Abstract
Selenium (Se), an essential trace element, is linked to poor prognosis in heart failure (HF) and kidney disease. Se deficiency (serum Se < 70 μg/L) has been associated with increased cardiovascular mortality. Selenoprotein P (SELENOP), the main Se transporter, reflects bioavailable Se. Selective glomerular hypofiltration syndrome (SGHS), defined by a cystatin C-based eGFR < 0.7 of creatinine-based eGFR, signals early kidney dysfunction and worsens HF outcomes. The prognostic role of SELENOP for SGHS and kidney-related hospitalization in HF remains unclear. PURPOSE: To assess whether SELENOP is associated with SGHS at baseline and future kidney disease hospitalization in acute HF patients. METHODS: In 570 patients hospitalized for acute HF, creatinine and cystatin C were analyzed; SELENOP was measured in the first 320 using an immunoassay. Kidney hospitalizations (ICD-10 N17-N19) were identified from regional registries. Logistic and Cox regression models evaluated SELENOP's association with SGHS and hospitalization risk, adjusting for age, sex, blood pressure, BMI, eGFR and NT-proBNP. RESULTS: Among 320 patients (mean age 75 years, 69% male), 58% had Se deficiency, and 30% had SGHS. During a median 43-month follow-up, 28 patients were hospitalized for kidney disease. Higher SELENOP was linked to lower odds of SGHS (OR 0.69; p = 0.002) and reduced risk of hospitalization for AKI or CKD (HR 0.60; p = 0.010), particularly AKI (HR 0.42; p = 0.002). SELENOP-deficiency (<3.23 mg/L) predicted AKI hospitalization (HR 4.02; p = 0.035). CONCLUSIONS: Low SELENOP is associated with SGHS and increased risk of kidney disease hospitalization, especially AKI, suggesting Se status may influence HF and renal outcomes.