Adaptive change in ammonia excretion in renal insufficiency.
Experiments were performed to study the mechanism of the compensatory increase in the excretion of metabolic acid by residual nephrons after reduction in renal mass. Despite a decrease in nephron population to 20% of control, total excretion of acid remained similar to pair-fed controls due to an increase in nephron excretion from 5.4 +/- 0.5 in controls to 22.3 +/- 1.9 nEq/24 hr (P < 0.25), including a threefold rise in ammonia excretion and a ninefold increase in excretion of titratable acid. Further studies showed that the in vivo production of ammonia by residual nephrons paralleled, in general, the nephron excretion rate, and increased from the control value of 0.23 +/- 0.02 to 0.54 +/- 0.09 ng/min (P < 0.05). Because the production rate of ammonia per milligram of DNA was not increased in experimental animals above control and because changes were not found in enzymes and substrates associated with increased ammoniagenesis in the rat, these data suggest that formation of additional ammonia-producing cells, due to hyperplasia, plays a role in the compensatory increase in ammonia excretion by residual nephrons. During acute acidosis, cellular ammonia production rose in a parallel manner in control and experimental kidneys, indicating that the capacity to form ammonia is not impaired in chronic renal insufficiency.
D000138:Acidosis / Q000378:metabolism; D000641:Ammonia / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D000818:Animals; D004247:DNA / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007674:Kidney Diseases / Q000378:metabolism*; D008297:Male; D009399:Nephrons / Q000378:metabolism; D051381:Rats
D000641:Ammonia; D004247:DNA