الفهرس 
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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)