Hepatorenal syndrome
Hepatorenal syndrome is functional renal failure in a patient with cirrhosis and ascites, driven by splanchnic vasodilation and compensatory renal vasoconstriction, and it is diagnosed only after excluding shock, nephrotoxins, and structural kidney disease and after creatinine fails to improve with diuretic withdrawal and an albumin challenge. Treatment is a splanchnic vasoconstrictor (terlipressin first-line) with intravenous albumin as a bridge to liver transplantation, the only curative therapy.
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What this article covers
- Overview
Definition: hepatorenal syndrome (HRS) is functional renal failure in a patient with cirrhosis, portal hypertension, and ascites, caused by intrarenal vasoconstriction driven by splanchnic arterial…
- Epidemiology
Occurs in advanced liver disease: most patients who develop HRS have cirrhosis with ascites, though alcohol-associated hepatitis and acute liver failure are also associated with HRS.
- Risk factors
Cirrhosis with ascites: the necessary substrate; HRS does not occur without portal hypertension and ascites (cirrhotic ascites).
- Pathophysiology
Portal hypertension drives splanchnic vasodilation: nitric oxide and other vasodilators released with portal hypertension dilate the splanchnic arterial bed.
- Clinical features
Rising serum creatinine in a patient with known cirrhosis and ascites: the presenting abnormality, often noted after a precipitating event such as infection.
- Differential diagnosis
Prerenal azotemia from volume depletion: vomiting, diarrhea, hemorrhage, or diuretic overuse; distinguished by a history of volume loss and rapid creatinine improvement with fluid resuscitation, which HRS does not show.
- Diagnosis
HRS is a diagnosis of exclusion established by meeting all of the following criteria in a patient with cirrhosis and ascites: Cirrhosis with ascites.
- Management
Treat the precipitating condition immediately: if spontaneous bacterial peritonitis or another infection is identified, start source-appropriate antibiotics without delay; if gastrointestinal…
- Complications
Progression to renal replacement dependence: failure to reverse the functional renal failure can necessitate ongoing hemodialysis.
- Prognosis
Failure to respond to initial vasoconstrictor and albumin therapy is a poor prognostic sign and predicts a high risk of death without renal replacement therapy or transplantation.
- Prevention
Give albumin with large-volume paracentesis: 6 to 8 g per liter of ascitic fluid removed when more than 5 liters are removed at a single session, to prevent post-paracentesis circulatory dysfunction that can precipitate HRS.
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Related articles
- Cirrhosis
Cirrhosis is end-stage hepatic fibrosis with regenerative nodules, staged as compensated or decompensated by the onset of ascites, variceal hemorrhage, encephalopathy, or jaundice. Severity is graded by Child-Pugh class and MELD, and management centers on treating the underlying cause, surveillance for varices and hepatocellular carcinoma, and timely transplant referral once decompensation appears.
- Cirrhotic ascites
Cirrhotic ascites is fluid accumulation in the peritoneal cavity driven by portal hypertension and splanchnic vasodilation, confirmed by a serum-ascites albumin gradient of 1.1 g/dL or more on diagnostic paracentesis. Management proceeds from sodium restriction and combination diuretics to large-volume paracentesis with albumin and TIPS for refractory disease, with every new or worsening episode screened for spontaneous bacterial peritonitis.
- Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis is a monomicrobial infection of cirrhotic ascitic fluid without a surgical source, diagnosed by an ascitic fluid neutrophil count of 250 cells/microL or higher on paracentesis. Treatment is prompt IV third-generation cephalosporin plus IV albumin in patients with renal or hepatic dysfunction, followed by indefinite secondary antibiotic prophylaxis because recurrence is common.
- Portal hypertension
Portal hypertension is elevated pressure in the portal venous system, most often from cirrhosis, that drives the major decompensating complications of chronic liver disease: varices, ascites, splenomegaly, and encephalopathy. Diagnosis rests on imaging and endoscopy for its downstream signs, and management combines treating the underlying cause with nonselective beta-blockade and, for refractory complications, TIPS.
- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Hepatocellular carcinoma
Hepatocellular carcinoma is a primary liver cancer that arises almost exclusively in cirrhosis and can be diagnosed non-invasively when multiphase CT or MRI shows arterial-phase hyperenhancement with portal-venous washout in a lesion at least 1 cm. Treatment is stratified by tumor burden, liver function, and vascular or extrahepatic spread, ranging from resection or ablation through transplantation and transarterial chemoembolization to systemic atezolizumab-bevacizumab for advanced disease.