Hepatorenal Syndrome – Acute Kidney Injury (HRS-AKI): Advances in Definition, Diagnosis and Management: Review Article

Document Type : Original Article

Abstract

Background: Hepatorenal Syndrome – Acute Kidney Injury (HRS-AKI) is a severe and frequently fatal complication that happens in cases with advanced liver illness, particularly those with liver cirrhosis. Acute kidney injury (AKI) in cirrhotic patients is related to high morbidity and death, and differentiating HRS-AKI from other causes including prerenal azotemia (PRA) and acute tubular necrosis (ATN) that remains a major clinical challenge because of overlapping features.
Objective: This study aimed to provide an updated overview of the current understanding of HRS-AKI, emphasizing its evolving definitions, pathophysiology, diagnostic challenges, and therapeutic approaches. Methods: A systematic search was conducted using PubMed, Google Scholar, and Scopus, with keywords including: Acute kidney injury, Liver cirrhosis, Hepatorenal syndrome and Fractional Excretion of urea. The writers evaluated relevant literature references as well. Documents written in languages other than English have been ignored. Papers that were not regarded as significant scientific research included dissertations, oral presentations, conference abstracts and unpublished manuscripts were excluded.
Conclusion: The pathogenesis of HRS-AKI is primarily linked to profound circulatory dysfunction, leading to renal vasoconstriction and reduced renal perfusion. Recent research, however, has highlighted the important role of systemic inflammation, sepsis, and multi-organ failure in disease progression. Traditional diagnostic tools, including fractional excretion of sodium (FENa), are often unreliable in patients receiving diuretics. Therefore, the fractional excretion of urea (FEUrea) has emerged as a more accurate and accessible biomarker to differentiate functional kidney injury (HRS-AKI and PRA) from structural injury (ATN). Management focuses on early identification, discontinuation of nephrotoxic agents, volume expansion with intravenous albumin, and vasoconstrictor therapy using terlipressin, norepinephrine, or midodrine with octreotide. For refractory cases, transjugular intrahepatic portosystemic shunt (TIPS) and liver transplantation remain definitive options. Early diagnosis and tailored management of HRS-AKI are essential for improving survival. Continued research on novel biomarkers and therapeutic strategies offers promise for better outcomes in this complex syndrome.

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