Norby L H, Weidig J, Ramwell P, Slotkoff L, Flamenbaum W
Lancet. 1978 Nov 25;2(8100):1118-22. doi: 10.1016/s0140-6736(78)92275-4.
A 57-year-old woman with hypertension and moderate renal insufficiency had chronic unexplained hyperkalaemia. Metabolic balance studies confirmed a diagnosis of hyporeninaemic hypoaldosteronism. Two observations suggested that impaired renal prostaglandin production contributed to the pathogenesis of the patient's disorder. Baseline renal-prostaglandin synthesis (as determined by urinary excretion of P.G.E and P.G.F) was was substantially depressed when compared with that in nine normal females. Infusion of low doses of P.G.A1 produced a significant increase in serum-aldosterone and urinary potassium excretion; it also led to a dramatic fall in blood-pressure and serum-potassium. It appears from these studies that a defect in renal prostaglandin synthesis has an important role in the pathogenesis of hyporeninaemic hypoaldosteronism.
一名患有高血压和中度肾功能不全的57岁女性患有慢性不明原因高钾血症。代谢平衡研究确诊为低肾素性低醛固酮血症。两项观察结果提示，肾脏前列腺素生成受损促成了该患者疾病的发病机制。与九名正常女性相比，基线肾脏前列腺素合成（通过尿中P.G.E和P.G.F排泄量测定）显著降低。输注低剂量的P.G.A1可使血清醛固酮和尿钾排泄量显著增加；还导致血压和血清钾急剧下降。从这些研究看来，肾脏前列腺素合成缺陷在低肾素性低醛固酮血症的发病机制中起重要作用。
