[Tubular interstitial disorders in the nephrotoxic action of antibiotics].
Experimental and clinical evaluation of antibiotic nephrotoxicity suggest a conclusion that these drugs may cause tubular damage in relatively unaffected function of tubular apparatus. Progression of tubular dysfunction results from accumulation of high concentrations of antibiotics in renal parenchyma due to tubular filtration and secretion of the drug by tubular epithelium cells. In the majority of patients the disease manifestations were directly associated with antibiotics administration. Tubular dysfunctions present as concentration, acid-excretion, glucose transport and beta 2-microglobulin reabsorption abnormalities. Though renal lesions proved benign, there were occasional cases of acute renal insufficiency in the absence of arterial hypertension.
Potapova
A V
AV
Dzgoeva
F U
FU
Kutyrina
I M
IM
Zozulia
O V
OV
Okunev
D Iu
DIu
Milovanov
Iu S
IuS
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000617:Aminoglycosides; D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects / Q000633:toxicity*; D001707:Biopsy, Needle; D005260:Female; D006801:Humans; D007671:Kidney Concentrating Ability / Q000187:drug effects; D007684:Kidney Tubules / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D001613:beta 2-Microglobulin / Q000032:analysis
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D001613:beta 2-Microglobulin