Renal dysfunction and acceleration of coronary disease

Abstract

Tens of millions of persons worldwide have combined cardiovascular disease (CVD) and CKD.¹ In the USA alone, over 300 000 individuals are on renal replacement therapy (RRT),² which confers a five- to 40-fold increased risk of fatal cardiovascular events.^{3w1 w2} CKD is commonly defined as an estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m², or the presence of a raised urinary albumin to creatinine ratio > 30 mg/g on a spot urine sample. Although conventional risk factors such as hypertension, diabetes mellitus, and dyslipidaemia are commonly associated with CKD and its attendant long term CVD morbidity, these risk factors alone do not fully explain the prevalence of CVD in this population.⁴ Figure 1 depicts the independent and dominant effect of renal disease on coronary heart disease death rates among diabetics. Novel risk factors such as homocysteinaemia (Hcy), raised lipoprotein Lp(a), oxidative stress, endothelial dysfunction, diminished transforming growth factor β1 (TGF-β1), chronic inflammation, and vascular calcification are increasingly linked to accelerated rates of atherogenesis in the setting of CKD. Furthermore, patients with CKD have inferior clinical outcomes following percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) independent of procedural success.