Proteolytic activity in patients with hypercatabolic renal failure.
Proteolytic enzymes exist in ultrafiltrated plasma, concentrated dialysates and urine fractions of patients with posttraumatic renal failure. Differences in digestion pattern of phosphorylase kinase suggest the existence of different proteases in patients with hypercatabolic renal failure. Trypsin binding capacity is reduced in RDT patients and markedly lower in patients with posttraumatic ARF. Protein catabolism is inhibited in vitro by alpha 2-macroglobulin. From our in vitro studies we favour the application of fresh frozen plasma instead of the available plasma protein solutions to hypercatabolic patients. Hemodialysis may enhance proteinase inhibitory capacity of the plasma. Hemodialysis therapy induces the increase of plasma E-X1 PI. The continuous release of granulocyte elastase during hemodialysis therapy may enhance the risk for the development of destructive lung disease.
D058186:Acute Kidney Injury / Q000201:enzymology*; D001798:Blood Proteins / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D009504:Neutrophils / Q000201:enzymology; D010196:Pancreatic Elastase / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood / Q000378:metabolism* / Q000652:urine; D010764:Phosphorylase Kinase; D011480:Protease Inhibitors / Q000378:metabolism; D006435:Renal Dialysis; D000515:alpha 1-Antitrypsin
D001798:Blood Proteins; D011480:Protease Inhibitors; D000515:alpha 1-Antitrypsin; D010764:Phosphorylase Kinase; D010447:Peptide Hydrolases; D010196:Pancreatic Elastase