Figure 1.

Mechanisms for excessive CV events in patients with CKD arising from reduced excretion from the kidney or reduced hormone (erythropoietin and calcitriol) production from the kidney. Accumulation of salt and water leads to sympathetic overactivity and renin-angiotensin-aldosterone system activation that results in changes to the left ventricle and arterioles that affect systemic vascular resistance. Accumulation of uremic toxins leads to platelet activation causing endothelial dysfunction that generates oxidative stress and inflammation, which also involves liver and adipocytes. Finally, phosphate retention leads to endothelial dysfunction, which has effects on the parathyroid gland, bone, and vessels. Reduced production of calcitriol adds to parathyroid gland, bone, heart, and vessel problems. Reduced production of erythropoietin leads to anemia that affects heart and vessels. CKD, chronic kidney disease; CV cardiovascular; RAAS, renin-angiotensin systems