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


The Latest on Twitter

Kidney Week

Abstract: TH-PO230

Recombinant Erythropoietin Reduces Endothelium-Mediated Vasodilation in Patients with CKD – A Prospective Controlled Study

Session Information

Category: Anemia and Iron Metabolism

  • 202 Anemia and Iron Metabolism: Clinical


  • Sun, Zoe Dong yang, University of Cambridge, Cambridge, United Kingdom
  • Selvarajah, Viknesh, University of Cambridge, Cambridge, United Kingdom
  • Hubsch, Annette, University of Cambridge, Cambridge, United Kingdom
  • Pritchard, Nicholas R., Cambridge University Hopitals NHS Foundation Trust, Cambridge, United Kingdom
  • Cheriyan, Joseph, University of Cambridge, Cambridge, United Kingdom
  • Wilkinson, Ian, University of Cambridge, Cambridge, United Kingdom
  • Hiemstra, Thomas F., University of Cambridge, Cambridge, United Kingdom

Recombinant erythropoietin (rhEPO) is used for the treatment of CKD-associated anaemia, despite the hypertension and cardiovascular risks. Postulated mechanisms include endothelial dysfunction. Given the emergence of non-rhEPO treatments, elucidating the vascular effects of rhEPO in CKD-associated anaemia is important for comparative studies with non-rhEPO treatments.


We conducted a single centre open-label prospective non-randomised matched-control study in pre-dialysis rhEPO-naïve patients with CKD (n=12) and matched-healthy controls (n=12) to assess the effect of rhEPO on endothelial function (NCT02987465). Forearm blood flow responses to intra-arterial acetylcholine (ACh endothelium-dependent vasodilator), noradrenaline (NA) and BQ123 (ETA receptor antagonist) were assessed using venous occlusion plethysmography in CKD patients before and 6-weeks after rhEPO and in controls at baseline. Blood pressure, blood parameters and aortic stiffness (carotid-femoral pulse-wave velocity PWV) were measured. The primary outcome was change in log-transformed forearm blood flow compared using mixed-effects ANOVA.


Baseline characteristics were similar between CKD patients and controls (age±SD 65±16 vs 64±16 years, male 83% vs male 83%). Although median eGFR (16, IQR 13-25 vs 83, IQR 78-90 ml/min, p<0.001) and haemoglobin (Hb 97±11 g/L vs 140±9 g/L, p<0.001) were lower, mean arterial pressure (110±21 vs 92±9 mmHg, p=0.02) and PWV (11.5±4.8 vs 8.3±2.2 m/s, p=0.04) were higher in patients with CKD. Response to ACh did not differ significantly between CKD patients and controls at baseline. In the CKD group, rhEPO increased haemoglobin (Hb) to 110 ± 17g/L (p<0.001) after 6 weeks, and reduced endothelium-dependent vasodilation by 23% (95% CI, 5% to 40%, p=0.009). The response to BQ123 did not differ after rhEPO treatment (-5%, 95% CI, -13% to 2%, p=0.15), but there was a greater vasoconstrictor response to NA (10%, 95% CI, 2% to 17%, p=0.01). Blood pressure and arterial stiffness did not change significantly after rhEPO.


Endothelium-dependent vasodilation is impaired after rhEPO treatment in patients with CKD, and NA-induced vasoconstriction is enhanced, suggesting possible mechanisms for rhEPO-associated hypertension and adverse cardiovascular outcomes.


  • Commercial Support