In hepatic cirrhosis with portal hypertension, patients develop hyperdynamic circulation (high CO, low SVR) and eventually hepatorenal syndrome (HRS). The primary mechanism of renal vasoconstriction in HRS type 1 is:

• A Direct hepatic toxin accumulation causing renal tubular necrosis
• B Splanchnic vasodilation from portal hypertension reduces effective arterial blood volume → baroreceptor activation → RAAS + SNS + ADH (AVP) mediated intense renal vasoconstriction with preserved tubular integrity ✓
• C Elevated portal pressure directly compresses renal veins, reducing GFR by raising renal venous pressure
• D Bilirubin nephrotoxicity causing progressive glomerular injury

Explanation

In cirrhotic portal hypertension, excess nitric oxide from splanchnic endothelium causes splanchnic vasodilation, sequestering blood volume and reducing effective arterial blood volume (EABV) despite high total CO. This relative hypovolemia activates arterial baroreceptors, triggering: RAAS (renin → AngII → aldosterone), sympathetic nervous system, and non-osmotic ADH release. Together these cause intense renal afferent arteriolar vasoconstriction, dramatically reducing GFR, while tubular function is initially preserved (distinguishing HRS from ATN — urine Na⁺ <10 mEq/L, FENa <1%). No structural tubular damage occurs in HRS type 1; kidneys transplanted from HRS patients function normally in recipients.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.