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2015 ; 16
(ä): 178
Nephropedia Template TP
gab.com Text
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English Wikipedia
Putative novel mediators of acute kidney injury in critically ill patients:
handling by continuous venovenous hemofiltration and effect of anticoagulation
modalities
#MMPMID26519056
Schilder L
; Nurmohamed SA
; ter Wee PM
; Paauw NJ
; Girbes AR
; Beishuizen A
; Beelen RH
; Groeneveld AB
BMC Nephrol
2015[Oct]; 16
(ä): 178
PMID26519056
show ga
BACKGROUND: 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 effect of
continuous venovenous hemofiltration (CVVH) and different anticoagulation
regimens on plasma levels were studied. METHODS: At 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. RESULTS: Concentrations 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. CONCLUSION: Novel 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.