Klaus D
Klin Wochenschr. 1984 Aug 16;62(16):747-52. doi: 10.1007/BF01721771.
Aldosterone deficiency is caused by various defects of aldosterone biosynthesis in the adrenal gland or hyporeninism. The most important symptoms are hyponatremia and hyperkalemia. These electrolyte disturbances are also found in pseudohypoaldosteronism. Pseudohypoaldosteronism type I is characterized by insensitivity of the distal nephron for aldosterone. Hyperabsorption of chloride in the distal nephron leads to pseudohypoaldosteronism type II, which is linked with hypertension, whereas blood pressure in the other mentioned disorders is decreased. Renal tubular acidosis, mainly type 4, with impaired production of ammonia due to hyperkalemia, is frequently observed in hypoaldosteronism and both types of pseudohypoaldosteronism as well. The therapeutic regimen is different: low doses of fludrocortisone in hypoaldosteronism, potassium restriction, sodium bicarbonate and loop diuretics in type I of pseudohypoaldosteronism, and sodium restriction and chloruretic diuretics (thiazide) in type II of pseudohypoaldosteronism. In some cases hyperkalemia requires the use of potassium-binding resins.
醛固酮缺乏症由肾上腺醛固酮生物合成的各种缺陷或低肾素血症引起。最重要的症状是低钠血症和高钾血症。这些电解质紊乱在假性醛固酮增多症中也有发现。I型假性醛固酮增多症的特征是远端肾单位对醛固酮不敏感。远端肾单位氯化物的过度吸收导致II型假性醛固酮增多症，其与高血压有关，而其他上述疾病的血压则降低。肾小管酸中毒，主要是4型，由于高钾血症导致氨生成受损，在醛固酮缺乏症以及两种类型的假性醛固酮增多症中也经常观察到。治疗方案不同：醛固酮缺乏症使用低剂量氟氢可的松，I型假性醛固酮增多症限制钾摄入、使用碳酸氢钠和袢利尿剂，II型假性醛固酮增多症限制钠摄入和使用氯噻嗪类利尿剂。在某些情况下，高钾血症需要使用钾结合树脂。
