Jovanovic D, Dimitrijevic J, Varagic J, Jovovic D, Starcevic A, Djukanovic L
Institute of Urology and Nephrology, Clinical Center of Serbia, Belgrade, Yugoslavia.
Ren Fail. 1998 May;20(3):451-8. doi: 10.3109/08860229809045134.
Antihypertensive therapy has been shown to slow down the progression of chronic renal failure. Angiotensin converting enzyme inhibitors and calcium antagonists have been emphasized as the agents with the most protective effect. Our previous study showed that captopril slowed down renal function deterioration in the early course of adriamycin (ADR) nephropathy in spontaneously hypertensive rats (SHR). The present study was undertaken with the aim to examine morphologic changes associated with that slower renal function deterioration. Adult (24 weeks) female SHR were randomly divided into the following groups: the control group (n = 12) was given tap water to drink; the adriamycin (ADR) group (n = 25) was treated with ADR; the ADR-captopril (ADR-C) group (n = 27) was treated with ADR and thereafter with captopril (60 mg/kg/day). Rats were sacrificed at weeks 6, 12 and 18 and histologic analysis was semiquantitatively performed. In the control group the glomeruli exhibited only minor changes at the end of the study. In the ADR group slight glomerular mesangial hypercellularity appeared in the sixth week and progressed in focal and segmental sclerosis. Some glomeruli showed segmental proliferation and increased fibrular matrix of a tuft adherent to a fibrocellular crescents. In the ADR-C group, glomeruli with a slight increase of mesangial matrix were seen at the end of the sixth week, mesangial hypercellularity developed until the end of the sixth week, mesangial hypercellularity developed until the end of the 12th week and segmental glomerulosclerosis until the end of the study. Semiquantitative analysis revealed that the mean semiquantitative scores for mesangial expansion and glomerular sclerosis were significantly lower in ADR-C group than in ADR group throughout the study. We concluded that captopril slowed down mesangial expansion and reduced the development of glomerular sclerosis.
抗高血压治疗已被证明可减缓慢性肾功能衰竭的进展。血管紧张素转换酶抑制剂和钙拮抗剂被强调为具有最强保护作用的药物。我们之前的研究表明,卡托普利可减缓自发性高血压大鼠(SHR)阿霉素(ADR)肾病早期的肾功能恶化。本研究旨在检查与肾功能恶化减缓相关的形态学变化。成年(24周)雌性SHR被随机分为以下几组:对照组(n = 12)饮用自来水;阿霉素(ADR)组(n = 25)接受ADR治疗;阿霉素 - 卡托普利(ADR-C)组(n = 27)接受ADR治疗,之后给予卡托普利(60 mg/kg/天)。在第6、12和18周处死大鼠并进行组织学半定量分析。对照组在研究结束时肾小球仅表现出轻微变化。ADR组在第6周出现轻微的肾小球系膜细胞增多,并进展为局灶性和节段性硬化。一些肾小球显示节段性增生和与纤维细胞性新月体粘连的肾小球丛纤维基质增加。在ADR-C组,在第6周结束时可见系膜基质略有增加的肾小球,系膜细胞增多发展至第6周结束,系膜细胞增多发展至第12周结束,节段性肾小球硬化发展至研究结束。半定量分析显示,在整个研究过程中,ADR-C组系膜扩张和肾小球硬化的平均半定量评分显著低于ADR组。我们得出结论,卡托普利减缓了系膜扩张并减少了肾小球硬化的发展。