Department of Critical Care, University of Groningen, University Medical Center Groningen, P.O. 30.001, Hanzeplein 1, 9700 RB, Groningen, Netherlands.
Department of Pathology & Medical Biology, Medical Biology Section, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, Netherlands.
Crit Care. 2018 Dec 27;22(1):359. doi: 10.1186/s13054-018-2287-3.
The histopathology of sepsis-associated acute kidney injury (AKI) in critically ill patients remains an understudied area. Previous studies have identified that acute tubular necrosis (ATN) is not the only driver of sepsis-AKI. The focus of this study was to identify additional candidate processes that may drive sepsis-AKI. To do this we immunohistochemically characterized the histopathological and cellular features in various compartments of human septic kidneys.
We studied the following histopathological features: leukocyte subsets, fibroblast activation, cellular proliferation, apoptosis, and fibrin deposition in the glomerulus and the tubulointerstitium in human post-mortem kidney biopsy tissue. Biopsy tissue samples from 27 patients with sepsis-AKI were collected 33 min (range 24-150) after death in the ICU. The unaffected part of the kidneys from 12 patients undergoing total nephrectomy as a result of renal carcinoma served as controls.
Immunohistochemical analysis revealed the presence of more neutrophils and macrophages in the glomeruli and more neutrophils in the tubulointerstitium of renal tissue from patients with sepsis compared to control renal tissue. Type II macrophages were predominant, with some macrophages expressing both type I and type II markers. In contrast, there were almost no macrophages found in control kidneys. The number of activated (myo)fibroblasts was low in the glomeruli of sepsis-AKI kidneys, yet this was not observed in the tubulointerstitium. Cell proliferation and fibrin deposition were more pronounced in the glomeruli and tubulointerstitium of sepsis-AKI than in control kidneys.
The extensive heterogeneity of observations among and within patients emphasizes the need to thoroughly characterize patients with sepsis-AKI in a large sample of renal biopsy tissue from patients with sepsis.
危重病患者脓毒症相关性急性肾损伤（AKI）的组织病理学仍未得到充分研究。既往研究已确定，急性肾小管坏死（ATN）并非脓毒症性 AKI 的唯一驱动因素。本研究的重点是确定可能导致脓毒症性 AKI 的其他候选过程。为此，我们通过免疫组织化学方法对各种人类脓毒症肾脏部位的组织病理学和细胞特征进行了特征描述。
我们研究了以下组织病理学特征：白细胞亚群、成纤维细胞激活、细胞增殖、细胞凋亡和肾小球及小管间质中的纤维蛋白沉积。从 ICU 死亡后 33 分钟（范围 24-150 分钟）收集了 27 例脓毒症性 AKI 患者的尸检肾活检组织。作为对照，从 12 例因肾癌行全肾切除术的患者的未受影响部分肾脏组织中收集了肾组织样本。
免疫组织化学分析显示，与对照组肾组织相比，脓毒症患者肾组织的肾小球中存在更多的中性粒细胞和巨噬细胞，小管间质中存在更多的中性粒细胞。II 型巨噬细胞占优势，有些巨噬细胞同时表达 I 型和 II 型标志物。相比之下，对照组肾脏中几乎没有发现巨噬细胞。脓毒症性 AKI 肾脏的肾小球中激活的（肌）成纤维细胞数量较少，但小管间质中未见此现象。与对照组肾脏相比，脓毒症性 AKI 患者的肾小球和小管间质中的细胞增殖和纤维蛋白沉积更为明显。
患者之间和患者内部观察结果的广泛异质性强调了在大量脓毒症患者肾活检组织中对脓毒症性 AKI 患者进行全面特征描述的必要性。
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