In hepatorenal syndrome type 1 (acute), renal blood flow and GFR fall dramatically despite structurally normal kidneys. Which circulatory mechanism is central to this pathophysiology?

• A Splanchnic vasodilation from portal hypertension-driven NO and prostacyclin release reduces effective arterial blood volume, activating RAAS and ADH and causing intense renal vasoconstriction that reduces GFR despite intact tubular function ✓
• B Elevated bilirubin directly impairs renal tubular mitochondrial function, causing a primary tubulotoxic process that reduces GFR
• C High portal pressure transmits directly to the renal vein via the mesentericorenal collaterals, elevating Bowman's capsule pressure and reducing effective filtration pressure
• D Hypoalbuminaemia reduces plasma oncotic pressure, causing interstitial oedema that compresses peritubular capillaries and reduces GFR

Explanation

In advanced cirrhosis, portal hypertension drives splanchnic vasodilation (mediated by NO, prostacyclin, CO, and endocannabinoids). This greatly expands the splanchnic vascular bed, sequestering blood and reducing effective arterial blood volume (EABV). Baroreceptors detect EABV reduction and reflexively activate the renin-angiotensin-aldosterone system, sympathetic nervous system, and non-osmotic ADH release. The resulting renal vasoconstriction (angiotensin II, catecholamines, ADH via V1 receptors, endothelin) dramatically reduces renal blood flow and GFR, while tubular function remains intact (the kidneys will function normally if transplanted). This is why HRS kidneys transplanted into patients with cirrhosis cause HRS in the recipient, and cirrhotic patients receiving normal livers see HRS resolve.

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

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