ArticleCureus2025
Hepatorenal Syndrome: A Critical Complication in Advanced Cirrhosis.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatorenal syndrome (HRS) is a life-threatening complication of advanced liver disease, especially cirrhosis. It involves functional kidney failure without structural damage. The main cause is severe splanchnic vasodilation from portal hypertension, which reduces effective blood volume. This triggers compensatory vasoconstriction, leading to reduced kidney perfusion. HRS is classified into two types. Type 1 is rapid and often triggered by infection or bleeding. Type 2 progresses slowly and is linked to refractory ascites. Diagnosis is clinical and requires ruling out shock, nephrotoxins, and kidney disease. Early diagnosis is vital due to its high mortality. We describe the case of a male patient, age 54, with a history of alcohol-induced cirrhosis. He had laboratory evidence of acute kidney injury, oliguria, hyponatremia, and progressive fatigue. Ultrasound showed a nodular liver with ascites, indicating cirrhosis and portal hypertension. Both kidneys retained their normal size and corticomedullary differentiation, ruling out intrinsic renal disease. Type 1 HRS was identified after all other possible causes of renal dysfunction were ruled out. Renal function partially improved after the patient received intravenous albumin and terlipressin. He was then referred to be evaluated for a liver transplant. This case highlights how complex the clinical and diagnostic aspects of HRS can be while also emphasizing the critical need for early detection and treatment. By combining sonographic findings, such as indicators of portal hypertension, with clinical and biochemical data, we can make a more informed diagnosis of HRS. Although pharmacological treatments may provide temporary relief, liver transplantation remains the gold standard for ensuring long-term survival in patients with advanced liver disease complicated by 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.