Hepatorenal syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

The pathology involved in the development of hepatorenal syndrome is thought to be an alteration in blood flow and blood vessel tone in the circulation that supplies the intestines (the splanchnic circulation) and the circulation that supplies the kidney. It is usually indicative of an end-stage of perfusion, or blood flow to the kidney, due to deteriorating liver function. Patients with hepatorenal syndrome are very ill, and, if untreated, the condition is usually fatal.

The renal failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the splanchnic circulation (which supplies the intestines). It is known that there is an overall decreased systemic vascular resistance in hepatorenal syndrome, but that the measured femoral and renal fractions of cardiac output are respectively increased and reduced, suggesting that splanchnic vasodilation is implicated in the renal failure.

There is activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, and profound vasoconstriction of the kidneys. Many vasocontrictor chemicals have been hypothesized as being involved in this pathway, including vasopressin, prostacyclin, thromboxane A2,, and endotoxin.

Microscopic Pathology

Liver pathology is altered in HRS while kidney histology is normal. The image is a trichrome stain of cirrhosis of the liver, the most common cause of HRS.

Differentiating Hepatorenal Syndrome from other Diseases

Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome. They include the following:

• Pre-renal failure: Pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum creatinine and the excretion of sodium.
• Acute tubular necrosis (ATN): This can be difficult to confidently diagnose. It may be an inability to concentrate the urine, if any is being produced. The urine sediment should be bland, microscopy may show hyaline casts. ATN may recover with supportive treatment only or progress to end-stage renal failure. In cirrhosis, urinary sodium is not a reliable guide to the development of ATN, as fractional sodium excretion may stay below 1 percent, due to the gradual worsening of renal ischaemia.
• Other causes may include glomerular disease secondary to Hepatitis B or Hepatitis C, drug toxicity (notably gentamicin) or contrast nephropathy.