Pathophysiology of hepatorenal syndrome-acute kidney injury. (IMAGE)
Caption
Pathophysiology of hepatorenal syndrome-acute kidney injury. Cirrhosis leads to an elevation in intrahepatic vascular resistance. Splanchnic vasodilation increases the production of vasodilators (nitric oxide, carbon monoxide, prostacyclins and endocannabinoids) within the splanchnic circulation. These vasodilators induce systemic vasodilation, consequently reducing the effective arterial blood volume (EABV) and systemic arterial pressure. To counterbalance this effect, systemic vasoconstrictor pathways, including the renin–angiotensin–aldosterone system, sympathetic nervous system, and arginine vasopressin, are activated to enhance the EABV. However, these compensatory mechanisms lead to sodium retention, impaired solute-free water excretion and renal vasoconstriction, ultimately resulting in reduced renal blood flow.
Credit
By Arnold J, Avila E, Idalsoaga F, et al.
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CC BY-NC