Pathogenesis of ascites and hepatorenal syndrome.

Ascites is one of the most common complications of cirrhosis and has a one year mortality of up to 50%. For fluid to accumulate in any clinical situation the amount of sodium ingested must exceed that excreted by the kidneys and the virtual absence of sodium from the urine of ascitic patients was first documented by Farnsworth and Krakusin in 1948.' Five years later Chart and Shipley showed such patients to have an excess of a sodium retaining hormone in their urine (later identified as aldosterone).2 Four decades after these discoveries the inter-relationship between renal function, hormonal changes and ascites formation remains controversial. At the other extreme of functional renal changes up to 85% ofpatients dying with cirrhosis have renal failure and, where there is no apparent cause other than the liver disease, is termed 'hepatorenal syndrome.' In 1863 Flint noted that proteinuria was uncommon and kidney morphology often normal, but some patients showed a variety of renal parenchymal changes.3 Hecker and Sherlock confirmed the absence of proteinuria and normal histology in many patients and reported very low urine sodium concentrations findings of a prerenal type of uraemia.