Ono H, Ono Y
Department of Internal Medicine, Dokkyo University School of Medicine, Tochigi, Japan.
Med Clin North Am. 1997 Nov;81(6):1273-88. doi: 10.1016/s0025-7125(05)70582-4.
In patients with benign nephrosclerosis, the histologic changes are characterized by hyaline degeneration of afferent arterioles with reduced kidney size. Although the glomeruli are nearly intact in patients with adult essential hypertension, the greatest numbers of sclerotic glomeruli are seen in nephrosclerosis with the aging process. Aging undoubtedly plays a role. In the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. Kidneys of elderly subjects also are associated with a large number of sclerotic glomeruli. Experimental evidence supports the notion that the pathogenesis of glomerulosclerosis with nephrosclerosis has been demonstrated as important factors: (1) the elevation of PG (glomerular hypertension); (2) mesangial dysfunction, such as mesangiolysis and increased mesangial matrix; and (3) genetic abnormalities (apoptosis) in mesangial cells with glomerular hypertension. Malignant nephrosclerosis is characterized histologically by vascular endothelial damage and fibrinoid necrosis of afferent and interlobular arteries. In an afferent arteriole or a glomerulus, NOS or endothelin produced in endothelial cells may play a role in the reduction or the maintenance of vascular tone. The frequency of malignant hypertension has decreased because of the effective treatment of essential hypertension with new antihypertensive agents: calcium antagonists, ACE inhibitors, and angiotensin II receptor antagonists. Therefore, the importance of the prevention of essential hypertension with these antihypertensive agents, by slowing and stopping the increase in blood pressure from mild hypertension, has received widespread recognition in the prevention of organ damage, such as cases of cardiovascular disease and ESRD. Thus, prevention of renal injuries is an important goal of antihypertensive therapy.
在良性肾硬化患者中，组织学改变的特征是入球小动脉玻璃样变性伴肾脏体积缩小。虽然成人原发性高血压患者的肾小球几乎完好无损，但在肾硬化伴衰老过程中可见到最多数量的硬化性肾小球。衰老无疑起了作用。根据作者的经验，老年受试者的肾脏，尽管血压正常且胆固醇水平正常，但系膜基质增加，血管中层平滑肌细胞肥大。老年受试者的肾脏也伴有大量硬化性肾小球。实验证据支持以下观点，即肾硬化伴肾小球硬化的发病机制已被证明是重要因素：（1）PG升高（肾小球高压）；（2）系膜功能障碍，如系膜溶解和系膜基质增加；（3）系膜细胞的基因异常（凋亡）伴肾小球高压。恶性肾硬化的组织学特征是血管内皮损伤以及入球动脉和小叶间动脉的纤维蛋白样坏死。在内皮细胞中产生的一氧化氮合酶或内皮素可能在入球小动脉或肾小球中对血管张力的降低或维持起作用。由于使用新型抗高血压药物（钙拮抗剂、ACE抑制剂和血管紧张素II受体拮抗剂）有效治疗原发性高血压，恶性高血压的发生率已降低。因此，通过减缓并阻止血压从轻度高血压开始升高来预防原发性高血压，在预防诸如心血管疾病和终末期肾病等器官损伤方面的重要性已得到广泛认可。因此，预防肾损伤是抗高血压治疗的一个重要目标。
