Editing Hepatorenal syndrome (section)

==Diagnosis==
There can be many causes of kidney failure in individuals with cirrhosis or fulminant liver failure.  Consequently, it is a challenge to distinguish hepatorenal syndrome from other entities that cause kidney failure in the setting of advanced liver disease.  As a result, additional major and minor criteria have been developed to assist in the [[diagnosis]] of hepatorenal syndrome.<ref name=IAC/>

The '''major''' criteria include liver disease with [[portal hypertension]]; [[kidney failure]]; the absence of [[Shock (circulatory)|shock]], [[infection]], recent treatment with medications that affect the function of the kidney ([[nephrotoxin]]s), and fluid losses; the absence of sustained improvement in kidney function despite treatment with 1.5 litres of [[intravenous]] [[normal saline]]; the absence of [[proteinuria]] ([[protein]] in the [[urine]]); and, the absence of kidney disease or obstruction of kidney outflow as seen on [[ultrasound]].<ref name=IAC/>

The '''minor''' criteria are the following: a [[oliguria|low urine volume]] (less than {{convert|500|mL|0|abbr=on}} per day), low [[sodium]] concentration in the urine, a [[urine osmolality]] that is greater than that in the [[blood]], the absence of [[red blood cells]] in the urine, and a serum sodium concentration of less than 130&nbsp;mmol/L.<ref name=IAC/>

Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome.  Individuals with [[Kidney failure|pre-renal kidney failure]] do not have damage to the kidneys, but as in individuals with HRS, have kidney dysfunction due to decreased blood flow to the kidneys. Also, similarly to HRS, pre-renal kidney failure causes the formation of urine that has a very low sodium concentration. In contrast to HRS, however, pre-renal kidney failure usually responds to treatment with intravenous fluids, resulting in reduction in serum [[creatinine]] and increased excretion of sodium.<ref name=IAC/>  [[Acute tubular necrosis]] (ATN) involves damage to the tubules of the kidney, and can be a complication in individuals with cirrhosis, because of exposure to toxic medications or the development of decreased blood pressure.  Because of the damage to the tubules, ATN affected kidneys usually are unable to maximally resorb sodium from the urine.  As a result, ATN can be distinguished from HRS on the basis of laboratory testing, as individuals with ATN will have urine sodium measurements that are much higher than in HRS; however, this may not always be the case in cirrhotics.<ref name=emed/>  Individuals with ATN also may have evidence of [[hyaline cast]]s or [[muddy-brown cast]]s in the urine on microscopy, whereas the urine of individuals with HRS is typically devoid of cellular material, as the kidneys have not been directly injured.<ref name=IAC/>  Some viral infections of the liver, including [[hepatitis B]] and [[hepatitis C]] can also lead to inflammation of the [[glomerulonephritis|glomerulus]] of the kidney.<ref>{{cite journal |author=Han SH |title=Extrahepatic manifestations of chronic hepatitis B |journal=Clin Liver Dis |volume=8 |issue=2 |pages=403–18 |year=2004 |pmid=15481347 |doi= 10.1016/j.cld.2004.02.003}}</ref><ref>{{cite journal |vauthors=Philipneri M, Bastani B |title=Kidney disease in patients with chronic hepatitis C |journal=Curr Gastroenterol Rep |volume=3 |issue=1 |pages=79–83 |date=February 2001 |pmid=11177699 |doi=10.1007/s11894-001-0045-0|s2cid=21358956 }}</ref>  Other causes of kidney failure in individuals with liver disease include drug toxicity (notably, the antibiotic [[gentamicin]]) or [[contrast nephropathy]], caused by intravenous administration of [[contrast medium|contrast]] agents used for medical imaging tests.<ref name=IAC/>