Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome

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Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome. / Møller, Søren; Bendtsen, Flemming; Henriksen, Jens H.

In: Scandinavian Journal of Gastroenterology, Vol. 40, No. 5, 2005, p. 491-500.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Møller, S, Bendtsen, F & Henriksen, JH 2005, 'Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome', Scandinavian Journal of Gastroenterology, vol. 40, no. 5, pp. 491-500. https://doi.org/10.1080/00365520510012064

APA

Møller, S., Bendtsen, F., & Henriksen, J. H. (2005). Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome. Scandinavian Journal of Gastroenterology, 40(5), 491-500. https://doi.org/10.1080/00365520510012064

Vancouver

Møller S, Bendtsen F, Henriksen JH. Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome. Scandinavian Journal of Gastroenterology. 2005;40(5):491-500. https://doi.org/10.1080/00365520510012064

Author

Møller, Søren ; Bendtsen, Flemming ; Henriksen, Jens H. / Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome. In: Scandinavian Journal of Gastroenterology. 2005 ; Vol. 40, No. 5. pp. 491-500.

Bibtex

@article{b81ad3701bc411df8ed1000ea68e967b,

title = "Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome",

abstract = "Hepatorenal syndrome (HRS) is a functional and reversible impairment of renal function in patients with severe cirrhosis. Major pathophysiological elements include liver dysfunction, a circulatory derangement with central hypovolaemia and neurohumoral activation of potent vasoactive systems leading to a pronounced renal vasoconstriction. The prognosis of patients with HRS is poor but recent research has spread new enthusiasm for treatment. Efforts at treatment should seek to improve liver function, to ameliorate arterial hypotension and central hypovolaemia, and to reduce renal vasoconstriction. Therefore a combined approach should be applied with reduction of portal pressure with e.g. ss-adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS), with amelioration of arterial hypotension and central hypovolaemia with vasoconstrictors such as terlipressin and plasma expanders. New experimental treatments with endothelin- and adenosine antagonists and long-acting vasoconstrictors may have a future role in the management of HRS.",

author = "S{\o}ren M{\o}ller and Flemming Bendtsen and Henriksen, {Jens H}",

note = "Keywords: Adenosine; Adrenergic beta-Antagonists; Endothelins; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hypotension; Hypovolemia; Kidney; Liver; Portasystemic Shunt, Transjugular Intrahepatic; Renal Veins; Vasoconstriction; Vasoconstrictor Agents",

year = "2005",

doi = "10.1080/00365520510012064",

language = "English",

volume = "40",

pages = "491--500",

journal = "Scandinavian Journal of Gastroenterology",

issn = "0036-5521",

publisher = "Taylor & Francis",

number = "5",

}

RIS

TY - JOUR

T1 - Pathophysiological basis of pharmacotherapy in the hepatorenal syndrome

AU - Møller, Søren

AU - Bendtsen, Flemming

AU - Henriksen, Jens H

N1 - Keywords: Adenosine; Adrenergic beta-Antagonists; Endothelins; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hypotension; Hypovolemia; Kidney; Liver; Portasystemic Shunt, Transjugular Intrahepatic; Renal Veins; Vasoconstriction; Vasoconstrictor Agents

PY - 2005

Y1 - 2005

N2 - Hepatorenal syndrome (HRS) is a functional and reversible impairment of renal function in patients with severe cirrhosis. Major pathophysiological elements include liver dysfunction, a circulatory derangement with central hypovolaemia and neurohumoral activation of potent vasoactive systems leading to a pronounced renal vasoconstriction. The prognosis of patients with HRS is poor but recent research has spread new enthusiasm for treatment. Efforts at treatment should seek to improve liver function, to ameliorate arterial hypotension and central hypovolaemia, and to reduce renal vasoconstriction. Therefore a combined approach should be applied with reduction of portal pressure with e.g. ss-adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS), with amelioration of arterial hypotension and central hypovolaemia with vasoconstrictors such as terlipressin and plasma expanders. New experimental treatments with endothelin- and adenosine antagonists and long-acting vasoconstrictors may have a future role in the management of HRS.

AB - Hepatorenal syndrome (HRS) is a functional and reversible impairment of renal function in patients with severe cirrhosis. Major pathophysiological elements include liver dysfunction, a circulatory derangement with central hypovolaemia and neurohumoral activation of potent vasoactive systems leading to a pronounced renal vasoconstriction. The prognosis of patients with HRS is poor but recent research has spread new enthusiasm for treatment. Efforts at treatment should seek to improve liver function, to ameliorate arterial hypotension and central hypovolaemia, and to reduce renal vasoconstriction. Therefore a combined approach should be applied with reduction of portal pressure with e.g. ss-adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS), with amelioration of arterial hypotension and central hypovolaemia with vasoconstrictors such as terlipressin and plasma expanders. New experimental treatments with endothelin- and adenosine antagonists and long-acting vasoconstrictors may have a future role in the management of HRS.

U2 - 10.1080/00365520510012064

DO - 10.1080/00365520510012064

M3 - Journal article

C2 - 16036500

VL - 40

SP - 491

EP - 500

JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 0036-5521

IS - 5

ER -

ID: 18052996