ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

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


The Latest on Twitter

Kidney Week

Abstract: PO0880

Progression of Coronary Artery Calcification in Unit vs. Nocturnal Haemodialysis Patients

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis


  • Brown, Karen E., Morriston Hospital, Swansea, Wales, United Kingdom
  • Bucknall, Thomas, Morriston Hospital, Swansea, Wales, United Kingdom
  • Greene, Giles, Public Health Wales, Cardiff, Cardiff, United Kingdom
  • Jefferies, Helen, Cardiff and Vale University Health Board, Cardiff, Cardiff, United Kingdom
  • Mikhail, Ashraf I., Morriston Hospital, Swansea, Wales, United Kingdom
  • Prior, Sarah L., Swansea University, Swansea, West Glamorgan, United Kingdom
  • Stephens, Jeffrey W., Swansea University, Swansea, West Glamorgan, United Kingdom
  • Obaid, Daniel R., Morriston Hospital, Swansea, Wales, United Kingdom

CT coronary artery calcium (CAC) predicts future cardiac events. Inflammation and deranged bone mineralisation may contribute to atherogenesis and arterial calcification. We compared progression of CAC in unit and nocturnal haemodialysis patients.


Patients commencing unit haemodialysis (UHD=7) and nocturnal haemodialysis (NHD=10) were prospectively enrolled. CAC scores (Agatson) were obtained at 0 and 12 months. Inflammatory (hsCRP, IL-18, hepcidin) and bone mineralisation (PO4-, Ca2+, PTH) biomarkers were obtained at 0, 3 and 12 months.


Groups were well matched for age, gender, aetiology of ESRD and cardiovascular risk factors. Average baseline CAC scores were similar between UHD and NHD but significant progression occurred only in UHD (Figure). The relative increase in CAC score was significantly higher for UHD (71.2%) than NHD (6.7%), p=0.04.

Over the study there were no significant changes in markers of bone mineralisation or inflammation for either group except patients undergoing NHD had a significant reduction in IL-18 (117pg/ml ± 59 to 75pg/ml ± 30, p=0.04).

Significant CAC progression (increase in CAC >20AU and >15% occurred in 4/7 (57%) of UHD patients compared with 2/10 (20%) undergoing NHD. CAC scores regressed in 1/7 (14%) of UHD patients and 4/10 (40%) of NHD. Hepcidin was the only biomarker associated with CAC progression, it was higher in the progressors: 370pg/mL [321– 398] than regressors: 243pg/ml [138–349], p=0.045 with increase in CAC score correlated to the level hepcidin r=0.51.


Extended hours NHD significantly decreased progression of CAC compared with UHD. Progression appeared to be more dependent on levels of inflammation than deranged bone mineralisation with hepcidin the best predictor of CAC progression, but larger scale studies are required.


  • Private Foundation Support