Background: Chronic kidney disease (CKD) affects over 35.5 million US adults. Serum α1-acid glycoprotein (α1-AGP), an acute-phase protein, exhibits anti-inflammatory properties in animal models, but its association with CKD in younger women remains underexplored. This study investigated the relationship between serum α1-AGP and CKD risk in US women aged 20–49 years. Methods: This nationally representative cross-sectional study used data on female adults in the US aged 20–49 years from the National Health and Nutrition Examination Survey 2015–2018 cycles. 2,137 individuals were included in the study after excluding individuals without serum α1-AGP, urine albumin, and creatinine data. Multivariate logistic regression models evaluated the association between serum α1-AGP and CKD. Moreover, we performed stratified and interaction analyses to see if the relationship was stable in different subgroups. Results: Among 2,137 participants (mean age 34.6 years, mean eGFR 111.7 mL/min/1.73 m²), CKD prevalence was 8.8% (n=188). Higher serum α1-AGP levels were associated with lower CKD risk in the fully adjusted model (OR 0.37, 95% CI 0.16–0.84, P = 0.017), with a dose-response trend across quartiles (P = 0.041). The association was stronger in women aged 40–49 years (OR 0.20, 95% CI 0.05–0.76) and Mexican Americans (OR 0.07, 95% CI 0.01–0.56), though interaction terms were not significant (P > 0.05). Conclusions: Higher serum α1-AGP levels are associated with lower CKD prevalence in young women, suggesting a protective role. Longitudinal studies are needed to confirm causality and explore α1-AGP as a biomarker for CKD risk stratification.

Background: Dysphagia is a common functional impairment in elderly populations, often leading to severe complications such as malnutrition and aspiration pneumonia, significantly increasing healthcare burdens. Currently, effective prognostic assessment tools are lacking. The absolute lymphocyte count (ALC), a biomarker reflecting immune-nutritional status, has potential predictive value in this context, though its role in dysphagia prognosis remains unclear. Methods: This retrospective cohort study included 253 dysphagic patients who received percutaneous endoscopic gastrostomy (PEG) or total parenteral nutrition (TPN) between 2014 and 2017. Five patients with missing ALC were excluded. Cox regression models assessed the association between ALC and mortality. ALC was analyzed as both continuous variable (using restriocted cubic splines) and categorical tertiles, with additional threshold analyses to assess non-linearity. Kaplan–Meier survival curves and subgroup analyses were also performed. Results: Lower ALC was associated with poorer nutritional status, higher inflammatory markers, and greater comorbidity burden. Higher ALC was independently associated with reduced mortality (adjusted HR: 0.60; 95% CI: 0.44–0.83; p = 0.002). Patients in the highest tertile had significantly better survival than those in the lowest (HR: 0.37; 95% CI: 0.23–0.59; P < 0.001). A non-linear threshold effect was identified at ALC = 1.899×10⁹/L (p for non-linearity = 0.009). Kaplan–Meier analysis confirmed improved survival with higher ALC (p < 0.0001). Subgroup analyses showed the protective effect of higher ALC was consistent across age, sex, BMI, PEG use, and comorbidity strata, with no significant interactions. Conclusions: ALC is an independent, non-linear predictor of mortality in older dysphagic patients and may aid clinical risk stratification across diverse patient subgroups.

Background: Hepatocellular carcinoma (HCC) faces significant challenges in early diagnosis and prognostic assessment, necessitating novel molecular biomarkers. The role of GCN1 in tumorigenesis remains unclear, warranting systematic investigation of its clinical value. Methods: Utilizing multi-omics data from 164 HCC patients in the TCGA database, we comprehensively evaluated the diagnostic and prognostic value of GCN1 through differential expression analysis, Cox proportional hazards regression, and gene set enrichment analysis (GSEA). Results: GCN1 expression was significantly upregulated in tumor tissues (P<0.001), with ROC analysis demonstrating an AUC of 0.921 (95% CI: 0.893-0.950) for discriminating tumor from normal tissue. Clinical correlation analysis revealed that high GCN1 expression significantly associated with advanced T stage (OR=1.941, P=0.002) and AFP levels >400 ng/ml (OR=3.697, P<0.001). Multivariate survival analysis confirmed its independent prognostic value (HR=1.454, P=0.038). Functional analysis indicated GCN1 promotes tumor progression by regulating cell cycle (NES=2.385) and axon guidance (NES=2.307) pathways. Conclusion: This study first elucidates the dual clinical value of GCN1 in HCC, providing a theoretical foundation for developing novel diagnostic biomarkers and prognostic evaluation systems. Future research should validate its molecular mechanisms and explore potential targeted therapies.