Conditions · Gastroenterology and hepatology
Hepatorenal syndrome !
Kidney failure that develops in people with advanced liver disease and ascites, although the kidneys themselves look normal. It is serious and often fatal.
Updated 2026-11-01
Structures involved
Tap one to see what it is and open it in 3D.
In the clinical exam
Why it happens
- Splanchnic and portal circulation
- The renin–angiotensin–aldosterone system
- Renal blood flow, autoregulation and tubuloglomerular feedback
- Physiology of acute and chronic kidney failure
- Nitric oxide (NO)
What it is
A functional kidney failure in patients with cirrhosis and ascites (or acute liver failure) caused by intense constriction of the renal arteries, without structural kidney damage. It is a diagnosis of exclusion and a marker of very advanced liver disease.
Who gets it
Occurs in a meaningful share of hospitalised patients with decompensated cirrhosis. In Colombia and Latin America, alcohol-related disease, viral hepatitis and metabolic (fatty) liver disease are the main causes of the cirrhosis behind it.
Causes
- Advanced cirrhosis with ascites and portal hypertension
- Acute liver failure or severe alcoholic hepatitis
- Precipitants: spontaneous bacterial peritonitis and other infections, gastrointestinal bleeding, large-volume paracentesis without albumin, excessive diuresis
Risk factors
- Refractory ascites and low serum sodium
- Low arterial pressure
- Infection, especially spontaneous bacterial peritonitis
- Nephrotoxic drugs (NSAIDs, aminoglycosides, contrast)
- Over-diuresis or vomiting and diarrhoea
Pathophysiology
Portal hypertension causes splanchnic vasodilation (nitric oxide), lowering effective arterial volume. The body responds with renin–angiotensin–aldosterone, sympathetic and vasopressin activation, which constrict the renal arteries and cut glomerular filtration. The kidney tissue is intact: kidneys transplanted from such patients work normally.
Classification
- HRS-AKI (formerly type 1): rapid rise in creatinine meeting AKI criteria
- HRS-NAKI / CKD (formerly type 2): slower, steadier decline, often with refractory ascites
Symptoms and signs
- Falling urine output (oliguria)
- Worsening ascites and abdominal distension
- Jaundice and other signs of decompensated cirrhosis
- Confusion or drowsiness from associated encephalopathy
- Nausea and fatigue
Diagnosis
- Clinical
- Cirrhosis with ascites and acute kidney injury that does not respond to stopping diuretics and expanding volume with albumin for 48 hours, without shock, current nephrotoxic drugs or signs of structural kidney disease.
- Tests
- Rising serum creatinine (AKI criteria), very low urine sodium, bland urine sediment with proteinuria under 500 mg/day and no haematuria. Diagnostic paracentesis to look for spontaneous bacterial peritonitis; blood cultures; electrolytes.
- Imaging
- Renal ultrasound shows normal-sized kidneys without obstruction; it also assesses the liver and ascites.
Differential diagnosis
- Prerenal azotaemia from bleeding, vomiting or over-diuresis (responds to volume)
- Acute tubular necrosis (shock, sepsis, nephrotoxins)
- Glomerulonephritis linked to hepatitis B or C
- Obstructive uropathy
- Drug-induced nephrotoxicity
Goal of treatment
Treat precipitants, restore renal perfusion with vasoconstrictors and albumin as a bridge, and refer early for liver transplantation, the only definitive cure.
Treatment
- Acute
- Stopping diuretics, beta-blockers and nephrotoxic drugs; treating infection or bleeding; volume expansion with intravenous albumin.
- Medical
- Vasoconstrictors combined with albumin: terlipressin is first line; noradrenaline in intensive care, or midodrine with octreotide where others are unavailable.
- Procedure
- Renal replacement therapy (dialysis) as a bridge to transplant; TIPS in selected patients.
- Surgical
- Liver transplantation, sometimes combined liver–kidney transplant when renal failure has been prolonged.
- Follow-up
- Strict fluid balance and urine output, daily creatinine and electrolytes, oxygen saturation during albumin and terlipressin (risk of fluid overload and ischaemia), mental status.
Complications
- Hyperkalaemia, metabolic acidosis and fluid overload
- Progression to multiorgan failure
- Hepatic encephalopathy
- Death, often from infection or bleeding
Prognosis
Poor without transplant: untreated HRS-AKI has a median survival of only weeks. Response to terlipressin with albumin improves short-term survival and serves as a bridge to transplant.
Prevention
- Albumin after large-volume paracentesis and in spontaneous bacterial peritonitis
- Antibiotic prophylaxis of spontaneous bacterial peritonitis in high-risk patients
- Avoiding NSAIDs and nephrotoxins in cirrhosis
- Careful diuretic dosing with monitoring of creatinine and sodium
Test yourself
Think of the answer, then tap the question to see it.
What is the basic mechanism of hepatorenal syndrome?
Splanchnic vasodilation from portal hypertension causes intense renal vasoconstriction, so filtration falls while the kidney tissue is structurally normal.
What urine findings are typical of hepatorenal syndrome?
Very low urine sodium with a bland sediment, minimal proteinuria and no haematuria.
Which test distinguishes HRS from prerenal azotaemia?
Lack of improvement after stopping diuretics and giving albumin for 48 hours.
What is the first-line drug treatment of HRS-AKI?
Terlipressin (a vasoconstrictor) combined with intravenous albumin.
What is the definitive treatment for hepatorenal syndrome?
Liver transplantation.
Related conditions
- Cirrhosis
- Portal hypertension
- Ascites and spontaneous bacterial peritonitis
- Acute kidney injury
- Acute liver failure
- Hepatic encephalopathy
- Upper gastrointestinal bleeding
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Hepatorenal syndrome: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2024).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.
