A 52-year-old man with a 15-year history of alcohol use disorder presents to the emergency department with haematemesis and melaena. On examination, he is hypotensive (BP 85/50), tachycardic (HR 118/min), and has clinical signs of chronic liver disease including spider angiomas, palmar erythema, and ascites. Abdominal ultrasound shows cirrhotic liver morphology with portal vein diameter of 14 mm. Upper endoscopy reveals large oesophageal varices with active bleeding. After initial resuscitation and variceal ligation, the patient stabilizes. One week later, he develops acute kidney injury (creatinine rises from 1.2 to 3.8 mg/dL) with oliguria despite adequate fluid resuscitation. Urine sodium is <10 mEq/L and fractional excretion of sodium (FENa) is <0.1%. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Hepatorenal Syndrome Type 1 ### Key Clinical Features **Key Point:** Hepatorenal syndrome (HRS) is a form of functional renal failure occurring in advanced cirrhosis, characterized by severe renal vasoconstriction in the setting of systemic vasodilation and portal hypertension. ### Diagnostic Criteria for HRS Type 1 | Feature | HRS Type 1 | HRS Type 2 | ATN | |---------|-----------|-----------|-----| | **Creatinine doubling** | Within 2 weeks | Gradual | Variable | | **Baseline Cr** | Often normal | Often elevated | Often elevated | | **FENa** | <0.1% | <0.1% | >2% | | **Urine Na** | <10 mEq/L | <10 mEq/L | >40 mEq/L | | **Clinical context** | Acute decompensation | Chronic progression | Sepsis/hypotension | | **Response to fluids** | Poor | Poor | May improve | ### Why This Case Fits HRS Type 1 1. **Precipitating event:** Variceal haemorrhage with acute decompensation is a classic trigger for HRS Type 1. 2. **Rapid renal deterioration:** Creatinine tripled within 1 week—hallmark of HRS Type 1 (by definition, doubling within 2 weeks). 3. **Functional renal failure:** FENa <0.1% and urine Na <10 mEq/L indicate intense renal vasoconstriction, not tubular damage. 4. **Cirrhotic liver disease:** Advanced cirrhosis (ascites, portal hypertension, varices) is the essential prerequisite. 5. **Haemodynamic context:** Post-haemorrhage, the patient likely has splanchnic vasodilation with compensatory renal vasoconstriction. ### Pathophysiology **High-Yield:** HRS Type 1 results from: - Severe splanchnic vasodilation (mediated by nitric oxide, endotoxins) - Compensatory renal and systemic vasoconstriction (↑ sympathetic tone, ↑ renin–angiotensin–aldosterone system, ↑ vasopressin) - Acute reduction in renal perfusion pressure → oliguria and azotaemia - **No structural kidney damage** — kidneys are histologically normal ### Management Implications **Clinical Pearl:** HRS Type 1 carries a mortality of ~50% without treatment. Management includes: - Vasoconstrictor therapy: terlipressin + albumin (first-line) or noradrenaline + albumin - Avoid nephrotoxins and further hypotension - Liver transplantation (definitive treatment) - Renal replacement therapy as bridge therapy ### Mnemonic: HRS Triggers **SPADE** — Sepsis, Paracentesis (large-volume), Acute variceal bleeding, Diuretics (excessive), Encephalopathy (worsening) [cite:Robbins 10e Ch 18]