O'Donnell M P, Kasiske B L, Daniels F X, Keane W F
Diabetes. 1986 Sep;35(9):1011-5. doi: 10.2337/diab.35.9.1011.
Loss of renal mass in rats with experimental diabetes mellitus leads to exaggerated hypertrophy of remaining nephrons and accelerated diabetic glomerulopathy. To examine factors responsible for glomerular injury in this setting, rats with preexisting diabetes were subjected to unilateral nephrectomy. Micropuncture studies and evaluation of glomerular morphology were performed 2-3 mo later. Nephrectomized diabetic rats demonstrated significant increases in kidney weight, superficial nephron glomerular filtration rate, and superficial nephron plasma flow compared with two-kidney diabetic rats and nephrectomized nondiabetic controls. Glomerular capillary hydraulic pressure was comparable in two-kidney and nephrectomized diabetic rats and was significantly reduced compared with nephrectomized nondiabetic controls. Nephrectomized diabetic rats demonstrated significant albuminuria, mesangial matrix expansion, and focal glomerulosclerosis, whereas two-kidney diabetic rats and nephrectomized nondiabetic controls showed only minimal alterations in glomerular morphology. It is concluded that diabetic rats can undergo glomerular functional compensation in response to nephron loss. Moreover, accelerated glomerular injury caused by nephron loss in diabetic rats could not be attributed to increased glomerular capillary pressure.
实验性糖尿病大鼠肾实质减少会导致剩余肾单位过度肥大及糖尿病性肾小球病变加速。为了研究此情况下导致肾小球损伤的因素,对已患糖尿病的大鼠进行单侧肾切除术。2至3个月后进行微穿刺研究及肾小球形态学评估。与双肾糖尿病大鼠和肾切除的非糖尿病对照大鼠相比,肾切除的糖尿病大鼠肾重量、浅表肾单位肾小球滤过率及浅表肾单位血浆流量显著增加。双肾及肾切除的糖尿病大鼠肾小球毛细血管液压相当,与肾切除的非糖尿病对照大鼠相比显著降低。肾切除的糖尿病大鼠出现显著蛋白尿、系膜基质扩张及局灶性肾小球硬化,而双肾糖尿病大鼠和肾切除的非糖尿病对照大鼠肾小球形态仅出现轻微改变。结论是糖尿病大鼠可对肾单位丢失做出肾小球功能代偿。此外,糖尿病大鼠肾单位丢失所致的肾小球损伤加速不能归因于肾小球毛细血管压力增加。