Hepatorenal syndrome: Update on diagnosis and treatment

Abstract

Acute kidney injury (AKI) is a common complication in patients with end-stage liver disease and advanced cirrhosis regardless of the underlying cause. Hepatorenal syndrome (HRS), a functional form of kidney failure, is one of the many possible causes of AKI. HRS is potentially reversible but involves highly complex pathogenetic mechanisms and equally complex clinical and therapeutic management. Once HRS has developed, it has a very poor prognosis. This review focuses on the diagnostic approach to HRS and discusses the therapeutic protocols currently adopted in clinical practice.

Keywords: Acute kidney injury; Cirrhosis; Diagnosis; Hepatorenal syndrome; Liver support system; Terlipressin; Treatment.

Figure 1

Hepatorenal syndrome: Pathogenesis. In cirrhotic patients portal hypertension can lead to markedly dilated splanchnic arterial vessels. The bacterial translocation of intestinal germs, the gradual decrease in systemic vascular resistances, the hepatic vascular neoformation are potential risk factors. The fall in mean arterial pressure is compensated by increase in cardiac output and by activation of renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) to improve systemic vascular resistence. The response mechanisms to the decreased effective circulating volume caused by Enhanced vascular capacitance (so-called “arterial underfilling”) include the non-osmotic release of vasopressin accounting for renal tubular sodium resorption and water retention leading to the onset of ascites, edema and hypervolemic hyponatremia. These compensatory mechanisms ultimately have repercussions on kidney function causing reduced glomerular filtration rate (GFR) and further water retention thereby worsening the water overload.