Pathophysiology of the hepatorenal syndrome acute kidney injury (HRS-AKI) (IMAGE)

Xia & He Publishing Inc.

Pathophysiology of the hepatorenal syndrome acute kidney injury (HRS-AKI)

Caption

The progressive worsening of liver cirrhosis and portal hypertension (HTN) decreases intra-hepatic nitric oxide (NO), which is counterbalanced by increased NO secretion from adjacent endothelial cells. Bacterial translocation from ascites and gut barrier disruption lead to increased production of inflammatory cytokines and mediators into the systemic circulation, including interleukin (IL) 6 and 12, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs). Both processes lead to splanchnic vasodilation, decreased systemic vascular resistance, and underfilling of the effective circulation. A compensatory mechanism occurs, and the renin-angiotensin-aldosterone system (RAAS) is activated, causing increased water retention, heart rate, and cardiac output. This increases renal vasoconstriction and decreases renal blood flow (RBF). Persistent vasodilation ultimately leads to renal hypoperfusion, sustained renal vasoconstriction, and may also contribute to cirrhotic cardiomyopathy, all contributing to the development of HRS-AKI. DAMPs, damage-associated molecular patterns; HRS-AKI, hepatorenal syndrome acute kidney injury; IL, interleukin; NO, nitric oxide; PAMPs, pathogen-associated molecular patterns; Portal HTN, portal hypertension; RAAS, renin-angiotensin aldosterone system; RBF, renal blood flow.

Credit

Ahmed H. Abdelwahed

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License

CC BY-NC

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