Abstract
Renal acidification in 18 healthy elderly subjects was studied using furosemide 80 mg orally, as a substance to stimulate H+ and K+ secretion by enhancing Na+ delivery and transport in the cortical collecting duct. In five subjects, group 2 (n=5), the furosemide failed to lower urinary pH below 5.5, but resulted in an increase in potassium excretion and decrease in net acid excretion. These effects were obliterated by amiloride, a drug which decreases transtubular epithelial voltage (lumen-negative) in the cortical collecting tubule (CCT) by blocking Na+ reabsorption. The serum bicarbonate in this group was normal, and they were considered as suffering from incomplete distal renal tubular acidosis (IC-DRTA). In group 1 (n=13), the furosemide resulted in a fall in urinary pH below 5.5, and in an increase in net acid excretion. Our results show that in a subgroup of elderly subjects there is a proton pump defect located in the cortical collecting duct, and that the elderly are susceptible to metabolic acidosis during stress conditions or high protein diet.
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