[Pharmacokinetic perturbations in kidney failure. Anomalies of metabolites and tissue diffusion (author's transl)].
Complex pharmacokinetic perturbations follow kidney failure. Delayed excretion affects not only the original substance but also metabolites, as illustrated by the behaviour of glipizide and glibenclamide. Moreover, abnormal absorption, distribution, and metabolism of these drugs also often occur and are particularily evident for some beta-blocking agents. Analysis of tissue pharmacokinetics shows that aminosides accumulate in the renal cortexand persist there for several months. This phenomenon is markedly enhanced in acute obstructive kidney failure and largely accounts for the nephrotoxicity of these drugs.
D000042:Absorption; D000617:Aminoglycosides / Q000378:metabolism; D000818:Animals; D000900:Anti-Bacterial Agents / Q000378:metabolism; D005913:Glipizide / Q000378:metabolism; D005905:Glyburide / Q000378:metabolism; D006801:Humans; D007672:Kidney Cortex / Q000378:metabolism; D007674:Kidney Diseases / Q000378:metabolism*; D007679:Kidney Medulla / Q000378:metabolism; D007700:Kinetics; D011412:Propanolamines / Q000097:blood; D051381:Rats; D014018:Tissue Distribution
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D011412:Propanolamines; D005905:Glyburide; D005913:Glipizide
Perturbations pharmacocinétiques dans l'insuffisance rénale. Anomalies des métobolites et de la diffusion dans les tissus.