Zusammenfassung
Das hepatorenale Syndrom (HRS) ist eine schwere Komplikation der
Leberzirrhose, die mit einer hohen Mortalität verbunden ist. Entsprechend
dem klinischen Verlauf werden zwei Formen des HRS unterschieden: Das HRS Typ I
ist gekennzeichnet durch einen raschen Anstieg der Retentionsparameter
(Verdoppelung des Serumkreatinins auf
Werte > 2,5 mg/dl) oder einen raschen Abfall der
Kreatininclearance < 20 ml/min innerhalb von 14 Tagen.
Das HRS Typ II entspricht dem chronischen Verlauf der Erkrankung mit nur
mäßig erhöhten Retentionswerten
(Kreatinin > 1,5 mg/dl). Hämodynamischen
Veränderungen wird in der Pathophysiologie des HRS eine wesentliche Rolle
beigemessen: So findet sich bei diesen Patienten neben portaler Hypertension
eine periphere, vor allem splanchnische Vasodilatation, welche zu einer Abnahme
des zentralen, effektiven Blutvolumens führt. Dies wiederum hat eine
Aktivierung Volumen und Natrium retinierender Hormonsysteme wie des
Renin-Angiotensin-Aldosteron-Systems und des sympathischen Nervensystems zur
Folge. Hieraus resultieren eine Abnahme des renalen Blutflusses, der
glomerulären Filtrationsrate und der freien Wasserclearance bei
gleichzeitiger Steigerung der Natriumrückresorption. Neuere therapeutische
Strategien zielen nun auf eine Korrektur der zugrunde liegenden
hämodynamischen Veränderungen: So senkt der transjuguläre
intrahepatische portosystemische Shunt den Pfortaderdruck, während
verschiedene vasoaktive Substanzen über eine periphere und splanchnische
Vasokonstriktion wirken. Zahlreiche, meist unkontrollierte Studien konnten
einen günstigen Effekt dieser Strategien auf die Nierenfunktion belegen.
In der vorliegenden Übersicht wird eine zusammenfassende Analyse
durchgeführt, die zeigt, dass sich dieser positive Effekt auch auf das
Überleben von Patienten mit HRS Typ 1 auswirken kann.
Abstract
HRS is a serious complication in patients with cirrhosis and ascites
and associated with a poor prognosis unless liver transplantation can be
performed. Two different types of HES are being differentiated according to the
clinical presentation: while HRS type I is characterised by rapid deterioration
of renal function indicated by a two-fold increase of serum creatinine to
values above 2.5 mg/dl or a decrease of creatinine clearance to values
below 20 ml/min, HRS type II shows moderately increased serum creatinine
above 1.5 mg/dl remaining stable over a longer period. The most
prominent circulatory alterations in patients with chronic liver disease
comprise portal hypertension and peripheral (mainly splanchnic) arterial
vasodilation. This leads to a decreased centrally effective blood volume in
cirrhotic patients. As a consequence, activation of sodium- and
volume-retaining neurohumoral systems such as the renin-angiotensin-aldosterone
system and the sympathetic nervous system and a non-osmotic release of
arginine-vasopressin can be observed. These neurohumoral alterations induce
renal sodium and water retention which are responsible for accumulation of
ascites and deterioration of renal function. Recent therapeutic strategies of
the hepatorenal syndrome take into account these pathophysiologic
considerations: whereas the transjugular intrahepatic portosystemic shunt
lowers portal hypertension, infusion of vasoactive drugs increases systemic
vascular resistance in cirrhotic patients. Several uncontrolled trials have
reported a positive effect of these strategies on renal function. The present
analysis of combined data from these reports shows that this positive effect on
renal function also may improve survival of patients with HRS type I.
Schlüsselwörter
hepatorenales
Syndrom - Therapie - Vasokonstriktoren - TIPS
Key words
Hepatonenal
syndrome - therapy - vasoconstrictors - TIPS
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Veit Gülberg, M.D.
Department of Medicine II, Klinikum of the Ludwig-Maximilians
University · Großhadern
Marchioninistr. 15
81377 München
Email: Veit.Guelberg@med2.med.uni-muenchen.de