Category: Gastrointestinal

Hepatorenal Syndrome

Pathogenesis: Increased NO generation in splanchnic circulation secondary to portal HTN. This causes systemic vasodilation, which reduces PVR and BP, causing renal hypoperfusion. In turn, compensatory mechanisms such as RAAS, SANS and ADH increase water and sodium retention worsen volume overload.

Risk factor: Severe cirrhosis with portal HTN and edema

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