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Hepatorenal Syndrome (HRS)

Impaired renal function which occurs in patients with severe liver disease (secondary to poor renal perfusion - with greatly reduced peripheral vascular resistance and low arterial pressure). Usually occurs in advanced cirrhosis with portal hypertension, but can be seen in acute liver failure or alcoholic hepatitis. HRS is often precipitated by events lowering blood pressure - eg bacterial infections, large volume paracentesis without volume expansion, or haemorrhage (hypovolaemia).¹

Presentation Patients with ascites and other signs of severe liver disease (jaundice, bleeding disorders, malnutrition, stigmata of chronic liver disease) develop renal failure (oligouria or just increasing serum creatinine levels). There is salt and water retention with increased ascites and peripheral oedema - although pulmonary oedema is uncommon. Hyponatraemia is almost universally present (dilutional hyponatraemia); hyperkalaemia is common (and should be aggressively treated).

Diagnosis This is made after excluding other causes of renal failure in patients with liver failure:

• Pre-renal causes (eg a history of dehydration, over diuresis, gastrointestinal fluid loss);
• Any nephrotoxic drugs?
• Any history of shock before renal failure (which would suggest acute tubular necrosis)?
• Any proteinuria ±haematuria? - suggests a parenchymal renal disease (renal USS may be helpful) - particularly glomerulonephritis (associated with Hepatitis B/C or chronic alcoholism).

Management HRS has been divided into 2 types depending on rate of progression:

• Type 1 Severe renal failure - defined as a doubling of serum creatinine to >221 µmol/l in less than 2 weeks. These patients have a very low GFR (<20 mL/min) and very poor prognosis. Admit to hospital, restrict fluid and monitor electrolytes. Treat any precipitating infections aggressively. Start vasoconstrictors and iv albumin. Renal replacement therapy may be necessary. Transjugular porto-hepatic shunts (TIPS) are sometimes used to reduce ascites in patients with portal hypertension (c/i in severe liver failure), although best chance of long term survival would seem to be liver transplantation.
• Type 2 - More gradual and more moderate renal failure, with ascites (resistant to Rx) being the most predominant feature. Usually treated as outpatient. Restrict dietary sodium - use diuretics carefully (hyperkalaemia) and only if they induce significant sodium excretion. Again treat infections aggressively. Repeated paracentesis may be necessary to control gross ascites. Some recommend Transjugular porto-hepatic shunts although may not be associated with increased survival.² Consider vasocontrictors or liver transplantation.

Complications Life threatening bacterial infections (septicaemia, spontaneous bacterial peritonitis, pneumonia).

Prevention It may be possible to reduce the incidence of HRS in patients with spontaneous bacterial peritonitis by administering iv albumin³; and in patients with alcoholic cirrhosis by giving pentoxifylline⁴ (needs confirmation in larger trial).

References

1. Gines P, Guevara M, Arroyo V, Rodes J. Hepatorenal syndrome. Lancet 2003 362:1819-27
2. Gines P, Uriz J, Calahorra B, Garcia-Tsao G, Kamath PS, Del Arbol LR, Planas R, Bosch J, Arroyo V, Rodes J. Transjugular intrahepatic portosystemic shunting versus paracentesis plus albumin for refractory ascites in cirrhosis. Gastroenterology. 2002 Dec; 123(6):1839-47.
3. Sort P, Navasa M, Arroyo V, Aldeguer X, Planas R, Ruiz-del-Arbol L, Castells L, Vargas V, Soriano G, Guevara M, Gines P, Rodes J. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis.N Engl J Med. 1999 Aug 5; 341(6):403-9.
4. Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O. Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial. Gastroenterology. 2000 Dec; 119(6):1637-48.

Acknowledgements EMIS is grateful to Dr Huw Thomas for adding to this article. The final copy has passed peer review of the independent Mentor GP authoring team. ©EMIS 2006.

Last issued 05 Jul 2006