Hrnciar J
Interná klinika a nemocnice F. D. Roosevelta, Banská Bystrica.
Vnitr Lek. 1996 Jun;42(6):394-9.
Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
在病程持续10年或更长时间的糖尿病患者中,75%会出现孤立性醛固酮减少症。偶尔也见于先天性自主神经病变、急性肾小球肾炎、痛风肾、肾小管间质性肾炎、肾移植后、使用丝裂霉素等情况。在对糖尿病患者进行血浆肾素活性和醛固酮对呋塞米给药及直立位反应的动态测试中,与非糖尿病高血压患者相比,记录到反应明显降低。18.3%的患者无反应(特发性醛固酮减少症失代偿型)。糖尿病高血压患者在长期使用β受体阻滞剂治疗时表现与对照高血压患者相似。在特发性醛固酮减少症失代偿型患者中,使用干扰交感神经 - 肾素 - 血管紧张素 - 醛固酮系统(SNS - RAAS)活性的药物(如血管紧张素转换酶抑制剂、螺内酯等)后,可能会发生高钾血症危象,使患者面临酸中毒、脱水、肌无力、肌肉痉挛的风险,尤其是致命的心律失常。前列腺素合成酶阻滞剂(非甾体类抗风湿药)和其他药物也可能产生类似作用。糖尿病患者特发性醛固酮减少症的病因是多种致病因素共同作用:1. 在糖尿病肾病(DN)发病初期,心房利钠肽(ANF)分泌过多伴高渗性高血糖高血容量和超滤过;2. 交感神经自主神经病变早期发展;3. DN早期肾素和前列腺素生成减少;4. 肾外异肾素生成减少;5. 肾素原转化为活性肾素减少;6. 由于糖尿病患者血糖水平波动导致对抗调节激素周期性激活,使肾小球球状带对血管紧张素II(AII)、高钾血症和促肾上腺皮质激素(ACTH)的反应性降低,影响其功能重建;7. 由于肾小管间质改变,远端肾小管对醛固酮的反应降低。因此,特发性醛固酮减少症是糖尿病另一种严重但很少被诊断出的晚期并发症,其发生仅部分取决于DN的阶段。然而,在选择治疗动脉高血压和胰岛素抵抗综合征及5H综合征(即高胰岛素血症代偿胰岛素抵抗与高血糖(非胰岛素依赖型糖尿病)、高血压、高脂蛋白血症和女性多毛症(所谓的斯坦 - 莱文塔尔综合征)的关联)的药物时,必须对其进行诊断并予以重视。