Hepatorenal syndrome (HRS) is a functional form of acute kidney injury occurring in advanced cirrhosis where the kidneys are structurally normal but fail due to extreme renal vasoconstriction. The pathophysiology begins with portal hypertension driving splanchnic arterial vasodilation (mediated by excess nitric oxide, prostacyclins, and other vasodilators produced by the congested portal circulation). This vasodilation reduces effective arterial blood volume (despite total plasma volume being expanded as ascites), triggering compensatory activation of vasoconstrictive systems: the renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system (SNS), and arginine vasopressin (AVP). These vasoconstrictors preferentially constrict the renal vasculature while failing to overcome the splanchnic vasodilation, producing a catastrophic reduction in renal blood flow and GFR. The kidneys are structurally normal — if transplanted into a healthy recipient, they would function normally. HRS is classified into HRS-AKI (formerly type 1 — rapid doubling of creatinine to >2.5 mg/dL within 2 weeks, median survival 2 weeks untreated) and HRS-NAKI (formerly type 2 — gradual creatinine rise, associated with refractory ascites, median survival 6 months). Precipitating factors include spontaneous bacterial peritonitis (SBP — most common trigger), large-volume paracentesis...