1. Afferent mechanisms of sodium retention in cirrhosis and hepatorenal syndrome 
Juan A. Oliver, Elizabeth C. Verna 
Kidney International 
Volume 77, Issue 8, Pages (April 2010)
DOI: /ki
Copyright © 2010 International Society of Nephrology Terms and Conditions

2. Figure 1
Variable effects of a decrease in cardiac output on plasma renin and extra-cellular fluid volume (ECFV) as a function of time and severity of disease. An acute decrease in cardiac output led to increased renin secretion and plasma renin (top). Activation of the renin–angiotensin–aldosterone system caused renal sodium retention (middle) and expansion of the ECFV, evidenced as weight gain (bottom). When the decrease in cardiac output was modest (green lines), as a response to the expanded ECFV, renin secretion was inhibited and plasma renin ‘normalized.’ This allowed restoration of sodium balance at the sodium intake of the experiment. However, when the decrease in cardiac output was severe (pink lines), despite expanded ECFV, renin secretion was not suppressed and renal sodium retention and edema formation continued unabated.
Adapted from Watkins et al.61
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

3. Figure 2
Temporal relationships between systemic hemodynamics and extra-cellular fluid volume (ECFV) during evolution of cirrhosis. During the early stages of disease, peripheral vascular resistance (PVR) and cardiac output (CO) were normal despite renal sodium retention and plasma volume expansion. Detectable systemic vasodilation and increased cardiac output occurred only after marked ECFV expansion (evidenced by the appearance of ascites).
Redrawn from Levy and Allotey.80
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

4. Figure 3
Hepatic circulation. (a) The normal liver receives two-thirds of its blood flow from the portal vein (PV) and the remaining one-third from the hepatic artery (HA). (b) Both the portal venules and the hepatic artrioles drain into hepatic sinusoids, but the exact arrangement that allows forward flow of the mixed venous and arterial bloods remains unclear.167 (c) Cirrhosis increases intra-hepatic vascular resistance and sinusoidal pressure. In addition, portal vein flow is markedly decreased and hepatic arterial flow is either unchanged or increased. HV, hepatic vein.
(adapted from WC Aird)
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

5. Figure 4
Hepatic vascular hemodynamics and sodium balance. (a) Cirrhosis or restriction of hepatic vein flow increases intra-hepatic vascular resistance and sinusoidal pressure, markedly decreasing portal vein (PV) flow and increasing hepatic artery (HA) flow. Changes in the physical forces or in the composition of the hepatic blood trigger sodium retention and edema formation. (b) Insertion of a side-to-side porto-caval shunt decreases sinusoidal pressure and maintains mixing of portal venous and hepatic arterial bloods, irrigating the liver. Under these conditions and despite cirrhosis, there is no sodium retention. (c) Insertion of an end-to-side porto-caval shunt only partially decreases the elevated sinusoidal pressure and prevents mixing of the venous and arterial hepatic blood supplies as the portal vein blood is diverted to the inferior vena cava. Under these conditions and despite normalization of portal vein pressure, sodium retention continues unabated. HV, hepatic vein; IVC, inferior venacava.
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions