Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Department of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Biomed Pharmacother. 2020 May;125:109978. doi: 10.1016/j.biopha.2020.109978. Epub 2020 Feb 12.
Severe acute pancreatitis (SAP), a critical inflammatory pathological disease of the pancreas, is crucial for the manifestation of lethal multiple organ dysfunction syndrome and systemic inflammatory response syndrome. Acute kidney injury (AKI) is one of the most severe complications of severe acute pancreatitis. Yet, the specific pathogenesis of AKI following SAP is defectively understood, and involves in multiple pathological processes in a "network-regulative" pattern, including dysfunction of the intestinal barrier, prolonged activation of coagulation, elevated discharge of damage-associated molecular patterns, complication of abdominal compartment syndrome, excessive release of inflammatory mediators, overexpression of procalcitonin, and incitement of chronic metabolic diseases. Therefore, in this review, we summarize the current knowledge on the pathogenesis of kidney injury following SAP to provide a better understanding of the interactions involved and to encourage the identification of novel targeted therapies to treat SAP and associated AKI.
严重急性胰腺炎（SAP）是一种胰腺的危急炎性病理疾病，对致命性多器官功能障碍综合征和全身炎症反应综合征的表现至关重要。急性肾损伤（AKI）是严重急性胰腺炎最严重的并发症之一。然而，SAP 后 AKI 的具体发病机制尚不清楚，涉及多个病理过程的“网络调节”模式，包括肠屏障功能障碍、凝血的长期激活、损伤相关分子模式的释放增加、腹腔间隔室综合征的并发症、炎症介质的过度释放、降钙素原的过度表达以及慢性代谢性疾病的激发。因此，在这篇综述中，我们总结了 SAP 后肾损伤发病机制的现有知识，以更好地了解所涉及的相互作用，并鼓励确定治疗 SAP 和相关 AKI 的新型靶向治疗方法。
