Hepatorenal Syndrome (HRS-AKI) Due to Intrarenal Vasoconstriction
This patient has hepatorenal syndrome-acute kidney injury (HRS-AKI), which results from intrarenal vasoconstriction secondary to splanchnic arterial vasodilation (Answer E).
Diagnostic Features Supporting HRS-AKI
This clinical presentation meets all diagnostic criteria established by the International Ascites Club for HRS-AKI 1, 2:
- Cirrhosis with tense ascites and serum creatinine ≥1.5 mg/dL (2.40 mg/dL in this case) 2
- Rapid progression of renal dysfunction (creatinine increased from 1.0 to 2.40 mg/dL over two weeks), characteristic of Type 1 HRS-AKI 1, 2
- No response to volume expansion with albumin following large-volume paracentesis, with continued deterioration despite intervention 2, 3
- Prerenal laboratory pattern with urine sodium 8 mEq/L and FENa 0.3%, indicating avid sodium retention with intact tubular function 2
- Bland urinary sediment excluding acute tubular necrosis and glomerulonephritis 2
- Absence of structural obstruction on ultrasound (no hydronephrosis) 2
- No shock or nephrotoxic drug exposure 1, 3
Pathophysiological Mechanism
The fundamental mechanism is extreme splanchnic arterial vasodilation leading to decreased effective arterial blood volume, which triggers intense intrarenal vasoconstriction 1, 2, 4:
- Portal hypertension causes splanchnic vasodilation through increased production of nitric oxide, prostacyclin, and endocannabinoids 5
- This creates "effective hypovolemia" despite total body fluid overload 5
- Compensatory activation of the renin-angiotensin-aldosterone system and sympathetic nervous system causes profound renal vasoconstriction 1, 3
- The result is marked renal hypoperfusion and progressive kidney failure despite preserved tubular function 4, 6
Why Other Options Are Incorrect
Acute tubular necrosis (Option A) is excluded by:
- Bland urinary sediment without cellular casts 2
- Very low urine sodium (8 mEq/L) and FENa (0.3%), indicating intact tubular function 2
- No documented prolonged hypotension episode 1
Hepatitis C-associated glomerulonephritis (Option B) is ruled out by:
- Absence of proteinuria >500 mg/day 1, 2
- Absence of hematuria >50 RBCs per high-power field 1, 2
- Bland urinary sediment without dysmorphic RBCs or RBC casts 2
Renal vein thrombosis (Option C) is unlikely because:
- Ultrasound would typically show abnormalities 1
- Clinical presentation lacks flank pain or gross hematuria 2
- This is not a common complication in cirrhosis without additional risk factors 2
Obstructive uropathy (Option D) is excluded by:
- Ultrasound showing no hydronephrosis 1, 2
- Absence of abdominal compartment syndrome 2
- Ascitic fluid does not cause urinary tract compression 2
Prognosis and Management Implications
This diagnosis carries a grave prognosis with median survival of approximately 1 month if untreated 1, 3. The patient requires:
- Immediate vasoconstrictor therapy (terlipressin or norepinephrine) plus continued albumin administration to reverse splanchnic vasodilation and restore renal perfusion 1, 2, 3
- Urgent liver transplantation evaluation, as this is the only definitive treatment 2, 3
- Close monitoring in an intensive or semi-intensive care setting for fluid status and hemodynamics 1
The failure to improve despite albumin and paracentesis confirms that albumin alone is insufficient once HRS-AKI is established 2, 3, and vasoconstrictor therapy is mandatory 1, 2.