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

Please note that you are viewing an archived section from 2021 and some content may be unavailable. To unlock all content for 2021, please visit the archives.

Abstract: PO1798

Platelet Activity Mediates Enhanced Cardiovascular Risk in Patients with CKD and Peripheral Artery Disease

Session Information

Category: Hypertension and CVD

  • 1402 Hypertension and CVD: Clinical, Outcomes, and Trials

Authors

  • Soomro, Qandeel H., New York University, New York, New York, United States
  • Cofer, Lucas, New York University, New York, New York, United States
  • Xia, Yuhe, New York University, New York, New York, United States
  • Luttrell-Williams, Elliot S., New York University, New York, New York, United States
  • Myndzar, Khrystyna, New York University, New York, New York, United States
  • Charytan, David M., New York University, New York, New York, United States
  • Berger, Jeffrey S., New York University, New York, New York, United States
Background

Chronic kidney disease (CKD) is common in patients with peripheral artery disease (PAD), and both are associated with poor cardiovascular (CV) outcomes. Platelets drive PAD pathogenesis and mediate atherothrombosis. Platelet function in CKD and the related CV risk is unclear. We investigated relationships between CKD, platelet activity, and incident CV events in a cohort of patients with PAD

Methods

The Platelet Activity and Cardiovascular Events (PACE) study enrolled 289 patients with PAD undergoing lower extremity revascularization (LER). CKD was defined as eGFR<60 mL/min/1.73m2 by the CKD-EPI equation. We measured platelet activity via light transmission aggregometry (LTA) in response to submaximal ADP, collagen, serotonin, epinephrine, and arachidonic acid (AA) prior to LER, and followed patients for a median of 18 months. The primary clinical endpoints were myocardial infarction (MI) and a composite of major adverse CV events (MACE; MI, stroke, death).

Results

There were 113 (40%) patients with and 172 (60%) without CKD. Patients with CKD (vs. non-CKD) were older and more likely to be female, Hispanic, have diabetes, heart failure, and critical limb ischemia (P<0.05 for each). There were no significant differences in prevalent coronary artery disease or use of antiplatelet therapy between groups. Platelet aggregation in response to submaximal ADP, serotonin, epinephrine, and AA was elevated in the CKD group (Figure). After multivariable adjustment, patients with CKD were at greater risk of MI (aHR 2.2 [95% CI: 1.02-4.9]; P=0.045) and MACE (1.9 [1.2-3.3]; P=0.01) than those without CKD. Platelet aggregation in response to submaximal agonist stimulation had a 25% and 12% mediating effect on the association of CKD with MI and MACE, respectively

Conclusion

In patients with PAD, CKD was associated with increased platelet activity and CV events. Heightened platelet activity is an important mechanism underlying increased CV risk in CKD