The fate of portal ammonia derived from intestinal urea degradation was examined in 15 experiments in patients with chronic renal failure. The kinetics of labelled urea metabolism were studied before and again during the administration of oral neomycin or kanamycin. Detectable absorption of both drugs generally occurred, but urea clearance and estimated glomerular filtration rate did not significantly change during antibiotic administration. In seven experiments a significant fall in urea degradation (65% to 95%) occurred during antibiotic administration. Analysis of the effect of antibiotics was confined to these seven experiments. In the control periods, there were no differences in urea metabolism or renal function between these patients and those in whom urea degradation was not suppressed. If ammonia derived from urea degradation is converted back to urea in the liver, then suppression of degradation would lead to an equal decrease in urea production, and the difference between production and degradation ('appearance') would remain constant. However, if urea derived ammonia is used for protein synthesis, suppression of degradation would permit the formerly degraded urea to appear in urine and body fluids and thus to increase measured urea appearance. In these seven experiments, we found no change in urea appearance during antibiotic administration. We conclude that portal ammonia is reincorporated into urea in chronic renal failure and is not utilized significantly for protein synthesis.
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