Hepatorenal syndrome
From Medical-Wiki
Hepatorenal syndrome (HRS) is renal failure that occurs in the face of advanced liver disease — often fulminant failure — with portal hypertension and ascites. It is estimated that 40% of patients who have ascites and portal hypertension will develop HRS at some point during their course.
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Physiological origin of hepatorenal syndrome
It appears that the primary pathology of HRS is renal vasoconstriction. The interactions that are responsible for the syndrome are complex and poorly understood but their pattern is characterized by increased cardiac output, low arterial pressure, and reduced systemic vascular resistance. Renal vasoconstriction occurs without reduced cardiac output and blood volume — in contrast to most clinical conditions associated with renal hypoperfusion.
There are 2 main theories that are now used to explain HRS and cirrhosis — arterial vasodilation theory and the hepatorenal reflex theory. The former theory not only describes sodium and water retention in cirrhosis, but also may be the most rational hypothesis for the development of HRS. Splanchnic arteriolar vasodilatation in patients with compensated cirrhosis and portal hypertension may be mediated by several factors, the most important of which is probably nitrous oxide (NO). In the early phases of portal hypertension and compensated cirrhosis, this underfilling of the arterial bed causes a decrease in the effective arterial blood volume and results in homeostatic/reflex activation of the endogenous vasoconstrictor systems. [1]
Diagnosis of hepatorenal syndrome
The International Ascites Club has established criteria that must be met for the diagnosis of HRS.
- A patient must have a low glomerular filtration rate.
- There must be an absence of shock, ongoing bacterial infection, fluid losses and any exposure to nephrotoxic drugs.
- There should be no sustained improvement in renal failure following diuretic withdrawal and expansion of plasma volume.
- There should be proteinuria that is no greater than 500 mg/day and no ultrasonographic evidence of obstructive uropathy or parenchymal renal disease.
- The additional criteria are a urine volume lower than 500 ml/day, a urine sodium lower than 10 m/Eq/l, and urine osmolality greater than plasma osmolality, urine red blood cells less than 50 per high-power field, and serum sodium concentration lower than 130 mEq/l.
All major criteria must be present for the diagnosis of HRS to be made. Additional criteria are not necessary for the diagnosis—they do however provide supportive evidence.
Two types of heaptorenal syndrome
There are two types of hepatorenal syndrome—type I and type II. Type I is characterized by rapid and progressive impairment of renal function. This is defined by a doubling of the initial creatinine or a 50% reduction of the initial 24-hour creatinine clearance to a level lower than 20 ml/min in less than 2 weeks.
Type II is characterized by significant impairment in renal function —(creatanine 41.5 mg/dl) that does not meet the criteria of type I. [2]
The development of HRS, be it type I or type II, has ominous implications.
Type I HRS has a median survival time of 2 weeks.
Type II HRS has a median survival time of 6 months. [3]
Treatment for hepatorenal syndrome
One of the changes in treatment in the last five years has been derived from an increased understanding of its physiology.
Vasoconstrictor therapy is aimed at increasing systemic or splanchnic vasoconstriction. Increasing systemic vasoconstriction improves renal perfusion. Increasing splanchnic vasoconstriction redistributes part of the splanchnic volume to the systemic circulation — improving systemic perfusion in general.
In Europe, Terlipressin is the vasoconstrictor of choice. This drug has not been cleared in America. In America an alternative of the combination of midodrine and octreotide is used instead of Terlipressin.
Transjugular intrahepatic portosystemic stent shunt (TIPS) and extracorporeal albumin dialysis (ECAD) are also used to stabilize patients during attempts to arrange a liver transplant. [4]
