kidneytubularproximalmortalityapoptosisimpairmentirreversiblehypertrophy蒋素华histological
摘要：12.1 Kidney function2007244 Short-and long-term outcome of the kidney after acute ischemia-reperfusion injury. JIANG suhua(蒋素华), et al. Dept Nephrol, Zhongshan Hosp, Fudan Univ, Shanghai 200032. Chin J Nephrol 2007;23(4):246-250. Objective To investigate short-and long-term outcome of the kidney after acute ischemia-reperfusion (IR) injury. Methods Rat model of renal IR was established by clamping both pedicles for 40 min followed by reperfusion. Blood sample and kidneys were collected at indicated times. Serum creatinine levels, mortality and histological change were observed throughout the study. Transmission electron microscopy (TEM) was used to observe tubular ultra-structure. Apoptosis was confirmed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay. The extent of tubulointerstitial fibrosis was evaluated by Masson trichome staining. The expression of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) was determined by Western blot and immunohistochemical analysis. Results Extensive proximal tubular necrosis, functional impairment and high mortality (32%, 8/25) were found in the early phase after renal IR injury, accompanied by a small number of apoptotic cells. Patchy tubulointerstitial fibrosis was obvious at 5th and 10th week postischemia in correlation with renal hypertrophy and increased urinary output. Moreover, the expression of a-SMA and TGF-β1 increased significantly at first, 5th and 10th week in the kidneys of IR group compared to sham-operated group. The expression mentioned above was localized mainly in the injured tubulointerstitium, consistent with the distribution of renal fibrosis. Conclusion Severe renal IR injury may lead to acute tubular necrosis, functional disorder and high mortality in short term. The initial structural injury in the kidney is irreversible and tubulointerstitial fibrosis is the final outcome. Increased myofibrolasts (s-SMA positive) and overexpression of TGF-β1 maybe contribute t
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