with elevated β-hydroxybutyrate levels provide further evidence that disordered lipid metabolism may be involved in the pathogenesis of this phenomenon.
核下肾小管上皮细胞空泡化是糖尿病酮症酸中毒的一个标志物。尚不清楚这是由于高血糖还是酮症酸中毒所致。为了单独研究酮症酸中毒对肾细胞的影响,对5例无高血糖的致死性酒精性酮症酸中毒病例进行了检查(玻璃体液β-羟基丁酸:6.42 - 8.75 mM,平均7.66 mM;葡萄糖:0.1 - 4.2 mM,平均1.46 mM)。肾脏的显微镜检查显示,3例(60%)出现基底空泡。7例无酮症酸中毒的急性酒精中毒对照病例(血酒精:0.18 - 0.43%,平均0.31%;β-羟基丁酸:0.12 - 0.42 mM,平均0.21 mM)未出现这些变化。在本研究中,仅在显著酮症酸中毒的病例中发现基底上皮空泡化。尽管病例数较少,但在β-羟基丁酸水平升高的血糖正常病例中发现基底肾小管上皮空泡化,进一步证明脂质代谢紊乱可能参与了这一现象的发病机制。