Hepatorenal syndrome (HRS) is a severe functional renal disorder that occurs in patients with advanced liver disease, portal hypertension, and circulatory dysfunction. It represents one of the most serious complications of decompensated cirrhosis and acute-on-chronic liver failure, with very high morbidity and mortality if untreated. Contemporary understanding of HRS has evolved considerably over the past decade, resulting in revised diagnostic criteria, earlier recognition of acute kidney injury (AKI), and improved therapeutic strategies. Current classifications recognize HRS-AKI, HRS-non-AKI, and HRS-chronic kidney disease phenotypes, replacing the older type 1 and type 2 classifications. The pathophysiology of HRS is multifactorial and involves severe splanchnic vasodilation, systemic inflammation, neurohormonal activation, renal vasoconstriction, impaired cardiac output, and endothelial dysfunction. Diagnosis requires exclusion of structural kidney disease and other causes of renal dysfunction in cirrhotic patients. Current management strategies emphasize early albumin administration, withdrawal of nephrotoxic agents, treatment of precipitating factors, and vasoconstrictor therapy including terlipressin, norepinephrine, and midodrine-octreotide combinations. Liver transplantation remains the definitive therapy, although renal replacement therapy may serve as bridge treatment in selected patients. Emerging evidence on biomarkers, inflammatory pathways, and individualized therapy continues to refine management approaches. This descriptive review summarizes the current understanding, epidemiology, pathophysiology, clinical assessment, diagnostic challenges, management strategies, prognosis, and future directions in hepatorenal syndrome.