Steele T W, Györy A Z, Edwards K D
Br Med J. 1969 Apr 26;2(5651):213-6. doi: 10.1136/bmj.2.5651.213.
Comprehensive one-day renal function tests in 20 patients with a history of analgesic abuse showed varying degrees of chronic renal failure in all. There was no evidence of a selective defect in proximal tubular function, while a defective concentrating mechanism, usually considered necessary for the diagnosis of analgesic-induced renal damage, could be demonstrated in only 16 patients. A urinary acidification defect associated with a concentrating defect was found in nine cases and was thought to reflect specific collecting duct dysfunction. Urinary ammonium excretion was reduced in 13 subjects, owing to a reduced number of functioning nephrons or inadequate acidification, or both. Low citrate excretion was frequently encountered, and this, as well as defective urinary acidification, may play some part in predisposing patients with analgesic nephropathy to intrarenal calcification and progressive renal failure.
对20例有镇痛药滥用史的患者进行的为期一天的综合肾功能检查显示,所有人均有不同程度的慢性肾衰竭。没有证据表明近端肾小管功能存在选择性缺陷,而通常认为对镇痛药所致肾损害诊断必不可少的浓缩机制缺陷仅在16例患者中得到证实。9例患者发现存在与浓缩缺陷相关的尿酸化缺陷,认为这反映了特定的集合管功能障碍。13例受试者尿铵排泄减少,原因是有功能的肾单位数量减少或酸化不足,或两者兼而有之。经常发现柠檬酸盐排泄量低,这以及尿酸化缺陷可能在使镇痛药肾病患者易发生肾内钙化和进行性肾衰竭方面起一定作用。