Wen S F, Parthasarathy R, Iliopoulos O, Oberley T D
Department of Medicine, University of Wisconsin Center for Health Sciences, Madison.
Am J Kidney Dis. 1992 Sep;20(3):281-5. doi: 10.1016/s0272-6386(12)80702-5.
Two college students who developed reversible acute deterioration in renal function following binge drinking of beer and the use of nonsteroidal antiinflammatory drugs (NSAIDs) are reported. Both patients presented with back and flank pain with muscle tenderness, but showed no evidence of overt rhabdomyolysis. The first case had marked renal failure, with a peak serum creatinine reaching 575 mumol/L (6.5 mg/dL), and acute tubular necrosis was documented by renal biopsy. The second case had only modest elevation in serum creatinine, and renal function rapidly improved on rehydration. The contribution of the potential muscle damage associated with alcohol ingestion to the changes in renal function in these two cases is not clear. However, the major mechanism for the acute renal failure was thought to be related to inhibition of renal prostaglandin synthesis in the face of compromised renal hemodynamics secondary to alcohol-induced volume depletion.
报告了两名大学生,他们在大量饮用啤酒并使用非甾体类抗炎药(NSAIDs)后出现了可逆性急性肾功能恶化。两名患者均表现为背部和侧腹疼痛伴肌肉压痛,但未显示明显的横纹肌溶解证据。第一例患者出现严重肾衰竭,血清肌酐峰值达到575 μmol/L(6.5 mg/dL),肾活检证实为急性肾小管坏死。第二例患者血清肌酐仅轻度升高,补液后肾功能迅速改善。在这两例病例中,与酒精摄入相关的潜在肌肉损伤对肾功能变化的作用尚不清楚。然而,急性肾衰竭的主要机制被认为与在酒精引起的容量耗竭继发肾血流动力学受损的情况下,肾前列腺素合成受到抑制有关。