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Abstract Advanced chronic liver disease is responsible for a significant number of physiological changes that affect the circulation and kidney perfusion. Cirrhosis results in accumulation of vasodilatory mediators, in particular nitric oxide (NO), which specifically vasodilates the splanchnic circulation reducing the effective circulating blood volume and mean arterial pressure. Hypoperfusion of the kidneys leads to a reduction in the sodium concentration of tubular fluid reaching the distal tubule stimulating the macula densa, to release renin, thus activating the renin-angiotensin-aldosterone (RAA) axis (Slack et al.,2010) . Hepatorenal syndrome is defined as a unique functional form of acute kidney injury in patient with advanced cirrhosis (almost always associated with ascites ) or in patient with fulminant acute hepatic failure that can not explained by the common etiological factors that account for acute kidney injury in patient without underlying liver disease (venkat D and K,2010)Hepatorenal syndrome (HRS) is a potentially reversible clinical syndrome that occurs in patients with cirrhosis, ascites and liver failure, as well as in patients with acute liver failure or alcoholic hepatitis. It is characterized by impaired renal function, marked alterations in cardiovascular function and overactivity of the sympathetic nervous (SNS) and renin–angiotensin– aldosterone systems. The incidence of functional renal failure including HRS in nonazotemic patients with cirrhosis after the onset of ascites is estimated to be 23.6% at 1 year and 42% by 5 years. Older age, higher Child–Pugh score, and higher baseline creatinine are strong predictors for the development of functional renal failure including HRS, reflecting that a longer duration of disease, and more severe liver and renal dysfunction are strong risk factors for the development of HRS (Leung andWrong ,2011) . Hepatitis B virus can cause hepatitis as well as various extrahepatic complication through formation of immune complexes . these include nephrotic syndrome , polyarteritis nodosa and essential mixed cryoglobinemia.Many adult patients with HBVassociated nephropathy have symptom attributed to Introduction nephrotic syndrome and 30% of patients ultimately progress to renal failure (Nakahara et al.,2010) . Hepatitis C has long been associated with several glomerulopathies, most notably cryoglobulin- and noncryoglobulin associated membranoproliferative glomerulonephritis. The prevalence of cryoglobulinemia is around 50% , although extrarenal manifestations are often absent in the majority of these patients. Viral RNA, proteins and particles have been inconsistently isolated from kidney biopsy specimens, making it difficult to establish whether hepatitis C is causative in other forms of glomerulopathy . In seropositive hepatitis C populations, hepatitis C infection has been reported to be associated with focal segmental glomerulosclerosis, membranous nephropathy with or without nephrotic range proteinuria, IgA nephropathy, and proliferative glomerulonephritis (Slack et al.,2010 ) . Hypovolemia as a consequence of gastrointestinal bleeding , diarrhea ,or excessive administration of diuretics is a common cause of impaired renal functionin cirrhosis(Gines and schrier,2009) . Introduction Recent advances in the understanding of the natural history and pathophysiology of liver cirrhosis and in treatment of its complication have resulted in improved management, quality of life and life expectancy of patients (schuppan D and Afdhal NH,2008) |