Orth S, Nowicki M, Wiecek A, Ritz E
Department of Internal Medicine, Ruperto Carola University, Heidelberg, Germany.
Drugs. 1993;46 Suppl 2:189-95; discussion 195-6. doi: 10.2165/00003495-199300462-00029.
In most cases of renal disease, progression of renal failure occurs via nonspecific mechanisms that can be dissociated from the primary cause of renal damage. Progression of disease is accompanied by glomerulosclerosis and tubulointerstitial fibrosis. Loss of autoregulation and afferent renal vasodilation renders the glomerular microcirculation particularly susceptible to systemic hypertension. Glomerular growth is an ancillary factor permitting the development of glomerulosclerosis. Experimental and clinical studies indicate that angiotensin converting enzyme (ACE) inhibitors may prevent progressive renal deterioration. Furthermore, it appears that this effect can be dissociated, at least in part, from the haemodynamic effects of ACE inhibitors. Some evidence indicates that the renal-protective effects of ACE inhibitors results from their effects on glomerular growth and glomerular permselectivity. The role of reduced generation of angiotensin II or accumulation of kinins in the renal effects of ACE inhibitors is under investigation. Prospective clinical trials have demonstrated that ACE inhibitors reduce proteinuria and interfere with progression of renal disease to a greater degree than can be explained by their blood pressure lowering effects alone.
在大多数肾脏疾病病例中，肾衰竭的进展是通过非特异性机制发生的，这些机制可与肾脏损伤的主要原因相分离。疾病进展伴随着肾小球硬化和肾小管间质纤维化。自身调节功能丧失和肾入球小动脉扩张使肾小球微循环特别容易受到系统性高血压的影响。肾小球生长是导致肾小球硬化发展的一个辅助因素。实验和临床研究表明，血管紧张素转换酶（ACE）抑制剂可能预防肾脏进行性恶化。此外，这种作用似乎至少部分可与ACE抑制剂的血流动力学作用相分离。一些证据表明，ACE抑制剂的肾脏保护作用源于它们对肾小球生长和肾小球滤过选择性的影响。血管紧张素II生成减少或激肽在ACE抑制剂肾脏作用中的积累所起的作用正在研究中。前瞻性临床试验表明，ACE抑制剂降低蛋白尿并干扰肾脏疾病进展的程度，大于仅由其降压作用所能解释的程度。
