[Renal enzymology: experimental patterns and clinical symptoms].
This is a study of the changes, both in serum and urine, of a wide enzymatic pattern whose origin is well known to be the renal parenchyma (LDH, LAP, AP and lysozyme), in the course of two experimental prototype lesions induced in rats. Simultaneously a similar enzymatic study was carried out in a group of patients with nephropathies. The experimental lesions were a toxic tubular dysfunction using a mercury salt and an immune glomerulonephritis of two types: by foreign proteins (human albumin) and by rabbit nephrotoxic serum. In all these cases, there has been a convincing evidence, both direct (histological and inmunofluorescent) and indirect (marked proteinuria), of the induced lesions which were similar to the experimental models reported in the literature. The isolated enzymatic changes we observed in serum made us conceed less value to this pattern in comparison to the urinary one which proved to be more important in our study. It was possible to define the following urinary enzymatic patterns for each of the experimental groups: a) The acute toxic tubular dysfunction has a marked rise in the activity of LDH and LAP, and less so in the activity of AP and lysozyme. The retarded tubular lesion has a moderate rise in LAP. b) The glomerular lesion has a moderate and exclusive rise in the activity of LDH and LAP. Likewise the clear similarity between each experimental group and its clinical equivalent was demonstrated as refers to the urinary enzymatic pattern.
D000818:Animals; D004798:Enzymes / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007674:Kidney Diseases / Q000097:blood / Q000201:enzymology* / Q000652:urine; D051381:Rats
D004798:Enzymes
Enzimologia renal: patrones experimentales y semiologia clinica