New biomarkers of inflammation associated to hemodialysis
Clinical Kidney Journal, 2025
Guerrero F., Carmona A., Jiménez M., Ariza F., Obrero T., Berdud I., Carrillo-Carrión C., Rodríguez M., Soriano S., Muñoz-Castañeda J., Martín-Malo A.
| Disease area | Application area | Sample type | Products |
|---|---|---|---|
CVD Nephrology | Pathophysiology | Plasma |  Olink Target 96 |
Abstract
Background
The first year of hemodialysis (HD) carries the highest risk of mortality which to a large extent is attributed to the aggravation of inflammation. However, traditional markers, such as C-reactive protein and interleukin-6, show only minor changes during the first year, suggesting that there are other factors involved. The present study evaluates the effect of HD on microinflammation and oxidative stress of uremic patients.
Methods
Prospective observational longitudinal study, including 30 incident HD patients. Blood samples were collected at baseline, 6 and 12 months. Proinflammatory monocytes were quantified using flow cytometry. Proteomic analysis (Olink) was performed on serum. Concentrations of indoxyl sulfate (IS), growth differentiation factor 15 (GDF-15), oxidative status and circulating miRNAs expression were also determined.
Results
A new population of activated monocytes was identified which increased progressively at one year of HD. In addition, an increase in the serum concentration of up to twenty-nine inflammation-related proteins was detected, including interleukins, chemokines, TNF family molecules, cell activation molecules, and apoptosis-related proteins. Conversely, the leukemia inhibitory factor receptor (LIF-R) was downregulated. The concentration of IS was positively correlated with the GDF-15 levels. Furthermore, patients exhibited a decreased expression of miRNAs-126-3p, -130a-3p, -146a-5p, 223-3p, -let7a-5p and -let7b-5p.
Conclusions
This study highlights the impact of HD on inflammation and oxidative stress, manifested by an increase in activated monocytes and inflammatory markers. The observed subclinical inflammation associated to HD treatment may help to understand the mechanisms of cardiovascular damage of patients on HD.