Andreev E, Koopman M, Arisz L
Clinic of Nephrology, Medical University-Sofia, Bulgaria.
J Intern Med. 1999 Sep;246(3):247-52. doi: 10.1046/j.1365-2796.1999.00515.x.
This is a review of the available information about drugs which cause an increase in plasma creatinine concentration without decreasing glomerular filtration rate (GFR). The GFR is the main, but not the single, determinant of the plasma creatinine levels. Several drugs, such as cimetidine, trimethoprim, corticosteroids, pyrimethamine, phenacemide, salicylates and active vitamin D metabolites, have been reported to increase plasma creatinine without influencing its glomerular filtration. Cimetidine, trimethoprim, pyrimethamine and salicylates can inhibit secretion of creatinine by the proximal tubule. Corticosteroids and vitamin D metabolites probably modify the production rate and the release of creatinine. The exact mechanism of phenacemide-creatinine interaction is not fully explained. These drug-induced alterations in plasma creatinine concentration have clinical significance when GFR is estimated by using plasma creatinine.
这是一篇关于那些会导致血浆肌酐浓度升高而不降低肾小球滤过率(GFR)的药物的现有信息综述。GFR是血浆肌酐水平的主要但非唯一决定因素。据报道,几种药物,如西咪替丁、甲氧苄啶、皮质类固醇、乙胺嘧啶、非那西丁、水杨酸盐和活性维生素D代谢物,可在不影响其肾小球滤过的情况下增加血浆肌酐。西咪替丁、甲氧苄啶、乙胺嘧啶和水杨酸盐可抑制近端小管对肌酐的分泌。皮质类固醇和维生素D代谢物可能会改变肌酐的产生速率和释放。非那西丁与肌酐相互作用的确切机制尚未完全阐明。当通过血浆肌酐来估算GFR时,这些药物引起的血浆肌酐浓度变化具有临床意义。