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Part of the book series: Falk Symposium ((FASS,volume 160))

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Abstract

Definition and diagnostic criteria for hepatorenal syndrome (HRS) established in 19941 were based on the following three concepts:

  1. 1.

    Renal failure in HRS is functional and caused by marked intrarenal arteriolar vasoconstriction.

  2. 2.

    HRS occurs in the setting of a systemic circulatory dysfunction caused by extrarenal vasodilation.

  3. 3.

    Plasma volume expansion does not improve renal failure.

Four new concepts have emerged since then:

  1. 1.

    Extrarenal arterial vasodilation mainly occurs in the splanchnic bed, whereas other major vascular beds, such as the brain and the liver, may be vasoconstricted. This may contribute to some of the frequent extrarenal complications, i.e. progressive hepatic failure and encephalopathy.

  2. 2.

    Cardiac output in patients with HRS may be low, normal, or high, but all the same it is insufficient because of the reduced peripheral vascular resistance. This may aggravate the systemic circulatory dysfunction of HRS.

  3. 3.

    The most frequent trigger of type 1 HRS is bacterial infection, mainly spontaneous bacterial peritonitis (SBP).

  4. 4.

    HRS is not always a terminal event as it can be improved by medical treatment, and the improvement is associated with improved survival.

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Gerbes, A.L. (2008). Hepatorenal syndrome in cirrhosis. In: Ferkolj, I., Gangl, A., Galle, P.R., Vucelic, B. (eds) Pathogenesis and Clinical Practice in Gastroenterology. Falk Symposium, vol 160. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-8767-7_21

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  • DOI: https://doi.org/10.1007/978-1-4020-8767-7_21

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