Robbins M E, Bonsib S M
Department of Radiology, University of Iowa, Iowa City 52242, USA.
Scanning Microsc. 1995 Jun;9(2):535-60.
The marked radiosensitivity of renal tissue represents a limitation on the total radiotherapeutic dose that safely can be applied to treatment volumes that include the kidneys. Radiation nephropathy is characterized by a progressive reduction in renal hemodynamics associated with a severe anemia. The latter is often normochromic normocytic in character, but can progress to a microangiopathic hemolytic anemia. The pathogenic mechanisms responsible for the development of radiation nephropathy remain ill-defined. Experimental studies which allow serial determinations of functional, morphologic, and cell kinetic radiation-induced changes indicate that primarily glomerular but also tubular alterations occur in the primary stages of radiation nephropathy. Glomerular capillary endothelial cell loss is seen within several weeks of irradiation. Remaining endothelial cells exhibit increased permeability leading to a subendothelial transudate. Mesangiolysis also is observed. In contrast, podocytes appear to be relatively unaffected at this stage. The endothelial changes appear to resolve, but the mesangial lesions progress, with hypercellularity and/or hypertrophy, increased mesangial matrix, mesangial sclerosis, and ultimately, glomerulosclerosis. These mesangial changes are similar to those observed in other chronic glomerulopathies. Dietary protein restriction, corticosteroids, and ACE-inhibitors all can reduce the severity of experimental radiation nephropathy.
肾组织显著的放射敏感性限制了安全应用于包含肾脏的治疗体积的总放射治疗剂量。放射性肾病的特征是肾血流动力学逐渐降低，并伴有严重贫血。后者通常为正色素正细胞性，但可进展为微血管病性溶血性贫血。导致放射性肾病发生的致病机制仍不明确。允许对功能、形态和细胞动力学辐射诱导变化进行系列测定的实验研究表明，在放射性肾病的初级阶段主要发生肾小球改变，但肾小管也会发生改变。照射后数周内可见肾小球毛细血管内皮细胞丢失。剩余的内皮细胞表现出通透性增加，导致内皮下渗出液。也观察到系膜溶解。相比之下，此阶段足细胞似乎相对未受影响。内皮变化似乎会消退，但系膜病变会进展，出现细胞增多和/或肥大、系膜基质增加、系膜硬化，最终发展为肾小球硬化。这些系膜变化与其他慢性肾小球病中观察到的变化相似。饮食蛋白限制、皮质类固醇和血管紧张素转换酶抑制剂均可降低实验性放射性肾病的严重程度。
