ReviewWorld journal of gastroenterology2012
Hepatorenal syndrome.
Review in World journal of gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 54 citations in OpenAlex.
- Liver involvement in kidney disease and vice versa.Pediatric nephrology (Berlin, Germany) · 2018Review
- Induction of renal artery hyperresponsiveness by alpha1-adrenoceptor in hepatorenal syndrome.Oncotarget · 2017Article
- Modulation of splanchnic circulation: Role in perioperative management of liver transplant patients.World journal of gastroenterology · 2016Review
- Dialysis-dependent acute kidney injury in children with end-stage liver disease: prevalence, dialysis modalities and outcome.Pediatric nephrology (Berlin, Germany) · 2015Article
- Contemporary concepts of the medical therapy of portal hypertension under liver cirrhosis.World journal of gastroenterology · 2015Review
- D-Galactosamine Intoxication in Experimental Animals: Is it Only an Experimental Model of Acute Liver Failure?Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Primary biliary cirrhosis: Pathophysiology, clinical presentation and therapy.World journal of hepatology · 2015Review
- Management of hepatorenal syndrome.World journal of nephrology · 2015Review
- Gut-liver axis in liver cirrhosis: How to manage leaky gut and endotoxemia.World journal of hepatology · 2015Review
- Progressive Familial Intrahepatic Cholestasis: A Rare Cause of Cirrhosis in Young Adult Patients.Case reports in medicine · 2015Article
- Hepatorenal syndrome: outcome of response to therapy and predictors of survival.Gastroenterology research and practice · 2015Article
- Cholecystectomy in Patients with Liver Cirrhosis.Gastroenterology research and practice · 2015Article
- In silico evaluation of gadofosveset pharmacokinetics in different population groups using the Simcyp® simulator platform.In silico pharmacology · 2014Article
- Comprehensive review of post-liver resection surgical complications and a new universal classification and grading system.World journal of hepatology · 2014Review
- Effect of nitric oxide pathway regulation on water/sodium balance and renal function in a rodent model of acute liver and renal failure.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
- Renal dysfunction in patients with cirrhosis: Where do we stand?World journal of gastrointestinal pharmacology and therapeutics · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatorenal syndrome (HRS) is defined as a functional renal failure in patients with liver disease with portal hypertension and it constitutes the climax of systemic circulatory changes associated with portal hypertension. This term refers to a precisely specified syndrome featuring in particular morphologically intact kidneys, where regulatory mechanisms have minimised glomerular filtration and maximised tubular resorption and urine concentration, which ultimately results in uraemia. The syndrome occurs almost exclusively in patients with ascites. Type 1 HRS develops as a consequence of a severe reduction of effective circulating volume due to both an extreme splanchnic arterial vasodilatation and a reduction of cardiac output. Type 2 HRS is characterised by a stable or slowly progressive renal failure so that its main clinical consequence is not acute renal failure, but refractory ascites, and its impact on prognosis is less negative. Liver transplantation is the most appropriate therapeutic method, nevertheless, only a few patients can receive it. The most suitable "bridge treatments" or treatment for patients ineligible for a liver transplant include terlipressin plus albumin. Terlipressin is at an initial dose of 0.5-1 mg every 4 h by intravenous bolus to 3 mg every 4 h in cases when there is no response. Renal function recovery can be achieved in less than 50% of patients and a considerable decrease in renal function may reoccur even in patients who have been responding to therapy over the short term. Transjugular intrahepatic portosystemic shunt plays only a marginal role in the treatment of HRS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.