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 Twitter

Kidney Week

Abstract: TH-PO139

Progression of Endothelial Dysfunction, Atherosclerosis, and Arterial Stiffness in Kidney Transplant Patients

Session Information

Category: Transplantation

  • 1802 Transplantation: Clinical

Authors

  • Junarta, Joey, St. George's, University of London, London, United Kingdom
  • Hojs, Nina, University Clinical Centre Maribor, Maribor, Slovenia
  • Lowe-Jones, Racquel M., St. George's, University of London, London, United Kingdom
  • Kaski, Juan carlos, St. George's, University of London, London, United Kingdom
  • Banerjee, Debasish, St. George's, University of London, London, United Kingdom
Background

Cardiovascular events are the commonest cause of mortality and morbidity in kidney transplant recipients, yet little is known about the changes in vascular structure and function with time. This pilot study investigated changes vascular structure and function over time, in stable kidney transplant patients (KTxPs) compared to controls.

Methods

Brachial artery flow-mediated dilation (FMD), nitroglycerine-mediated dilation (NMD), carotid-femoral pulse wave velocity (cf-PWV), ankle-brachial pressure index (ABPI), and common carotid artery intima-media thickness (CCA-IMT) were assessed in 18 KTxPs and 17 controls at baseline and 3-6 months after. All subjects were recruited after written consent and all measurements were done in our vascular laboratory under standard conditions.

Results

There were more dyslipidaemics in KTxPs compared to controls (10 vs. 3; P=0.02). There was no difference in age (51.28 ± 13.29 vs. 45.82 ± 10.85; P=0.19), body mass index (25.56 ± 5.18 vs. 24.59 ± 2.59; P=0.49), or diabetes status (3 vs. 0; P=0.08). No difference existed in vascular markers between KTxPs and controls at baseline: FMD (4.34 ± 3.45 vs. 4.63 ± 3.02 %; P=0.79), NMD (15.15 ± 6.08 vs. 16.00 ± 5.47 %; P=0.67), cf-PWV (7.83 ± 1.76 vs. 6.96 ± 1.26 m/s; P=0.10), ABPI (1.27 ± 0.15 vs. 1.18 ± 0.08; P=0.47), CCA-IMT (5.73 ± 0.95 vs. 5.54 ± 1.08 mm; P=0.05).
Vascular measurements did not change in controls upon follow-up (see table 1). In KTxPs, FMD decreased (-1.52 ± 2.74 %; P=0.03), cf-PWV increased (0.62 ± 1.06 m/s; P=0.03), and CCA-IMT increased (0.35 ± 0.53 mm; P=0.02).

Conclusion

Markers of vascular structure and function worsened in stable kidney transplant patients follow-up. We propose that after initial improvement in cardiovascular health immediate post-transplant; the newly acquired cardio-vascular risk factors, immunosuppression and persistent mild CKD may cause further deterioration explaining the elevated risk for CV events.

Table showing the changes in vascular abnormalities over time in kidney transplant patients and controls