Hepatorenal Syndrome (HRS-AKI)
This patient has hepatorenal syndrome (HRS-AKI), specifically option E: intrarenal vasoconstriction secondary to splanchnic arterial vasodilation. The clinical presentation of cirrhosis with ascites, rising creatinine (1.0 to 2.4 mg/dL over two weeks), hyponatremia, extremely low urine sodium (8 mEq/L), FeNa of 0.3%, bland sediment, and absence of structural kidney disease on ultrasound all point definitively to HRS-AKI 1, 2.
Why This is HRS-AKI and Not the Other Options
The patient meets diagnostic criteria for HRS-AKI established by the International Club of Ascites: cirrhosis with ascites, serum creatinine ≥1.5 mg/dL (now 2.4), no shock, no nephrotoxic drugs, normal renal ultrasound (no hydronephrosis), and bland urinary sediment 1, 2.
Ruling Out Alternative Diagnoses
ATN (Option A) is excluded because the urinary sediment is bland—ATN would show muddy brown granular casts indicating tubular epithelial cell injury 3. Additionally, ATN typically presents with FeNa >1-2%, whereas this patient has FeNa of 0.3% 1.
Glomerulonephritis from Hepatitis C (Option B) is excluded because there is no proteinuria (>500 mg/d), no hematuria (>50 RBCs per high-power field), and bland sediment—glomerulonephritis would show RBC casts 1, 3.
Renal vein thrombosis (Option C) is excluded by the normal ultrasound findings and absence of typical features such as flank pain, hematuria, or acute onset 1.
Obstructive uropathy (Option D) is excluded by the ultrasound showing no hydronephrosis 1.
Pathophysiology: The Mechanism Behind HRS-AKI
The fundamental mechanism is extreme splanchnic arterial vasodilation leading to decreased effective arterial blood volume, which triggers intense intrarenal vasoconstriction 2, 1. This represents a functional rather than structural kidney injury.
The Pathophysiologic Cascade
Portal hypertension causes splanchnic vasodilation, reducing effective arterial blood volume despite total body sodium and water overload (manifested as ascites) 1, 4.
Compensatory activation of vasoconstrictor systems occurs: renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and arginine vasopressin (ADH) 1, 5, 6.
Progressive renal cortical ischemia develops from intense intrarenal vasoconstriction, causing marked reduction in renal blood flow and GFR 4, 2.
Tubular function remains intact, explaining the avid sodium retention (urine sodium 8 mEq/L, FeNa 0.3%) as the kidney appropriately responds to perceived volume depletion 7, 2.
Key Laboratory Pattern Recognition
The prerenal laboratory pattern with intact tubular function is characteristic of HRS-AKI:
FeNa of 0.3% indicates extreme sodium conservation, though FeNa <1% has 100% sensitivity but only 14% specificity for prerenal causes in cirrhosis 3, 7.
Urine sodium of 8 mEq/L reflects maximal sodium reabsorption throughout the nephron mediated by aldosterone, angiotensin II, and sympathetic activity 7, 2.
Bland urinary sediment confirms absence of structural kidney injury 1, 3.
Hyponatremia (128 mEq/L) results from non-osmotic ADH secretion causing impaired free water excretion, worsening water retention 5, 6.
Critical Pitfall: Why This is NOT Simple Prerenal AKI
Although the laboratory values suggest a prerenal pattern, this is HRS-AKI, not simple volume-responsive prerenal AKI. The distinction is critical because management differs fundamentally 8, 2:
Prerenal AKI responds to volume expansion with albumin (1 g/kg/day for 2 days) 1, 3.
HRS-AKI does not respond to albumin alone—lack of response to volume challenge is actually a diagnostic criterion 1, 2.
The rapid progression (creatinine doubling from baseline in <2 weeks) suggests Type 1 HRS-AKI, which carries poor prognosis 2, 8.
Immediate Management Algorithm
Step 1: Withdraw all nephrotoxic agents immediately including NSAIDs, ACE inhibitors, ARBs, aminoglycosides, and hold diuretics 1, 3.
Step 2: Administer albumin volume challenge at 1 g/kg/day (maximum 100 g/day) for 2 consecutive days, monitoring carefully for pulmonary edema 1, 3, 2.
Step 3: If creatinine remains ≥1.5 mg/dL after 2 days despite risk factor management, initiate vasoconstrictor therapy plus albumin to counteract splanchnic vasodilation and increase renal blood flow 1, 2. Terlipressin or noradrenaline are the vasoconstrictors of choice 4.
Step 4: Monitor for response: Complete response is return of creatinine to <0.3 mg above baseline; partial response is reduction but >0.3 mg above baseline 1.
Prognostic Implications
HRS-AKI carries substantial mortality without liver transplantation, which remains the definitive treatment 2, 4. Even with vasoconstrictor therapy and albumin, which can reverse HRS-AKI in many patients, close monitoring is mandatory with creatinine checks every 2-4 days during hospitalization and every 2-4 weeks for 6 months post-discharge 3.