[Evaluation of enzymuria as a tracer in nephrotoxicity: results of a multicenter study].

Urinary excretion of three enzymes of different subcellular location in kidney tissue, alanine aminopeptidase (AAP), gammaglutamyltransferase (GGT), N acetyl-beta-D glucosaminidase (NAG), was carried out in 79 healthy adults and 108 healthy children and in 69 adults with various therapies: antibiotics (32 cases), non steroidal anti-inflammatory drugs (NSAIDs) (22 cases), cisplatinum (12 cases) and cyclosporine (3 cases). A circadian rhythm has been shown in children. In patients treated with antibiotics, the importance and duration of the increased enzymes urinary excretion were variable but the excretion of AAP was always higher than that of GGT and NAG. Short term therapies by NSAIDs were without influence on enzymuria but long term therapies produced a moderate increase of NAG excretion. Enzymuria increased immediately after cisplatinum administration and decreased after each daily dose, except in patients with previously high creatininemia. Cyclosporine induced a slight increase in AAP and NAG excretion. Enzymuria, thus, increased early reflecting a toxic effect of the drug at the cellular level whereas creatininemia increase, marker of renal fonctionnal insufficiency, occurs only occasionally and lately.