The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p < 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 ± 16 μeq/min (mean ± SEM) to 310 ± 49 μeq/min (p < 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O (CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV.UKV fell acutely from 91 ± 13 to 45 ± 5 μeq/min (p < 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 ± 15 to 143 ± 18 μg/min and fractional excretion of calcium increased from 0.55 ± 0.13 to 1.24 ± 0.21% (p < 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 ± 0.05 to 4.30 ± 0.03 mg/dl (p < 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independent of changes in parathyroid hormone (as reflected by urinary cAMP).
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism