What is the most likely explanation for impaired renal function in a patient with cirrhosis, tense ascites, and worsening abdominal distention, despite large-volume paracentesis and albumin administration?

Hepatorenal Syndrome Type 1 (HRS-AKI)

This patient has hepatorenal syndrome-acute kidney injury (HRS-AKI), characterized by intrarenal vasoconstriction secondary to splanchnic arterial vasodilation—the correct answer is E.

Diagnostic Features Supporting HRS-AKI

This presentation demonstrates the classic hallmarks of HRS-AKI as defined by the International Ascites Club and American Association for the Study of Liver Diseases 1:

• Rapid progression of renal dysfunction: Serum creatinine increased from 1.0 to 2.40 mg/dL over two weeks, with continued deterioration despite large-volume paracentesis and albumin administration 1
• Prerenal laboratory pattern with intact tubular function: Urine sodium of 8 mEq/L and fractional excretion of sodium (FENa) of 0.3% indicate avid sodium retention, distinguishing this from acute tubular necrosis 1
• Bland urinary sediment: Absence of cellular casts or significant proteinuria excludes glomerulonephritis and acute tubular necrosis 2
• No structural obstruction: Ultrasound excluded hydronephrosis and portal vein thrombosis 2
• Lack of response to volume expansion: Despite albumin administration with paracentesis, kidney function continued to deteriorate—a diagnostic criterion for HRS-AKI 1

Pathophysiologic Mechanism

The fundamental mechanism is extreme splanchnic arterial vasodilation leading to decreased effective arterial blood volume, which triggers intense intrarenal vasoconstriction 1, 3. This represents the most severe expression of circulatory dysfunction in advanced cirrhosis 4. The hemodynamic instability (pulse 102/min, BP 92/58 mmHg) reflects this profound circulatory derangement 3.

Why Other Options Are Incorrect

Acute tubular necrosis (Option A) is excluded by:

• Bland urinary sediment without tubular epithelial cells or muddy brown casts 2
• Very low FENa of 0.3% (ATN typically shows FENa >1-2%) 1
• No documented prolonged hypotensive episode severe enough to cause ischemic tubular injury 2

Hepatitis C-associated glomerulonephritis (Option B) is ruled out by:

• Absence of proteinuria >500 mg/day 2
• Absence of hematuria >50 RBCs per high-power field 2
• Bland urinary sediment without dysmorphic RBCs or RBC casts 2

Renal vein thrombosis (Option C) is unlikely because:

• Ultrasound did not demonstrate this finding 2
• Clinical presentation lacks flank pain or gross hematuria typical of acute renal vein thrombosis 2

Obstructive uropathy (Option D) is definitively excluded by:

• Ultrasound showing no hydronephrosis 2
• Ascites does not cause urinary tract obstruction; abdominal compartment syndrome (intra-abdominal pressure >20 mmHg) is rare and would present differently 2

Immediate Management Required

The patient requires vasoconstrictor therapy in combination with continued albumin administration 1, 2. The European Association for the Study of the Liver and American Association for the Study of Liver Diseases recommend:

• Terlipressin plus albumin as first-line therapy where available, or norepinephrine plus albumin in North America 2
• Continue albumin at therapeutic doses (not just for paracentesis), as albumin alone is insufficient once HRS-AKI is established 1, 5
• Urgent evaluation for liver transplantation, which is the definitive treatment for HRS-AKI 2, 6

Critical Clinical Pitfall

The key error to avoid is assuming that albumin administration with paracentesis alone is adequate treatment for HRS-AKI 1. Once HRS-AKI is established, vasoconstrictors are mandatory to reverse the splanchnic vasodilation and restore renal perfusion 2. Meta-analyses confirm that vasoconstrictor therapy increases mean arterial pressure, improves kidney function, and provides short-term survival benefit 2.