A network-regulative pattern in the pathogenesis of kidney injury following severe acute pancreatitis.

Abstract 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.