Perlmutter E P, Sweeney D, Herskovits G, Kleiner M
Nephrology Division, Department of Medicine, Staten Island University Hospital, New York, USA.
Am J Med Sci. 1996 Feb;311(2):84-5. doi: 10.1097/00000441-199602000-00006.
A case is reported of a 96-year-old woman with congestive heart failure, hypertension, and chronic obstructive pulmonary disease who presented with altered mental status and severe hyperkalemia, a serum potassium 9.3 meq/L, and electrocardiograph changes. The patient was discharged 1 week prior, with a normal serum potassium, receiving trimethoprim-sulfamethoxazole for urinary tract infection and pneumonia. Serum potassium measurements returned to normal after discontinuation of the drug. Other causes of hyperkalemia were ruled out. Mild hyperkalemia due to trimethoprim-sulfamethoxazole was first reported in 1983 in a 69-year-old woman in whom leukemia with leukopenia developed. In literature to date, mild hyperkalemia in younger geriatric patients has been described. Trimethoprim is thought to act by inhibiting amiloride sensitive sodium channels in the distal nephron and impairing renal potassium secretion in a dose dependent manner. The authors report the case, review the literature, and discuss age-related reduction in renal function as a possible etiology.
报告了一例96岁女性患者，患有充血性心力衰竭、高血压和慢性阻塞性肺疾病，出现精神状态改变和严重高钾血症，血清钾为9.3毫当量/升，并伴有心电图改变。该患者1周前出院时血清钾正常，因尿路感染和肺炎接受甲氧苄啶-磺胺甲恶唑治疗。停药后血清钾测量值恢复正常。排除了高钾血症的其他病因。1983年首次报道了一名69岁女性因甲氧苄啶-磺胺甲恶唑导致轻度高钾血症，该患者患有白血病并伴有白细胞减少。在迄今为止的文献中，已描述了老年患者中的轻度高钾血症。甲氧苄啶被认为是通过抑制远端肾单位中阿米洛利敏感的钠通道并以剂量依赖方式损害肾脏钾分泌而起作用。作者报告了该病例，回顾了文献，并讨论了与年龄相关的肾功能减退作为可能病因的情况。
