Steinhardt G F, Liapis H, Phillips B, Vogler G, Nag M, Yoon K W
Department of Surgery (Divisions of Urology and Neurosurgery), St. Louis University School of Medicine, Missouri, USA.
J Urol. 1995 Aug;154(2 Pt 2):690-3. doi: 10.1097/00005392-199508000-00093.
Others have previously demonstrated that the administration of insulin-like growth factor-I accelerates recovery from ischemic acute tubular necrosis in the rat kidney. We investigated the effect of insulin-like growth factor-I on the histology of unilaterally obstructed kidneys in the pouch young of the North American opossum, Didelphis virginiana. In this model complete unilateral ureteral obstruction reliably induces statistically significant degrees of caliceal dilatation, tubular cystic change, and cortical and medullary fibrosis in kidneys examined 1 week after the creation of complete obstruction. Cortical and medullary inflammation is also increased after 1 week of obstruction in this model but not to a degree that is statistically different than control (sham operated) animals. We administered insulin-like growth factor-I to opossum pups with complete unilateral obstruction created at a length of 5 cm. (age 25 days, human equivalent 18 to 20 weeks). Insulin-like growth factor-I (400 mcg/kg.) was injected subcutaneously on the day of operation and again on days 2 and 4 postoperatively. The animals were sacrificed 1 week after obstruction and the formalin fixed, paraffin embedded kidneys were assessed histologically. In the obstructed kidney insulin-like growth factor-I ameliorated the development of fibrosis (cortical and medullary) and caliceal dilatation such that these characteristics did not differ significantly from those of sham operated animals. Tubular cystic change in the obstructed kidneys was also decreased by insulin-like growth factor-I administration but not to significant levels. Insulin-like growth factor-I treatment in obstructed animals resulted in significantly more inflammation (cortical and medullary) than in the sham operated animals. We also administered insulin-like growth factor-I to normal pups with no other intervention. These insulin-like growth factor-I treated pups did not differ from sham pups for any characteristic studied. Our study suggests that there is protective effect of insulin-like growth factor-I on renal architecture when administered in the setting of experimental fetal ureteral obstruction.
其他人先前已证明,给予胰岛素样生长因子-I可加速大鼠肾脏缺血性急性肾小管坏死的恢复。我们研究了胰岛素样生长因子-I对北美负鼠(弗吉尼亚负鼠)育儿袋幼崽单侧梗阻肾脏组织学的影响。在该模型中,完全性单侧输尿管梗阻在梗阻形成1周后检查时,可靠地诱导出具有统计学意义的肾盂扩张、肾小管囊性改变以及皮质和髓质纤维化程度。在该模型中,梗阻1周后皮质和髓质炎症也会增加,但程度与对照(假手术)动物相比无统计学差异。我们对在5厘米处造成完全性单侧梗阻的负鼠幼崽给予胰岛素样生长因子-I。(年龄25天,相当于人类18至20周)。在手术当天皮下注射胰岛素样生长因子-I(400微克/千克),术后第2天和第4天再次注射。梗阻1周后处死动物,对用福尔马林固定、石蜡包埋的肾脏进行组织学评估。在梗阻的肾脏中,胰岛素样生长因子-I改善了纤维化(皮质和髓质)和肾盂扩张的发展,使得这些特征与假手术动物相比无显著差异。给予胰岛素样生长因子-I也可减少梗阻肾脏中的肾小管囊性改变,但未降至显著水平。梗阻动物接受胰岛素样生长因子-I治疗后,其皮质和髓质炎症明显多于假手术动物。我们还对未进行其他干预的正常幼崽给予胰岛素样生长因子-I。这些接受胰岛素样生长因子-I治疗的幼崽在任何研究特征方面与假手术幼崽均无差异。我们的研究表明,在实验性胎儿输尿管梗阻的情况下给予胰岛素样生长因子-I对肾脏结构具有保护作用。