-
PDF
- Split View
-
Views
-
Cite
Cite
Makrouhi Sonikian, Eugenia Karakou, Theodoros Hiras, Jacob Skarakis, Pagona Sklapani, Constantinos Skandalis, Nikolaos Trakas, FP614
POST-DIALYSIS ACID-BASE BALANCE AND CALCIUM-PHOSPHATE CHANGES IN HEMODIALYSIS PATIENTS WITH VASCULAR CALCIFICATIONS, Nephrology Dialysis Transplantation, Volume 33, Issue suppl_1, May 2018, Page i249, https://doi.org/10.1093/ndt/gfy104.FP614 - Share Icon Share
INTRODUCTION AND AIMS: Vascular calcifications are influenced by changes in acid-base balance. Alkalinization is thought to promote calcium phosphate precipitation. Raising plasma bicarbonate(BIC) by dialysis in hemodialysis(HD) patients may lead to excessive correction of metabolic acidosis and promote vascular calcifications.Post-dialysis acid-base balance and calcium-phosphate alterations are described in HD patints with and without vascular calcifications.
METHODS: 20 patients on standard HD with dialysate BIC and Ca2+ concentrations of 32mM and 1,5mM respectively and serum PTH of 340±274pg/ml were studied. Calcification degree was scored using hands and pelvis X-ray films divided into four parts by mutually vertical lines. Each part could be scored 0 or 1 according to calcification absence or presence respectively and patients could get final calcification scores(CaS) from 0 to 8. Two patient groups were formed: group A(GA) included 11 patients with CaS≤1(0,18±0,4) and group B(GB) 9 patients, with CaS>1(6,44±1,8)-p<0,001. In all patients blood was sampled before(preD), at the end(postD) and one hour after session(1hpostD) for pH, BIC, ionized Ca(iCa), phosphate(P), total Ca, albumin(Alb), urea and Mg. Corrected for Alb Ca(Ca) and CaxP product values were calculated.
RESULTS: In GA, postD pH(7,42±0,05) and 1hpostD pH(7,42±0,05) were higher than preD pH(7,32±0,04)-p<0,001 respectively; BIC showed similar increases: 26,4±1,8 and 25,8±2,5 vs 20,5±1,9mM-p<0,001 respectively. Similarly in GB, postD pH(7,43±0,05) and 1hpostD pH(7,42±0,05) were higher than preD pH(7,34±0,05)-p<0,001 respectively; BIC showed similar increases: 26,2±1,6 and 25,2±2,2 vs 21,5±2,4mM-p<0,001 respectively. In GA, only postD Ca(10,1±1mg/dl) was higher than preD Ca(8,9±0,7mg/dl)-p=0,02; 1hpostD Ca(9,8±0,7mg/dl) was not statistically different from preD Ca or postD Ca, whereas both postD Alb(4,6±0,5g/dl) and 1hpostD Alb(4,5±0,4g/dl) were higher than preD Alb(4±0,3g/dl)-p<0,05 respectively. In contrary, in GB both postD Ca(10,3±0,5mg/dl) and 1hpostD Ca(10,3±0,9 mg/dl) were higher than preD Ca(9,2mg/dl)-p<0,05 respectively, whereas there was no significant changes in Alb. In both groups postD P was decreased: GA, 5,7±1,5 to 2,9±0,7mg/dl-p<0,001 and GB, 5,6±1,6 to 3,2±0,7mg/dl-p<0,001; 1hpostD P was also lower than preD P with no significant rebound: GA, 3,8±1,1mg/dl-p=0,002 and GB, 3,8±0,8mg/dl-p=0,004. CaxP values followed P changes in both groups. No difference between groups was observed in postD and 1hpostD iCa and Mg changes. In all patients significant negative correlations of 1hpostD Ca were observed with PTH(p=0,04) and preD urea(p=0,03).
CONCLUSIONS: In conclusion, all patients experienced similar postD pH and BIC increases remaining one hour after session. Only patients with high calcification score had increased 1hpostD Ca under alkaline pH in the absence of Alb increase. The relationship of this finding with postD metabolic alkalosis in patients with vascular calcifications needs further investigation.
Comments