TUBULAR PEPTIDE HYPERMETABOLISM AND URINARY AMMONIA IN CHRONIC-RENAL-FAILURE IN MAN - A MALADAPTIVE RESPONSE

Excessive renal tubular peptide uptake and degradation reflecting hype rcatabolism may be a maladaptive response in chronic renal failure (CR F). It may also offer an explanation for the increased ammoniagenesis, per surviving nephron, observed in CRF but as yet unexplained. Neithe r has been explored in man. We have shown in patients with normal rena l function and heavy (>5.0 g/24 h) proteinuria that tubular catabolism of a technetium-labelled peptide marker, aprotinin, and urinary ammon ia were increased compared to others with less proteinuria. We now mea sure tubular kinetics of aprotinin and urinary ammonia in 16 CRF patie nts with variable proteinuria. Metabolism and turnover of aprotinin an d ammonia excretion were increased, corrected for glomerular filtratio n rate, to levels found in patients with normal function and heavy pro teinuria.