Abstract
BackgroundNovel putative mediators of acute kidney injury (AKI) include immune-cell derived tumour necrosis factor-like weak inducer of apoptosis (TWEAK), angiopoietin-2 (Ang-2) and protein pentraxin-3 (PTX3). The effect of continuous venovenous hemofiltration (CVVH) and different anticoagulation regimens on plasma levels were studied.MethodsAt 0, 10, 60, 180 and 720 min of CVVH, samples were collected from pre- and postfilter blood and ultrafiltrate. No anticoagulation (n = 13), unfractionated heparin (n = 8) or trisodium citrate (n = 21) were compared.ResultsConcentrations of TWEAK, Ang-2 and PTX3 were hardly affected by CVVH since the mediators were not (TWEAK, PTX3) or hardly (Ang-2) detectable in ultrafiltrate, indicating negligible clearance by the filter in spite of molecular sizes (TWEAK, PTX3) at or below the cutoff of the membrane. Heparin use, however, was associated with an increase in in- and outlet plasma TWEAK.ConclusionNovel AKI mediators are not cleared nor produced by CVVH. However, heparin anticoagulation increased TWEAK levels in patient’s plasma whereas citrate did not, favouring the latter as anticoagulant in CVVH for AKI.
Highlights
Novel putative mediators of acute kidney injury (AKI) include immune-cell derived tumour necrosis factor-like weak inducer of apoptosis (TWEAK), angiopoietin-2 (Ang-2) and protein pentraxin-3 (PTX3)
TWEAK Concentrations at in- and outlet were higher in the heparin group than other groups (P = 0.043 and P = 0.001, respectively), especially after 10 min of continuous venovenous hemofiltration (CVVH), and concentrations at in- and outlet decreased over time in the heparin group but not in the other groups (P = 0.001 and P = 0.007, respectively)
The present study shows that plasma levels of putative novel AKI mediators in critically ill patients are not affected by CVVH; there is no clearance, absorption nor production across the system
Summary
Novel putative mediators of acute kidney injury (AKI) include immune-cell derived tumour necrosis factor-like weak inducer of apoptosis (TWEAK), angiopoietin-2 (Ang-2) and protein pentraxin-3 (PTX3). The pathogenesis of AKI is multifactorial, novel mediators have been described that are implicated in the development of AKI, for instance in the course of sepsis. These mediators include TNF-associated weak inducer of apoptosis (TWEAK), a member of the super tumor necrosis factor (TNF) family, which can be expressed in renal and immune cells [2, 3]. The anticoagulation regimen applied during CVVH could influence release of proinflammatory factors and specific AKI mediators by activated immune cells and platelets in the patient and hemofilter
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