Lynn K L, Bailey R R, Swainson C P, Sainsbury R, Low W I
N Z Med J. 1985 Aug 14;98(784):629-33.
In one year 19 patients aged 73 SD 8 yr were referred with renal failure (plasma creatinine 0.14-0.52 mmol/l; urea 7.9-39.5 mmol/l; potassium 2.9-6.1 mmol/l, who were taking amiloride/hydrochlorothiazide (ten), amiloride alone (one) or triamterene/hydrochlorothiazide (eight). Six patients were taking other diuretics. Sixteen patients were being treated for hypertension and three for fluid retention; five hypertensive patients were also taking non-steroidal anti-inflammatory drugs (NSAID). Four patients were hypokalaemic, three were volume-depleted. All potassium-sparing diuretics and NSAID were stopped (four required another diuretic). Six-100 days later renal function was improved in 17 patients, unchanged in one and one patient had died of uraemia. Blood pressure was satisfactory on no therapy in 11 patients and two normotensive patients were oedema-free. In elderly patients with renal impairment potassium-sparing diuretics may cause renal failure, sometimes secondary to hypovolaemia, and NSAID may potentiate the effect.
在某一年,19名年龄为73±8岁的患者因肾衰竭前来就诊(血浆肌酐0.14 - 0.52 mmol/L;尿素7.9 - 39.5 mmol/L;钾2.9 - 6.1 mmol/L),他们正在服用阿米洛利/氢氯噻嗪(10人)、单独服用阿米洛利(1人)或氨苯蝶啶/氢氯噻嗪(8人)。6名患者正在服用其他利尿剂。16名患者正在接受高血压治疗,3名患者因液体潴留接受治疗;5名高血压患者还在服用非甾体抗炎药(NSAID)。4名患者低钾血症,3名患者容量不足。所有保钾利尿剂和NSAID均停用(4人需要换用另一种利尿剂)。6 - 100天后,17名患者肾功能改善,1名患者肾功能无变化,1名患者死于尿毒症。11名患者未接受治疗时血压令人满意,2名血压正常的患者无水肿。在老年肾功能损害患者中,保钾利尿剂可能导致肾衰竭,有时继发于血容量不足,NSAID可能会增强这种作用。