Abstract

BackgroundNightly extended hours hemodialysis may improve left ventricular hypertrophy and function and endothelial function but presents problems of sustainability and increased cost. The effect of alternate nightly home hemodialysis (NHD) on cardiovascular structure and function is not known.MethodsSixty-three patients on standard hemodialysis (SHD: 3.5-6 hours/session, 3-5 sessions weekly) converted to NHD (6-10 hours/session overnight for 3-5 sessions weekly). 2Dimensional transthoracic echocardiography and ultrasound measures of brachial artery reactivity (BAR), carotid intima-media thickness (CIMT), total arterial compliance (TAC) and augmentation index (AIX) were performed post dialysis at baseline and 18-24 months following conversion to NHD. In 37 patients, indices of oxidative stress: plasma malonyldialdehyde (MDA) and anti-oxidant enzymes: catalase (CAT), glutathione peroxidase (GPX) and superoxide dismutase (SOD) activity and total antioxidant status (TAS) were measured at baseline, 3 and 6 months.ResultsLeft ventricular mass index (LVMI) remained stable. Despite significant derangement at baseline, there were no changes in diastolic function measures, CIMT, BAR and TAC. AIX increased. Conversion to NHD improved bone mineral metabolism parameters and blood pressure control. Interdialytic weight gains increased. No definite improvements in measures of oxidative stress were demonstrated.ConclusionsDespite improvement in uremic toxin levels and some cardiovascular risk factors, conversion to an alternate nightly NHD regimen did not improve cardiovascular structure and function. Continuing suboptimal control of uremic toxins and interdialytic weight gains may be a possible explanation. This study adds to the increasing uncertainty about the nature of improvement in cardiovascular parameters with conversion to intensive hemodialysis regimens. Future randomized controlled trials will be important to determine whether increases in dialysis session duration, frequency or both are most beneficial for improving cardiovascular disease whilst minimizing costs and the impact of dialysis on quality of life.

Highlights

  • Extended hours hemodialysis may improve left ventricular hypertrophy and function and endothelial function but presents problems of sustainability and increased cost

  • Vascular disease occurs in two main forms: 1) arteriosclerosis with diffuse arterial wall dilatation, thickening, fibrosis and calcification resulting in stiffening and 2) atherosclerosis with abnormal endothelial function and patchy intimal plaques, causing abnormal regulation of vascular tone, fibrinolysis and smooth muscle proliferation with narrowing or obstruction of the arterial lumen

  • Demographic Data and Dialysis Prescription Eighty-seven percent of the eligible home hemodialysis population agreed to participate in the study

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Summary

Introduction

Extended hours hemodialysis may improve left ventricular hypertrophy and function and endothelial function but presents problems of sustainability and increased cost. Left ventricular hypertrophy (LVH), dilatation and systolic and diastolic dysfunction are common and independently associated with mortality [2,3]. These changes are postulated to result from chronic volume overload (due to salt and water retention, chronic anemia and arteriovenous fistulae), pressure overload (due to hypertension, atherosclerosis, vascular and cardiac valvular calcification), metabolic (acidosis, malnutrition, inflammation and oxidative stress) and neuroendocrine factors (renin-angiotensin-aldosterone and sympathetic activation) [4,5]. Vascular disease occurs in two main forms: 1) arteriosclerosis with diffuse arterial wall dilatation, thickening, fibrosis and calcification resulting in stiffening and 2) atherosclerosis with abnormal endothelial function and patchy intimal plaques, causing abnormal regulation of vascular tone, fibrinolysis and smooth muscle proliferation with narrowing or obstruction of the arterial lumen. The resulting increased pressure load on the left ventricle (LV) during systole promotes LV hypertrophy and the reduced pressure in diastole reduces coronary artery perfusion, promoting myocardial ischemia [6,7]

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