Ghimire Anukul, Li David, Amin Leena
Department of Medicine, University of Alberta, Edmonton, Canada.
Grey Nuns Community Hospital, Edmonton, AB, Canada.
Can J Kidney Health Dis. 2023 Jun 26;10:20543581231183813. doi: 10.1177/20543581231183813. eCollection 2023.
Renal tubular acidosis (RTA) is a cause of non-anion gap metabolic acidosis (NAGMA) that is infrequently diagnosed and is due to various underlying etiologies that impair the kidney's ability to retain bicarbonate or excrete acid. Ibuprofen is an over-the-counter non-steroidal anti-inflammatory medication that is used by patients widely for a variety of reasons. Although it is well known that ibuprofen and other non-steroidal anti-inflammatory drugs may have nephrotoxic effects, the role of ibuprofen as a cause of RTA and hypokalemia is not well recognized.
A 66-year-old man with chemotherapy-treated lymphoma in remission and ongoing heavy ibuprofen use for chronic pain presented to hospital with a 1-week history of increasing lethargy and otherwise unremarkable review of systems. Investigations showed acute kidney injury, hypokalemia, hyperchloremia, and NAGMA with elevated urinary pH and positive urine anion gap.
The final diagnosis of distal RTA secondary to ibuprofen was made after ruling out gastrointestinal bicarbonate loss and additional secondary causes of RTA, including other medications, autoimmune conditions, and obstructive uropathy.
The patient was admitted and treated with intravenous sodium bicarbonate for 24 hours with correction of hypokalemia via oral supplementation. His ibuprofen-containing medication was discontinued.
His acute kidney injury and electrolyte abnormalities resolved within 48 hours of initiating treatment with concurrent resolution of his lethargy. He was discharged home and advised to stop taking ibuprofen.
We report a case of patient with hypokalemia and NAGMA secondary to ibuprofen and highlight the importance of monitoring for this side effect in patients taking ibuprofen.
肾小管酸中毒（RTA）是导致非阴离子间隙代谢性酸中毒（NAGMA）的原因之一，其诊断并不常见，是由多种潜在病因引起的，这些病因会损害肾脏保留碳酸氢盐或排泄酸的能力。布洛芬是一种非处方非甾体抗炎药，患者因各种原因广泛使用。虽然众所周知布洛芬和其他非甾体抗炎药可能具有肾毒性作用，但布洛芬作为RTA和低钾血症病因的作用尚未得到充分认识。
一名66岁男性，化疗后缓解的淋巴瘤患者，因慢性疼痛持续大量服用布洛芬，因嗜睡加重1周就诊，其他系统检查无异常。检查显示急性肾损伤、低钾血症、高氯血症、NAGMA，尿pH值升高，尿阴离子间隙阳性。
在排除胃肠道碳酸氢盐丢失和RTA的其他继发原因，包括其他药物、自身免疫性疾病和梗阻性尿路病后，最终诊断为布洛芬继发的远端RTA。
患者入院，静脉输注碳酸氢钠24小时，并通过口服补充纠正低钾血症。停用含布洛芬的药物。
在开始治疗后48小时内，他的急性肾损伤和电解质异常得到缓解，同时嗜睡症状也得到缓解。他出院回家，并被建议停止服用布洛芬。
我们报告了一例因布洛芬导致低钾血症和NAGMA的病例，并强调了对服用布洛芬的患者监测这种副作用的重要性。
