The pathogenic mechanism of severe acute pancreatitis complicated with renal injury: a review of current knowledge

Dig Dis Sci. 2008 Feb;53(2):297-306. doi: 10.1007/s10620-007-9866-5. Epub 2007 Jun 28.


The onset of severe acute pancreatitis (SAP) is clinically harmful as it may rapidly progress from a local pancreatic inflammation into proemial systemic inflammatory reactions. Patients with SAP have a high mortality, with most cases of death resulting from complications involving the failure of organs other than the pancreas. The distinctive feature of SAP is that once it starts, it may aggrevate the clinical condition of the patient continuously, so that the levels of injury to the other organs surpass the severity of the pancreatic lesion, even causing multiple organ failure and, ultimately, death. In clinical practice, the main complications in terms of organ dysfunctions are shock, acute respiratory failure, acute renal failure, among others. The acute renal injury caused by SAP is not only able to aggravate the state of pancreatitis, but it also develops into renal failure and elevates patients' mortality. Studies have found that the injury due to massive inflammatory mediators, microcirculation changes and apoptosis, among others, may play important roles in the pathogenic mechanism of acute renal injury.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Disease
  • Animals
  • Humans
  • Hyperuricemia / physiopathology
  • Inflammation Mediators / physiology
  • Kidney / physiopathology
  • Microcirculation / physiology
  • NF-kappa B / physiology
  • Pancreatitis / complications
  • Pancreatitis / physiopathology*
  • Phospholipases A2 / physiology
  • Platelet Activating Factor / physiology
  • Trypsin / blood
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / physiology


  • Inflammation Mediators
  • NF-kappa B
  • Platelet Activating Factor
  • Tumor Necrosis Factor-alpha
  • Phospholipases A2
  • Trypsin