The Bony Issue of Cardiovascular Disease After Kidney Transplantation.

Abstract

People living with kidney failure have a significant burden of cardiovascular disease (CVD), which is their leading cause of death.1 Although kidney transplantation is successful at attenuating this CVD risk, generic and transplant-specific cardiometabolic risk factors contribute to posttransplantation cardiovascular morbidity and mortality.2 Our success as an international transplant community in improving short-term outcomes has led to a shift in focus to strategies that can lead to improvement of long-term outcomes after kidney transplantation. Reducing the burden of CVD and the spectrum of cardiometabolic risk factors that contribute to morbidity and mortality is therefore of critical importance if we wish to improve the longevity and quality of life of kidney transplant recipients. All kidney transplant recipients should be considered at heightened CVD risk and counseled as such before transplantation, but some patients are likely to be at greater risk. Although these individuals may be identifiable based on risk factor stratification, biomarkers that provide added value over-and-above risk factor profiling would be of clinical value. Serum osteoprotegerin (OPG) is a key regulator in bone metabolism and has been implicated in the pathophysiology of CVD.3 To date, no study has investigated the role of serum OPG as a biomarker and its association with CVD events after kidney transplantation.