Dtsch Med Wochenschr 2015; 140(14): 1083-1092
DOI: 10.1055/s-0041-102647
Fachwissen
CME
© Georg Thieme Verlag KG Stuttgart · New York

Diagnostik und Therapie des hepatorenalen Syndroms

Diagnosis and therapy of the hepatorenal syndrome
Sandra Blomeyer*#
1   Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Universität Duisburg-Essen
,
Bartosz Tyczynski*
2   Klinik für Nephrologie, Universitätsklinikum Essen
,
Guido Gerken*
1   Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Universität Duisburg-Essen
,
Ali Canbay*#
1   Klinik für Gastroenterologie und Hepatologie, Universitätsklinikum Essen, Universität Duisburg-Essen
› Author Affiliations
Further Information

Publication History

Publication Date:
16 July 2015 (online)

Zusammenfassung

In Folge einer fortgeschrittenen Leberzirrhose kommt es zu einer portalen Hypertension, die für den überwiegenden Teil letaler Komplikationen bei Leberzirrhose verantwortlich ist. Die kompensatorische, splanchnische Vasodilatation führt langfristig zu einer Gegenregulation unter anderem über das Renin-Angiotensin-Aldosteron-System und dadurch zu einer Erhöhung des renalen Gefäßwiderstands. Hierdurch kann ein hepatorenales Syndrom (HRS) entstehen. Das HRS stellt sich als Nierenfunktionseinschränkung mit erhöhten Kreatinin-Werten dar. Das HRS wird über eine komplexe Ausschlussdiagnostik erkannt und rasch mittels Albumin und Vasokonstriktoren therapiert. Für eine Heilung ist die Verbesserung der Leberfunktion essenziell, was in vielen Fällen die Notwendigkeit einer Lebertransplantation bedeutet. Zur Überbrückung bis zur Transplantation kann die Anlage eines TIPS sinnvoll sein, sofern keine hepatische Enzephalopathie vorliegt. Da eine spontane bakterielle Peritonitis (SBP) ein erhebliches Risiko für die HRS-Entstehung ist, ist bei Patienten mit Leberzirrhose und SBP neben der Antibiotikagabe eine Prävention mittels Albumin ratsam.

Abstract

Portal hypertension occurs frequently in advanced liver cirrhosis and accounts for the majority of lethal complications. Compensatory splanchnic vasodilation and counter regulatory mechanisms (e. g. activation of the renin-angiotensin-aldosterone system) increase renal vascular resistance, which may facilitate acute kidney injury and the development of hepatorenal syndrome (HRS). HRS represents a functional, yet reversible renal impairment with elevated serum creatinine levels. Establishing the diagnosis, fluid challenge test and several investigations are needed to exclude acute kidney injury and other causes of renal failure. Early treatment with albumin and vasoconstrictors improves the prognosis of HRS patients. The only curative treatment of HRS so far is improvement of liver function implying liver transplantation in many cases. TIPS placement may be useful as a bridging tool to transplantation unless hepatic encephalopathy is present. Spontaneous bacterial peritonitis (SBP) is a relevant, independent risk factor for HRS. In patients with liver cirrhosis and SBP in addition to antibiotics, preventive albumin treatment is recommended.

* Autoren des Hauptteils


# Autoren des konkreten Falls


 
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