Scolnik D, Halperin M L
Renal Divisions, Hospital for Sick Children, Toronto, Ont., Canada.
Nephron. 1993;63(3):342-6. doi: 10.1159/000187220.
This report focuses on the possible pathophysiology of a renal lesion that led to hypokalemia and the excessive excretion of potassium (K+) in a 2.5-year-old child. The rate of excretion of K+ was high, largely the result of forces leading to a very high concentration of K+ in the lumen of the terminal cortical collecting duct as revealed by very high values for the transtubular K+ concentration gradient (TTKG was 25 +/- 3). The TTKG was high despite undetectable levels of aldosterone in plasma and the absence of bicarbonaturia. The level of renin in plasma was not low and there was a tendency to contraction of the ECF volume when dietary intake was curtailed. These findings provided the basis to speculate that the underlying lesion might be a lower than normal 'permeability' of the cortical collecting duct for chloride.
本报告聚焦于一名2.5岁儿童因肾脏病变导致低钾血症及钾（K+）过度排泄的可能病理生理学机制。K+排泄率很高，这主要是由于导致终末皮质集合管管腔内K+浓度极高的因素所致，经测定跨管K+浓度梯度（TTKG为25±3）显示了这一点。尽管血浆醛固酮水平检测不到且无碳酸氢盐尿，但TTKG仍很高。血浆肾素水平不低，且当饮食摄入量减少时存在细胞外液量收缩的趋势。这些发现为推测潜在病变可能是皮质集合管对氯离子的“通透性”低于正常水平提供了依据。
