Hepatorenal syndrome type 1 (HRS-1) is a severe form of AKI that affects individuals with advanced cirrhosis and ascites. The main pillar of its pathogenesis is rooted in marked maladaptive renal vasoconstriction. Because of the lack of a gold standard, establishing the diagnosis requires a meticulous process of recognizing its phenotypical features and ascertaining the absence of strong evidence of an alternative etiology of AKI. This is particularly important because a diagnosis of AKI due to HRS-1 prompts initiation of a specific vasoconstrictor pharmacotherapy. Terlipressin and norepinephrine are the most effective therapeutic agents for HRS-1. Treatment eligibility and choice of agent should follow a systematic assessment of clinical presentation, drug safety profile, practical and logistical considerations around intensive care unit bed availability, and proximity of liver transplantation. Independently of the vasoconstrictor used, the goal of therapy is to target a sustained rise in mean arterial pressure to enable renal perfusion. Although intravenous albumin has been historically viewed as a key coadjuvant of vasoconstrictor therapy, newer data have emerged, demonstrating that intravenous albumin may increase the risk for fluid overload. Conversely, diuretics may be safely introduced when clinically applicable. In this review, we navigate through the common challenges faced during the assessment, diagnosis, and medical treatment of a patient with decompensated cirrhosis and AKI suspected to be due to HRS-1, emphasizing the newest lessons learned about the role of terlipressin, its safety profile, and the paradigm shift around the role of albumin in the management of HRS-1.