Renal potassium wasting in the absence of aldosterone. Insights into the mechanism for the secretion of potassium.

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.