Expansion
Splanchnic vasodilatation causes intense compensatory renal vasoconstriction
Expansion
The sequence:
- Portal hypertension causes release of nitric oxide and other vasodilators in the splanchnic bed
- Splanchnic vasodilatation pools blood, so the effective arterial blood volume falls even though total volume is increased
- Baroreceptors sense underfilling, activating the sympathetic nervous system, the renin-angiotensin-aldosterone system and antidiuretic hormone
- Intense renal vasoconstriction reduces renal blood flow and GFR
- Avid sodium and water retention causes ascites and dilutional hyponatraemia
The diagnostic hallmarks are a very low urinary sodium (typically under 10 mmol/l), bland urinary sediment, no proteinuria and no improvement with volume expansion after withdrawing diuretics.
Treatment targets the mechanism: terlipressin (a vasopressin analogue) constricts the splanchnic bed, combined with albumin to expand the circulating volume. Definitive treatment is liver transplantation, after which renal function typically recovers, confirming that the kidney itself was never the problem.