A 52-year-old man with a 10-year history of alcohol-related cirrhosis presents to the emergency department with hematemesis and melena. On examination, he is hypotensive (BP 88/56 mmHg), tachycardic (HR 118/min), with jaundice and spider angiomas. Abdominal examination reveals hepatomegaly and ascites. Upper endoscopy shows actively bleeding esophageal varices. After initial resuscitation and variceal ligation, the patient stabilizes. However, 48 hours later, he develops acute kidney injury (creatinine 2.8 mg/dL, up from 0.9 mg/dL), oliguria, and worsening encephalopathy despite adequate urine output before the bleed. What is the most likely diagnosis?

Explanation

## Diagnosis: Hepatorenal Syndrome Type 1 **Key Point:** Hepatorenal syndrome (HRS) is a form of functional acute kidney injury occurring in advanced cirrhosis, characterized by intense renal vasoconstriction in the setting of systemic vasodilation and portal hypertension. ### Clinical Features Supporting HRS-1 **High-Yield:** HRS-1 (previously HRS-acute) develops acutely over days to weeks, often precipitated by: - Variceal bleeding (as in this case) - Spontaneous bacterial peritonitis - Acute hepatitis - Other infections **Clinical Pearl:** The patient's presentation is classic for HRS-1: - Rapid rise in creatinine (0.9 → 2.8 mg/dL in 48 hours) - Oliguria despite adequate initial resuscitation - Absence of proteinuria or hematuria (rules out intrinsic renal disease) - Concurrent worsening encephalopathy (hepatic decompensation) - Variceal bleed as precipitant ### Diagnostic Criteria for HRS | Criterion | HRS-1 | HRS-2 | |-----------|-------|-------| | **Serum creatinine doubling** | < 2 weeks | > 2 weeks | | **Creatinine level** | > 2.5 mg/dL | 1.5–2.5 mg/dL | | **Prognosis** | Median survival ~2 weeks untreated | Months | | **Typical trigger** | Acute event (SBP, bleed) | Refractory ascites | ### Pathophysiology ```mermaid flowchart TD A[Advanced Cirrhosis + Portal Hypertension]:::outcome --> B[Splanchnic Vasodilation]:::outcome B --> C[Decreased Effective Arterial Blood Volume]:::outcome C --> D[Activation of RAAS & SNS]:::action D --> E[Renal Vasoconstriction]:::action E --> F[Decreased GFR & Oliguria]:::urgent G[Variceal Bleed] --> H[Acute Hypovolemia]:::urgent H --> I[Worsening Renal Perfusion]:::urgent I --> F F --> J[HRS-1: Rapid AKI]:::outcome ``` ### Management Approach **Key Point:** Treatment includes: 1. **Vasoconstrictor therapy** (terlipressin or noradrenaline) + albumin 2. **Avoid nephrotoxins** (NSAIDs, ACE inhibitors, contrast) 3. **Liver transplantation** (definitive therapy) 4. **TIPS** (transjugular intrahepatic portosystemic shunt) in selected cases **Warning:** Do NOT confuse HRS with prerenal azotemia — HRS is a diagnosis of exclusion after ruling out hypovolemia, infection, and intrinsic renal disease. This patient had adequate resuscitation, making pure hypovolemic AKI unlikely. [cite:Harrison 21e Ch 297]