Acute kidney injury (AKI) is common in patients with cirrhosis.
It occurs in up to 50% of hospitalized patients with cirrhosis and a 58% of such patients in the ICU.
Acute kidney injury is associated with high morbidity and mortality and an increased incidence of chronic kidney disease after liver transplantation for cirrhosis.
The major causes of AKI are hypoperfusion, which, in most cases is due to hypovolemia, intrinsic structure of kidney injury, and postrenal injury due to urinary obstruction.
Cirrhosis can causes AKI by renal hypoperfusion, known as the hepatorenal syndrome, which is the result of renal vasoconstriction.
Hypoperfusion from hypovolemia accounts for approximately half of the cases of AKI in patients with cirrhosis, intrinsic causes, such as acute tubular necrosis account for approximately 30%, and hepatorenal syndrome accounts were approximately 15 to 20% with less than 1% of cases attributable to post renal obstruction.
Patients with cirrhosis, especially those with ascites, have increased susceptibility to AKI because of hemodynamic alterations from portal hypertension.
Portal hypertension increases, intrahepatic resistance due to distorted liver architecture with fibrosis and nodules, and then increases in intrahatic vascular tone.
Activation of vasodilators in the splanchnic circulation, most importantly, nitric oxide, leads to progressive splanchnic and systemic vasodilation.
Increased translocation of bacteria and bacterial products due to intestinal
dysbiosis, bacterial overgrowth, and altered proteins, also contribute to vasodilatation resulting in the reduction in effective arterial blood volume that activates neurohormonal systems: renin angiotensin-aldosterone, sympathetic and arginine vasopressin systems, leading to sodium and water retention and ascites formation.
In advanced stages of cirrhosis, progressive dilatation leads to more retention of sodium and water, resulting in refractory, ascites and dilutional hyponatremia.