1863: Absence of histological changes to the kidney in some cirrhotics with renal failure 1863: Absence of histological changes to the kidney in some cirrhotics with renal failure 1956: 1st detailed description of the syndrome by Hecker and Sherlock 1960s: Reversal of renal failure with kidney transplant to patients with CKD 1970s: Reversal of HRS with liver transplantation
Functional renal failure Functional renal failure - Absence of Histological changes
Occurs in patients with chronic liver disease Can occur acutely in certain settings - Spontaneous bacterial peritonitis
- Large volume paracentesis without albumin
Marked renal vasoconstriction Reduced GFR
Hepatorenal Syndrome is a severe complication of end stage liver disease associated with an 80%-95% mortality at 2 weeks. Hepatorenal Syndrome is a severe complication of end stage liver disease associated with an 80%-95% mortality at 2 weeks. The only interventions that have been shown to improve survival are liver transplantation and more recently the vasopressin analogues and TIPS Type 1 (Acute) Type 2 (Chronic)
Type 1 Type 1 Rapid decline in renal function Doubling of serum Cr >132 or reduction in 24h CrCl to <40ml/min Less than 2 weeks Spontaneous Associated with SBP (20%) or large volume paracentesis w/o albumin (15%)
Type 2 Type 2 Slower decline in renal function Development of diuretic resistant or refractory ascites
Incidence Incidence - 7-10% in hospitalized cirrhotics with ascites
- 20% at 1 year, 40% at 5 years
Risk Factors - Advanced ascites (diuretic resistant)
- Large volume paracentesis w/o albumin (15%)
- SBP (20%)
Prognosis - Worst prognosis of all complications of cirrhosis
- Type 1 median survival: <2 weeks
- Type 2 median survival: ~6 months
Lack of specific testing Lack of specific testing Diagnosis of exclusion Differential Diagnosis of renal failure in cirrhosis - Hypovolaemia (GI hemorrhage, shock)
- Nephrotoxins (drugs, contrast)
- Glomerulonephritis (Hep B and C)
- Acute Tubular Necrosis
- Obstruction
Major Criteria Major Criteria Chronic or acute liver disease with advanced liver failure or portal hypertension Low GFR (Cr > 132mol/L OR CrCl < 40mL/min) Exclusion of shock, ongoing bacterial infection, volume depletion, and use of nephrotoxic drugs No improvement in renal function despite stopping diuretics and volume repletion with 1.5L of saline No proteinuria or ultrasonographic evidence of obstruction or parenchymal renal disease Arroyo et al; Hepatology 1996; 23: 164-76
Minor Criteria Minor Criteria Urine volume < 500mL/day Urine sodium < 10mEq/L Urine osmolality > plasma osmolality Urine RBCs < 50 per hpf Serum sodium < 130mEq/L Arroyo et al; Hepatology 1996; 23: 164-76
Splanchnic arteriolar vasodilatation - – Decreased effective arterial volume (EAV)
- – Decreased systemic vascular resistance
- – Hypotension
- – Activation of vasoconstrictor systems
- Renin-Angiotensin Angiotensin-Aldosterone-System
- Sympathetic Nervous System
- Anti-Diuretic Hormone
Hyperdynamic circulation Hyperdynamic circulation Hypotension from reduced effective art vol Low systemic vascular resistance (SVR) SNS activation leading to increased contractility Increased cardiac output
Vasoconstrictors Vasoconstrictors - Often combined with albumin
- Vasopressin analogues (Terlipressin)
TIPS Liver Transplantation
Synthetic vasopressin analogue Synthetic vasopressin analogue Most studied drug for treatment of HRS Mechanism: V-1 receptor agonist Adverse events (arrhythmia, ischemia) <5% IV bolus dosing
Reduce portal hypertension Reduce portal hypertension Increase effective arterial volume Reverse splanchnic vasodilatation Complications - Encephalopathy
- Shunt stenosis
- Haemolysis
- Hyperbilirubinaemia
Treatment of choice for HRS Limited by organ availability and mortality of HRS Higher rate of complications: - – Higher post operative mortality
- – More days in the ICU
- – Increased need for post-op RRT (35% vs. 5% w/o HRS)
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Improvement in renal function - – Increased GFR post-op vs. decline in non-HRS pts
- – Lower overall GFR compared to non HRS pts
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