Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome  Vicente Arroyo, Carlos Terra, Pere Ginès  Journal of Hepatology  Volume 46, Issue 5, Pages 935-946 (May 2007) DOI: 10.1016/j.jhep.2007.02.001 Copyright © 2007 Terms and Conditions

Fig. 1 Relationship between glomerular filtration rate (inulin clearance) and serum creatinine in patients with cirrhosis and ascites. Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions

Fig. 2 Survival of patients with cirrhosis and ascites without HRS (data obtained from Llach et al. [22]) and with type-1 and type-2 HRS (data obtained from Ginès P et al. [6]). Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions

Fig. 3 Peripheral arterial vasodilation hypothesis and renal dysfunction in cirrhosis. At initial phases, when cirrhosis is compensated, the increase in splanchnic arterial vasodilation is compensated by an increase in cardiac output (hyperdynamic circulation). The effective arterial blood volume and the activity of renin–angiotensin, sympathetic nervous system and plasma ADH are normal despite a reduction in systemic vascular resistance. With the progression of liver disease, splanchnic arterial vasodilation increases but not the cardiac output. An effective arterial hypovolemia therefore develops leading to activation of the renin–angiotensin and sympathetic nervous system and ADH. Systemic vascular resistance does not decrease due to vasoconstriction in extra-splanchnic organs. Type-2 HRS could be the extreme expression of renal vasoconstriction. Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions

Fig. 4 Peripheral vasodilation hypothesis (left graph) and modified peripheral vasodilation hypothesis (right graph). According to this latter hypothesis, impairment in arterial blood volume in cirrhosis could be the consequence of a progression of splanchnic arterial vasodilation and a decrease in cardiac output. Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions

Fig. 5 Upper graph: resistive index in the middle cerebral artery in patients with compensated cirrhosis, patients with ascites and healthy subjects. Lower graph: relationship between the renal resistive index and the resistive index in the middle cerebral artery in cirrhotic patients (Guevara et al. [47]). Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions

Fig. 6 HRS as a part of a multiorgan failure. Abbreviations: A-II, angiotensin II; NE, norepinephrine; ADH, antidiuretic hormone; HRS, hepatorenal syndrome. Journal of Hepatology 2007 46, 935-946DOI: (10.1016/j.jhep.2007.02.001) Copyright © 2007 Terms and Conditions