ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: TH-PO1182

Effect of Hemodialysis with Citrate on Vascular Calcification

Session Information

Category: Bone and Mineral Metabolism

  • 502 Bone and Mineral Metabolism: Clinical

Authors

  • O'Neill, W. Charles, Emory University, Atlanta, Georgia, United States
  • Navarrete, Jose E., Emory University, Atlanta, Georgia, United States
Background

Medial arterial calcification (MAC) is a serious problem in hemodialysis (HD) patients that leads to poor outcomes. Citrate, which can inhibit calcium crystallization, is used in some HD solutions but its effect on vascular calcification is unknown. We have shown that MAC can be conveniently measured on standard mammograms (MGs) and correlates with MAC in other locations and with cardiovascular outcomes. Therefore, we used mammography to measure changes in MAC in female HD patients during HD with and without citrate.

Methods

In this cross-over study in 4 outpatient units, patients with pre-existing MAC on MGs were recruited to 1 year periods of HD with and without citrate (Citrasate and Naturalyte, Fresenius) with MGs and measurements of serum Mg and ionized Ca (iCa), and plasma citrate every 6-months (NCT04956120). Lengths of calcified arteries were summed manually and the rate of change determined from the slope of values from the 3 MGs at the start, middle, and end of each arm. Data are means + SE with analysis by paired t-test, or medians (interquartile range) for MAC with analysis by Wilcoxon test.

Results

28 of 30 subjects have completed the study, 12 starting on the citrate arm. Durations of the arms did not differ (citrate: 383 + 8 days; no citrate 407 + 15). Dialysis adequacy, dialysate Ca, and pre-HD serum total Ca, iCa, and phosphorus did not differ between arms; pre-HD Mg was lower in the citrate arm (2.28 + 0.05 vs. 2.42 + 0.07 mg/dl, p=0.003. The change in serum Mg or iCa with HD did not differ significantly between arms. Pre-HD plasma citrate was similar (133 + 8 vs. 127 + 6 uM) but was substantially greater after HD with citrate (364 + 17 vs. 144 + 9 uM, p<0.001). The change in MAC was greater during citrate HD: 44 (21-121) mm/yr vs. 10 (-5-35), p=0.0002, or 35 (14-104) %/yr vs.12 (-3-23), p=0.002. 22 subjects had a greater change during citrate HD (median: 51 %/yr), while only 6 had a greater change without citrate (median: 14 %/yr). The change in MAC did not correlate with pre-HD serum iCa, P, or Mg.

Conclusion

Citrate HD unexpectedly promoted vascular calcification, which was not explained by changes in mineral metabolism or dialysis adequacy. This result may be related to known effects of citrate to promote or stabilize bone mineralization. Further studies are needed to determine the underlying mechanism and whether this is associated with adverse clinical outcomes.

Funding

  • Commercial Support – Fresenius Medical Care Renal Therapies Group