Abstract
<jats:p>Background. Hepatorenal syndrome (HRS) developing in the setting of decompensated portal hypertension (PH) is characterized by progressive renal failure, elevated serum creatinine levels, and worsening oliguria. HRS occurs in approximately one-third of patients with Child-Pugh class C liver cirrhosis. The purpose was to optimize early diagnosis and treatment, as well as to identify risk factors for the development of HRS and associated mortality. Materials and methods. A total of 126 medical records of patients with decompensated PH treated at the Kyiv City Emergency Hospital and the Department of Surgery, Dental Faculty, Bogomolets National Medical University, between 2022 and 2024 were analyzed. HRS was diagnosed in 51 (40.5 %) cases. Diagnostic criteria included an increase in serum creatinine > 150 µmol/L (1.69 mg/dL) or ≥ 26.5 µmol/L (0.3 mg/dL) within 48 hours in the presence of oliguria and absence of other signs of intrinsic renal injury, particularly hematuria. Patients were divided into two groups. The first group included 24 (47.1 %) patients in whom HRS and community-acquired spontaneous bacterial peritonitis (SBP) were diagnosed within the first 24 hours, and a restrictive transfusion strategy was applied. The second group comprised 27 (52.9 %) participants in whom HRS and nosocomial SBP were diagnosed on days 3–5 of hospitalization, and a liberal transfusion strategy was used. The impact of transfusion strategy, ascites severity, and SBP as mutually aggravating factors in HRS development was assessed. Results. Analysis showed that the combination of large-volume ascites, SBP, and a liberal transfusion strategy forms an unfavorable prognostic complex associated with a significantly increased risk of mortality. HRS development was more frequently associated with large-volume ascites (70.8 %), nosocomial SBP (37.0 %), and a liberal transfusion strategy (52.9 %). Among 126 patients, 27 (21.4 %) underwent surgery. In the postoperative period, HRS developed in 1 (4.2 %) patient in the first group and in 2 (7.4 %) patients in the second group. Overall mortality was 74.5 % (n = 38), with 14 deaths (58.3 %) in the first group and 24 (88.9 %) in the second group (p = 0.03). According to ROC analysis, the model demonstrated high predictive performance for mortality (AUC = 0.909; 95% CI 0.831–0.987), confirming strong discriminative ability for risk stratification in patients with HRS. Conclusions. HRS is a severe complication of decompensated PH associated with high mortality. A liberal transfusion strategy, severe ascites, and SBP increase the risk of its development and progression. Early monitoring of urine output and serum creatinine levels is critical for timely diagnosis, prevention, and management of HRS.</jats:p>