Compensatory Changes in Renal Electrolyte Excretion to Removal of Gastric HC1 in Normal and Uremic Man

Abstract

Renal compensatory changes were studied during gastric drainage in 4 normal men and in 3 patients with chronic glomerulonephritis. 4–500 ml gastric juice was removed daily during stimulation of HCl-secretion by a histamine analogue over a period of 4–7 days. In the normal subjects, the net effect of drainage was a loss of hydrogen ions nearly equivalent to the reduction in excretion of sodium ions, whereas urinary excretion of chloride was reduced corresponding to the amounts of chloride removed. Plasma bicarbonate concentration did not increase. In the uremic subjects, plasma bicarbonate increased from an average of 12 to 20 mEq/L. The reduction in renal excretion of chloride and sodium was less complete, and continued after gastric drainage when acidosis rapidly developed. Renal acid excretion was slightly reduced in both normal and uremic man. The reduction in potassium excretion corresponded to the gastric losses in both groups. The glomerular filtration rate remained unchanged. It is concluded that removal of HC1 stimulates renal tubular sodium reabsorption. An increase in renal secretion of potassium and hydrogen ions, as is usually observed after vomiting or HC1 removal in NaCl-deficient subjects, does not occur as long as sodium can be reabsorbed with chloride.

Key Words:

• Acid-base equilibrium
• extra-cellular space
• gastric juice
• hydrochloric acid
• hydrogen-ion concentration
• kidney failure, chronic
• kidney tubules
• natriuresis
• potassium
• sodium
• uremia
• glomerulonephritis