Abstract

An increased solute load per remaining functioning nephron may enhance K excretion and aid in maintaining K balance in chronic renal failure. An analogous model was sought by inducing progressive osmotic diuresis with urea in a) water-loaded dogs with minimal K excretion, b) dogs receiving K infusions at intermediate rates of 207–280 µEq/min, and c) dogs receiving K infusions at maximal tolerated rates of 400–600 µEq/min. Urea diuresis significantly augmented K excretion in experiments in which basal K excreted-to-K filtered ratios (KE:KF) were minimal (.02–.03) or intermediate (.20–.73), but when control ratios approached 1.0, urea loading became progressively less effective. The slight increment in K excretion with low basal KE:KF ratios (19 µEq/min) suggested partial inhibition of proximal reabsorption; the more marked increment in K excretion at intermediate KE:KF levels (130 µEq/min) is consistent with enhancement of K secretion following increased delivery of Na to the distal exchange sites. Once distal K secretion was maximally stimulated by K loading, however, it was not further affected by solute diuresis or augmented Na excretion.

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