Potapova A V, Dzgoeva F U, Kutyrina I M, Zozulia O V, Okunev D Iu, Milovanov Iu S
Urol Nefrol (Mosk). 1995 May-Jun(3):11-4.
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.
抗生素肾毒性的实验和临床评估表明,这些药物可能在肾小管装置功能相对未受影响的情况下导致肾小管损伤。肾小管功能障碍的进展是由于肾小管上皮细胞对药物的滤过和分泌,使得高浓度抗生素在肾实质中蓄积所致。在大多数患者中,疾病表现与使用抗生素直接相关。肾小管功能障碍表现为浓缩、酸排泄、葡萄糖转运及β2-微球蛋白重吸收异常。尽管肾脏病变被证实为良性,但在无动脉高血压的情况下偶尔也会出现急性肾功能不全的病例。