COMMENTARY

Complications of Portal Hypertension: Hepatorenal Syndrome

Rowen K. Zetterman, MD; Khalid Bashir, MD

Disclosures

December 05, 2011

In This Article

Hepatorenal Syndrome

Hepatorenal syndrome (HRS) is a unique, functional form of potentially reversible renal failure that occurs in the presence of severe acute or chronic liver disease.[1,2] Initially, the kidney structure is intact,[3] although continuing vasoconstriction associated with HRS can lead to acute tubular necrosis (ATN). HRS is often defined by the doubling of serum creatinine to 2.5 mg/dL or more within 2 weeks of the onset of azotemia.[4] HRS is uncommon in patients with compensated cirrhosis[5] and is most frequently associated with cirrhosis and ascites. A common complication of cirrhosis, ascites develops in 50% of patients within 10 years of diagnosis[6] and carries a 50% mortality within 2-5 years.[7] Patients with protracted ascites frequently develop spontaneous bacterial peritonitis and subsequent HRS.

Types of HRS

Two types of HRS have been described.[4] Type 1 HRS follows an initial precipitating event and is rapidly progressive, with worsening oliguria and azotemia. Type 2 HRS develops more slowly and typically occurs in patients with refractory ascites. Type 2 HRS is often nonoliguric and azotemia may be stable. Annually, HRS develops in up to 8% of patients with cirrhosis and ascites.[8] Median survival for untreated type 1 HRS is 2 weeks and for type 2 approximately 6 months.[4]

Pathophysiology of HRS

Type 1 HRS can be precipitated by hypovolemia, gastrointestinal bleeding, spontaneous bacterial peritonitis, sepsis, large-volume paracentesis, or receipt of nephrotoxic agents such as nonsteroidal anti-inflammatory drugs or radiographic contrast.[9,10] Underlying kidney disease and ATN may also result in azotemia in patients with liver disease.

Although the mechanism leading to HRS is unclear, patients develop renovascular vasoconstriction and alteration of intrarenal blood flow. These changes may be consequences of the increased splanchnic vasodilation, reduced systemic vascular resistance, and elevated cardiac output characteristic of patients with cirrhosis.[11,12] Splanchnic vasodilation occurs in response to elevated levels of splanchnic nitric oxide with portal hypertension.[13] The result is an effective reduction of circulating vascular volume and renal perfusion. To compensate for the lower effective intravascular volume, activation of the renin-angiotensin system and sympathetic nervous system plus secretion of antidiuretic hormone result in sodium and water retention coupled with renal vasoconstriction, reduced renal blood flow, and ultimately renal hypoperfusion.[14,15] As cirrhosis progresses, the continuing decline in systemic vascular resistance cannot be compensated by the increase in cardiac output, leading to a further deterioration of arterial blood flow.[16] Activation of the sympathetic nervous system results in renal vasoconstriction and reduced renal blood flow, leading to progressive renal failure, reduced glomerular filtration, and even ATN.

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