Late consequences of acute ischemic injury to a solitary kidney.
Late consequences of acute ischemic injury to a solitary kidney.
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发表时间：
1999-02
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通讯作者：
M. E. Pagtalunan;J. Olson;N. Tilney;T. Meyer
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作者：
M. E. Pagtalunan;J. Olson;N. Tilney;T. Meyer
在接受右肾切除术和左肾动脉短暂闭塞的大鼠中评估孤立肾急性缺血性损伤的后遗症;对照组大鼠仅接受右肾切除术。2周时缺血性损伤恢复不完全（血清肌酐水平为1.1 +/-0.2vs0.5 +/-0.1mg/dl，缺血组与对照组相比P < 0.05），20周时肾功能恶化（血清肌酸酐水平为1.7 +/-0.4vs0.7 +/-0.1mg/dl，缺血组与对照组相比P < 0.05）。形态学研究表明，缺血性损伤后的功能障碍与广泛的肾小管间质疾病有关。部分肾小管节段萎缩，部分呈囊状扩张，使肾小管细胞体积分数减少（37 +/- 4对53 +/-2%，P < 0.05），而管腔和间质体积分数增加（分别为31 +/- 4对23 +/- 2%和29 +/- 2对20 +/-1%，均P < 0.05）。许多肾小球保留开放的毛细血管袢，但不再与正常小管节段连接（63 +/- 8对15 +/- 7%的肾小球，P < 0.05）。缺血后20 wk肾小球滤过率与肾小球滤过率呈负相关（r ~ 2 = 0.79，P < 0.001）。当时的肾小管间质疾病伴有蛋白尿和广泛的节段性肾小球簇损伤。人类患者中类似过程的发生可能导致移植肾在移植过程中遭受缺血性损伤的损失。
The sequelae of acute ischemic injury to a solitary kidney were assessed in rats subjected to right nephrectomy and transient occlusion of the left renal artery; control rats underwent right nephrectomy alone. Incomplete recovery from ischemic injury at 2 wk (serum creatinine levels of 1.1 +/- 0.2 versus 0.5 +/- 0.1 mg/dl, P < 0.05 for ischemia versus control) was followed by deterioration of renal function at 20 wk (serum creatinine levels of 1.7 +/- 0.4 versus 0.7 +/- 0.1 mg/dl, P < 0.05 for ischemia versus control). Morphologic studies showed that impairment of function after ischemic injury was associated with widespread tubulointerstitial disease. Some tubule segments were atrophic and others exhibited cystic dilation, so that the tubular cell volume fraction was reduced (37 +/- 4 versus 53 +/- 2%, P < 0.05), while the tubular lumen and interstitial volume fractions were increased (31 +/- 4 versus 23 +/- 2% and 29 +/- 2 versus 20 +/- 1%, respectively, both P < 0.05). Many glomeruli retained open capillary loops but were no longer connected to normal tubule segments (63 +/- 8 versus 15 +/- 7% of glomeruli, P < 0.05). There was a strong inverse correlation between the prevalence of such glomeruli and the GFR at 20 wk after ischemia (r2 = 0.79, P < 0.001). Tubulointerstitial disease at that time was accompanied by proteinuria and widespread segmental glomerular tuft injury. The occurrence of similar processes in human patients could contribute to the loss of graft kidneys that suffer ischemic injury during transplantation.