Iversen B M, Kvam F I, Svarstad E
Medisinsk avdeling, Haukeland Sykehus, Bergen.
Tidsskr Nor Laegeforen. 1996 Jun 30;116(17):2022-6.
Hypertension is a common finding in patients with renal parenchymatous diseases. Development of hypertension causes increased proteinuria, decline in glomerular filtration rate and reduced life span in experimental models of glomerulonephritis. Hypertension has been shown to reduce glomerular filtration rate in man. It is therefore important to treat hypertension. The blood pressure should be reduced to about 140/80 mm Hg. Reduction of glomerular capillary pressure, inhibition of glomerular permeability, renal hypertrophy and inhibition of mesangial metabolism are the main mechanisms of renal protection during antihypertensive therapy. Autoregulation of the renal blood flow probably has an impact on these mechanisms. Impaired autoregulation is found in kidneys with low glomerular filtration rate and during treatment with calcium channel blockers. Alpha receptor blockers, angiotensin converting enzyme inhibitors (ACE-) and angiotensin II receptor blockers do not interfere with autoregulation. All types of antihypertensive drugs provide similar renal protection when the glomerular filtration rate is reduced. When calcium channel blockers are used in kidneys with normal or slightly reduced function, either blood pressure should be kept strictly at normal levels or these type of drugs should be combined with ACE inhibitors or angiotensin II receptor blockers.
高血压是肾实质疾病患者的常见表现。在肾小球肾炎实验模型中，高血压的发生会导致蛋白尿增加、肾小球滤过率下降以及寿命缩短。研究表明，高血压会降低人类的肾小球滤过率。因此，治疗高血压很重要。血压应降至约140/80 mmHg。降低肾小球毛细血管压力、抑制肾小球通透性、肾脏肥大以及抑制系膜代谢是降压治疗期间肾脏保护的主要机制。肾血流的自身调节可能对这些机制有影响。在肾小球滤过率低的肾脏以及使用钙通道阻滞剂治疗期间会出现自身调节受损。α受体阻滞剂、血管紧张素转换酶抑制剂（ACE-）和血管紧张素II受体阻滞剂不会干扰自身调节。当肾小球滤过率降低时，所有类型的降压药物都能提供相似的肾脏保护作用。当在功能正常或略有降低的肾脏中使用钙通道阻滞剂时，要么应将血压严格维持在正常水平，要么应将这类药物与ACE抑制剂或血管紧张素II受体阻滞剂联合使用。
