Korean J Gastroenterol.  2016 Nov;68(5):237-244. 10.4166/kjg.2016.68.5.237.

Acute Kidney Injury in Cirrhotic Patients with Portal Hypertension

Affiliations
  • 1Department of Internal Medicine, Dankook University College of Medicine, Cheonan, Korea. ihsong21@dankook.ac.kr

Abstract

Acute kidney injury (AKI) is one of the most common manifestations encountered in clinical practice. It is associated with high morbidity and mortality in cirrhotic pre- and post-transplantation patients. Hepatorenal syndrome (HRS), a special form of AKI in cirrhotic patients, was recognized as a consequence of renal vasoconstriction from systemic/renal hemodynamic alterations developed in advanced cirrhosis with portal hypertension. Recently, multiple factors"”such as infection/inflammation, underlying glomerulonephritis, bile cast, or increased abdominal pressure"”have been considered to contribute to renal dysfunction in cirrhotic patients, which were presumed to induce HRS. Moreover, in addition to changing the definition of AKI in the nephrologic guidelines, the new AKI definition for early diagnosis and intervention based on characteristics of liver cirrhosis has been proposed in an international meeting. This article provides a comprehensive and recent review of AKI definition, laying out the topics in accordance with the pathophysiologic mechanisms and therapeutic interventions of AKI in cirrhotic patients with portal hypertension.

Keyword

Acute kidney injury; Hepatorenal syndrome; Liver cirrhosis; Portal hypertension

MeSH Terms

Acute Kidney Injury*
Bile
Early Diagnosis
Fibrosis
Glomerulonephritis
Hemodynamics
Hepatorenal Syndrome
Humans
Hypertension, Portal*
Liver Cirrhosis
Mortality
Vasoconstriction

Figure

  • Fig. 1. Traditional and potential mechanisms of the development of acute kidney injury in cirrhotic patients with portal hypertension. NO, nitric oxide; CO, carbon monoxide; iNOS, inducible NO; TLR, toll like receptor; TNF, tumor necrosis factor; IL, interleukin; RAA, renin-angiotensin- aldosterone; SNS, sympathetic nervous system; PGE2, prostaglandin E2;6-keto PGF1, 6-keto-prostaglandin F1.


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