A patient with advanced liver cirrhosis develops renal failure with urine Na < 10 mEq/L, bland urine sediment, and no response to volume loading. Serum creatinine is 3.2 mg/dL. Which physiological mechanism underpins hepatorenal syndrome type 1?
- A Splanchnic vasodilation reduces effective arterial blood volume, triggering RAAS and SNS activation with severe afferent arteriolar vasoconstriction in the kidney ✓
- B Portal hypertension causes direct glomerular compression, reducing GFR
- C Hepatic encephalopathy releases nephrotoxins that cause tubular necrosis
- D Albumin deficiency reduces oncotic pressure in peritubular capillaries, impairing tubular reabsorption
Explanation
In hepatorenal syndrome (HRS), progressive splanchnic vasodilation (driven by NO and other vasodilators in portal hypertension) reduces effective arterial volume despite total body salt and water excess. This activates baroreceptor-mediated RAAS, sympathetic nervous system, and ADH secretion. These vasoconstrictors profoundly constrict the renal afferent arterioles, reducing GFR without structural tubular damage — explaining the bland sediment and avid sodium conservation (urine Na <10). The kidneys are functionally normal and can work in a transplant recipient's body.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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