Tubular metabolism of aprotinin 99mTc and urinary ammonia: effects of proteinuria.
Increased renal ammoniagenesis is pathogenic in animals. Thus, tubular degradation of filtered proteins to ammonia might link proteinuria to disease progression. The tubular uptake, metabolism and fractional degradation of aprotinin 99mTc (Trasylol), were measured in 26 glomerulonephritic patients with normal renal function, 10 with proteinuria > 5 g/24 h. In addition, urinary ammonia pH, and titratable acidity were measured. Patients with heavy proteinuria had a higher tubular metabolism, a lower uptake and a higher fractional degradation of aprotinin. Urinary ammonia and titratable acidity were also increased. Fractional degradation and urinary ammonia were strongly correlated as were urinary ammonia and proteinuria.
D000143:Acids / Q000652:urine; D000641:Ammonia / Q000652:urine*; D007611:Aprotinin / Q000378:metabolism*; D005921:Glomerulonephritis / Q000378:metabolism* / Q000652:urine; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000378:metabolism*; D011507:Proteinuria / Q000378:metabolism* / Q000652:urine; D017186:Titrimetry
D000143:Acids; D000641:Ammonia; D007611:Aprotinin