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Stimulation of the renal sympathetic nervous system (SNS) Ĭardiac dysfunction contributing to the circulatory derangements and renal hypoperfusion Īction of different cytokines and vasoactive mediators on the renal circulation and other vascular beds. Peripheral arterial vasodilation with hyperdynamic circulation and subsequent renal vasoconstriction The possible impact of each one of these pathways on renal vasoconstriction and the development of HRS varies from one patient to the other. Four interrelated pathways have been implicated in the pathophysiology of HRS. Type 2 HRS is gradually progressive and arises in association with the progression of cirrhosis, whereas type 1 is an acute deterioration in kidney function associated with severe renal vasoconstriction and failure of compensatory mechanisms that are responsible for maintenance of renal perfusion ( 8). The underlying mechanisms that are involved in HRS are incompletely understood but may include both increased vasoconstrictor and decreased vasodilator factors acting on the renal circulation. The hallmark of HRS is intense renal vasoconstriction that starts at an early time point and progresses with worsening of the liver disease ( 7). HRS is the most advanced stage of the various pathophysiologic derangements that take place in patients with cirrhosis. The present article provides an update on these recent developments. During the last 2 decades, knowledge of the pathogenesis and management of HRS has improved greatly. However, despite improved understanding, the prognosis of HRS remained poor, and in the 1970s, the term “terminal functional renal failure” was synonymous with HRS ( 6). ( 5) demonstrated without doubt that splanchnic and systemic vasodilation together with intense renal vasoconstriction is the pathophysiologic hallmark of HRS. The functional nature of HRS was confirmed further by the ability to transplant kidneys from patients with HRS and the normalization of renal function after liver transplantation ( 3, 4). On the basis of this hypothesis, their patients were treated with norepinephrine with dramatic but short-lived improvement in urine volume and without a significant change in serum creatinine or urea concentrations. The authors demonstrated the lack of major renal histologic changes despite the severity of kidney failure, linked the deterioration in renal function to impairment of the systemic circulation, and concluded that the underlying mechanism of kidney failure is peripheral arterial vasodilation. Almost 100 yr later, in a seminal article by Hecker and Sherlock ( 2), the pathogenesis of hepatorenal syndrome (HRS) was unraveled. In the late 19th century, reports by Frerichs (1861) and Flint (1863) noted an association among advanced liver disease, ascites, and oliguric renal failure in the absence of significant renal histologic changes ( 1).