Poirier T I
Drug Intell Clin Pharm. 1984 Jan;18(1):27-32. doi: 10.1177/106002808401800103.
A report of a probable case of acute, reversible renal failure and hyperkalemia, after an increase in dose of ibuprofen, is presented. Other cases of renal dysfunction associated with various nonsteroidal antiinflammatory drugs (NSAIDs) are reviewed. The ability of NSAIDs to inhibit prostaglandin synthesis may explain the various renal consequences. Possible predisposing factors to renal deterioration include the amount of drug consumed, presence of compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations, and high urinary prostaglandin excretion. Generally, the renal failure with NSAIDs is acute and reversible, though analgesic nephropathy with papillary necrosis and chronic renal failure are reported. Electrolytes, blood urea nitrogen, and serum creatinine levels need to be monitored in high-risk patients with predisposing factors and for chronic, long-term use of drugs that inhibit prostaglandin synthesis.
本文报告了1例布洛芬剂量增加后出现急性可逆性肾衰竭和高钾血症的疑似病例。同时回顾了其他与各种非甾体抗炎药（NSAIDs）相关的肾功能障碍病例。NSAIDs抑制前列腺素合成的能力可能解释了各种肾脏后果。导致肾脏恶化的可能易感因素包括药物摄入量、肾血流量受损、潜在的肾功能不全、肾毒性药物组合以及高尿前列腺素排泄。一般来说，NSAIDs引起的肾衰竭是急性且可逆的，不过也有关于伴有乳头坏死的镇痛性肾病和慢性肾衰竭的报道。对于有易感因素的高危患者以及长期慢性使用抑制前列腺素合成药物的患者，需要监测电解质、血尿素氮和血清肌酐水平。
