albumin (Pedialb / AlbuRel / AlbuRel LS)

Platelet-Albumin-Bilirubin Score Predicts In-Hospital Mortality in Patients with HFrEF Presenting with Acute Heart Failure.

Hekimsoy Vedat V, Tanık Veysel Ozan VO, Akbuğa Kürşat K, Taş Alperen A et al.

Patients with heart failure and reduced ejection fraction presenting with acute heart failure (HFrEF-AHF) carry a high in-hospital mortality. Conventional predictors do not fully capture the interplay between hepatic dysfunction, systemic inflammation, and nutritional decline. The platelet-albumin-bilirubin (PALBI) score, originally developed in hepatology, may offer incremental prognostic information in this setting. A total of 401 patients hospitalized with HFrEF-AHF were retrospectively studied. Baseline demographic, clinical, and laboratory data were collected. Platelet-albumin-bilirubin and albumin-bilirubin (ALBI) scores were calculated. The primary endpoint was all-cause in-hospital mortality. In-hospital mortality occurred in 47 patients (11.7%). Non-survivors were older, more frequently had chronic kidney disease (CKD), and showed lower albumin but higher bilirubin and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Both PALBI and ALBI were significantly higher in non-survivors. In multivariable Cox analysis, PALBI independently predicted mortality (hazard ratio = 2.638, 95% CI: 1.177-4.099, P < .001), along with age, CKD, and NT-proBNP. Receiver operating characteristic analysis showed that PALBI demonstrated slightly better performance than conventional predictors and, compared with ALBI (area under the curve = 0.737 vs. 0.708), yielded a modest but significant net reclassification improvement (~10%). Kaplan-Meier curves demonstrated clear separation in survival across PALBI strata (log-rank, P < .001), and restricted cubic spline analysis confirmed a graded, continuous association with risk. The PALBI score independently predicts in-hospital mortality in patients with HFrEF-AHF and may represent a simple and clinically useful tool for early risk stratification. External validation in larger, multicenter cohorts is warranted.

Methodological Considerations in the Bioequivalence Assessment of Recombinant Human Serum Albumin [Letter].

Chang Peng P, Shen Danfeng D

Methodological and Interpretative Considerations on the Uric Acid-to-Albumin Ratio in Acute Pulmonary Embolism.

Topal Salih S

Urinary Albumin-to-Creatinine Ratio Across Phenotypes of Polycystic Ovary Syndrome: A Phenotype-Based Evaluation.

Oner Oznur O, Akkus Canan C, Demircioglu Doga D, Karanlık Ilhan I et al.

Background/Aim: Albuminuria is a clinical marker associated with microvascular involvement and an independent predictor of cardiovascular risk. Polycystic ovary syndrome (PCOS) is associated with early metabolic and vascular abnormalities; however, whether albumin excretion differs across PCOS phenotypes remains unclear. This study aimed to evaluate the urinary albumin-to-creatinine ratio (U-ACR) across PCOS phenotypes and to examine its association with metabolic parameters. Materials and Methods: In this cross-sectional study, 180 women aged 18-35 years with PCOS and 51 age-matched healthy controls were included. PCOS phenotypes were classified according to the Rotterdam criteria as Phenotype A (n = 96), Phenotype B (n = 19), Phenotype C (n = 35), and Phenotype D (n = 30). Insulin resistance was assessed using the homeostasis model assessment for insulin resistance (HOMA-IR). Urinary albumin and creatinine levels were measured in morning urine samples, and U-ACR was calculated. Results: Age was comparable across all groups. Body mass index, waist circumference, diastolic blood pressure, and HOMA-IR were significantly higher in Phenotype A compared with controls and other phenotypes, reflecting a more adverse metabolic profile. Serum creatinine levels were similar across all groups. Despite this metabolic profile in Phenotype A, U-ACR was significantly elevated only in Phenotype B compared with controls (p = 0.018), and Phenotype D (p = 0.016). No significant correlations were observed between U-ACR and age, body mass index, or HOMA-IR. When participants were categorized according to U-ACR levels (<30, 30-299.9, and ≥300 mg/g creatinine), no significant differences in category distribution were observed between the total PCOS cohort, phenotype subgroups, and controls. Conclusion: Among PCOS phenotypes, U-ACR elevation was observed exclusively in Phenotype B despite similar renal function markers. This finding, in the presence of a more adverse metabolic profile in Phenotype A, suggests a dissociation between metabolic burden and early microvascular involvement across PCOS phenotypes. These findings suggest a potential phenotype-specific pattern that warrants further investigation.