死亡後腎小管產生腐敗或自溶的死後組織變化和急性腎小管損傷十分類似,在顯微組織檢查鑑別兩者相當困難。目前文獻上許多的證據顯示氧化壓力和急性腎小管損傷的致病機轉有關,而其中過氧化物還原酶3 為一種抗氧化劑,維持人體內氧化和還原反應的平衡。本篇研究納入30個切片確診急性腎小管損傷案例,10個腎小管出現死後組織變化的猝死案例和10個正常腎臟組織案例,利用數位影像分析軟體比較過氧化物還原酶3 的免疫組織化學染色在腎小管染色強度。結果顯示急性腎小管損傷在過氧化物還原酶3 染色表現上比腎小管死後組織變化組和正常腎臟組織組來的強,且統計上有顯著差異 (p值<0.0001)。而死後腎小管組織變化組和正常腎臟組織組兩組之間,在過氧化物還原酶3 染色強度上無統計上差異 (P值=0.1306)。本篇研究結論顯示,相比於死後腎小管組織變化的過氧化物還原酶3 免疫組織化學染色表現,當過氧化物還原酶3 在腎小管表現升高時,應考慮急性腎小管損傷的發生。
It is difficult to make the diagnosis of acute tubular injury at postmortem autopsy examination because the problems of postmortem change, leading to histologically similar feature of acute tubular injury. Many evidences exhibit that oxidative stress participates in pathogenesis of acute tubular injury and the peroxiredoxin 3, an antioxidant, maintains the balance between oxidation and reduction in body. We collected human renal tissues including 30 cases with biopsy-proven acute tubular injury, 10 sudden death cases with postmortem change and 10 control cases were enrolled for comparison of immunohistochemical peroxiredoxin 3 staining intensity at renal tubules by digital image analytic software. The results revealed that acute tubular injury showed more intense peroxiredoxin 3 staining than postmortem change and control with statistically significant difference (p value < 0.0001). Between postmortem change and control, no significance difference on staining intensity was observed (p value=0.1306). In conclusion, elevated immunohistochemical peroxiredoxin 3 expression at renal tubules indicated occurrence of antemortem acute tubular injury rather than postmortem change of renal tubules.