Schmiedt C W, Brainard B M, Hinson W, Brown S A, Brown C A
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA.
Vet Pathol. 2016 Jan;53(1):87-101. doi: 10.1177/0300985815600500. Epub 2015 Aug 28.
The objectives of this study were to define the acute and chronic effects of 1-hour unilateral in vivo renal ischemia on renal function and histology in cats. Twenty-one adult purpose-bred research cats were anesthetized, and 1 kidney underwent renal artery and vein occlusion for 1 hour. Serum creatinine and urea concentrations, urine protein:creatinine ratio, urine-specific gravity, glomerular filtration rate, hematocrit, platelet concentration and function, and white blood cell count were measured at baseline and variable time points after ischemia. Renal histopathology was evaluated on days 3, 6, 12, 21, 42, and 70 postischemia; changes in smooth muscle actin and interstitial collagen were examined. Following ischemia, whole animal glomerular filtration rate was significantly reduced (57% of baseline on day 6; P < .05). At the early time points, the ischemic kidneys exhibited severe acute epithelial necrosis accompanied by evidence of regeneration of tubules predominantly within the corticomedullary junction. At later periods, postischemic kidneys had evidence of tubular atrophy and interstitial inflammation with significantly more smooth muscle actin and interstitial collagen staining and interstitial fibrosis when compared with the contralateral control kidneys. This study characterizes the course of ischemic acute kidney injury in cats and demonstrates that ischemic acute kidney injury triggers chronic fibrosis, interstitial inflammation, and tubular atrophy in feline kidneys. These late changes are typical of those observed in cats with naturally occurring chronic kidney disease.
本研究的目的是确定1小时单侧体内肾缺血对猫肾功能和组织学的急性和慢性影响。21只成年的专门培育的实验猫被麻醉，一侧肾脏的肾动脉和肾静脉被阻断1小时。在缺血前的基线和不同时间点测量血清肌酐和尿素浓度、尿蛋白：肌酐比值、尿比重、肾小球滤过率、血细胞比容、血小板浓度和功能以及白细胞计数。在缺血后第3、6、12、21、42和70天评估肾脏组织病理学；检查平滑肌肌动蛋白和间质胶原的变化。缺血后，全动物肾小球滤过率显著降低（第6天为基线的57%；P < 0.05）。在早期时间点，缺血肾脏表现出严重的急性上皮坏死，并伴有主要在皮质髓质交界处的肾小管再生迹象。在后期，与对侧对照肾脏相比，缺血后肾脏有肾小管萎缩和间质炎症的迹象，平滑肌肌动蛋白和间质胶原染色以及间质纤维化明显更多。本研究描述了猫缺血性急性肾损伤的病程，并表明缺血性急性肾损伤会引发猫肾脏的慢性纤维化、间质炎症和肾小管萎缩。这些后期变化是自然发生的慢性肾病猫所观察到的典型变化。
