Impact of augmenting dialysis frequency and duration on cardiovascular function.
Conventional hemodialysis (CHD) only delivers 10% to 15% of renal function in a nonphysiological intermittent mode. Because it occurs nightly and is sustained over a longer dialysis time, the uremic clearance provided by nocturnal hemodialysis (NHD) far exceeds that of CHD. Increasing the dose and frequency of dialysis by NHD has been demonstrated, in both short- and long-term studies, to reverse several important risk factors for adverse cardiovascular events in patients with end-stage renal disease such as hypertension, left ventricular hypertrophy, systolic dysfunction, conduit artery stiffness, attenuated baroreflex regulation of heart rate, disturbed heart rate variability, sleep apnea, and endothelium-dependent vasodilation. In addition, the Toronto NHD experience has reported an emerging body of evidence demonstrating the benefits of NHD on anemia management, inflammation, and endothelial progenitor cell biology. The mechanism(s) by which nocturnal hemodialysis improves cardiovascular outcomes are under active investigation by our group. It is tempting to speculate that NHD has the potential to decrease endothelial/myocardial injury and restore simultaneously endothelial repair, thereby improving cardiovascular function in patients with end-stage renal disease. The objectives of the present document are (1) to review the mechanisms underlying dialysis-associated cardiovascular morbidity and (2) to describe the restorative potential of NHD on the cardiovascular system.
Ly
Joseph
J
Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada.
Chan
Christopher T
CT
D001071:Appointments and Schedules; D002318:Cardiovascular Diseases / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D006437:Hemodialysis, Home / Q000379:methods*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000473:pathology