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Hemodialysis (HD) is a critical life-supporting intervention for managing end-stage renal disease (ESRD). Despite its significance, this membrane-based therapy presents acute side-effects stemming from bioincompatibility concerns and challenges in effectively eliminating uremic toxins. The current investigation delves into the impact of hydrodynamic conditions employed during HD treatment on the inflammatory and thrombotic responses mediated by proteins.
We examined the influence of prescribed hemodialysis (HD) operating conditions on the release of inflammatory biomarkers in HD patients treated with the polyarylethersulfone (PAES) dialyzer. After obtaining Research Ethics Approval, we recruited twelve HD patients and two healthy controls from St. Paul’s Hospital dialysis center. Inclusion criteria for dialysis patients comprised a confirmed kidney disease diagnosis, regardless of gender, and age below 60. For the healthy controls, the criteria were the same for age and biological sex but included normal kidney function. Blood samples were collected from the dialysis patients before the dialysis session, at 30 minutes, 1 hour, and 4 hours (end of dialysis treatment). The samples were analyzed using Luminex assays and the Bio-Plex-200 system (Bio-Rad, Hercules, CA, USA) for the measurement of complement component 5a (C5a), properdin, tumor necrosis factor (TNF)-α, interleukin (IL)-1α, IL-1β, IL-6, serpin/antithrombin-III, and Von Willebrand factor (vWF).
We examined the impact of hemodialysis (HD) operating conditions on inflammatory biomarkers in patients using the PAES dialyzer. Prior to HD, patients and controls showed similar C5a and properdin levels. During the first hour, both factors followed similar trends, except for Qb = 400 mL/min (properdin decreased) and Qb = 500 mL/min (properdin increased). C5a remained higher in HD patients throughout. After 4 hours, the highest and lowest C5a levels occurred at Qb = 400 mL/min and Qb = 200 mL/min, respectively. Patients at Qb = 200 mL/min exhibited the greatest increases in both biomarkers. Serpin/antithrombin III levels decreased in the first 30 minutes, with higher levels at Qb = 200 mL/min at session's end. Pro-inflammatory cytokines and vWF varied during treatment, with some increases at Qb = 200 mL/min and reductions at higher flow rates.
In conclusion, our study reveals significant changes in biomarker concentrations following hemodialysis sessions at a Qb of 200 mL/min. Notably, C5a, properdin, serpin, IL-1α, IL-6, and vWF concentrations increased, while IL-1β and TNF-α declined. These findings emphasize the role of hydrodynamic conditions in influencing biomarker release, with lower flow rates triggering more adverse responses compared to higher flow rates. It's worth noting that serpin, serving as a clotting factor, exhibited a different pattern. These insights shed light on the interplay between flow rates and inflammatory and thrombotic responses in hemodialysis patients.