IMPROVING CARDIOVASCULAR OUTCOMES THROUGH PHOSPHATE LOWERING IN CKD? – BASELINE CHARACTERISTICS OF PARTICIPANTS IN THE ‘IMPACT OF PHOSPHATE REDUCTION ON VASCULAR END-POINTS IN CHRONIC KIDNEY DISEASE’ (IMPROVE-CKD) STUDY

N LIOUFAS1,2, N TOUSSAINT1,2, E PEDAGOGOS3, G ELDER4,5, S BADVE6, E PASCOE7,8,  A VALKS8, C HAWLEY7,8,9, ON BEHALF OF THE IMPROVE-CKD TRIAL INVESTIGATORS
1The Royal Melbourne Hospital, Parkville, Australia, 2The University of Melbourne, Parkville, Australia, 3Epworth Healthcare, Melbourne, Australia, 4Westmead Hospital, Westmead, Australia, 5Garvan Institute of Medical Research, Darlinghurst, Australia, 6St.George Hospital, Sydney, Australia, 7University of Queensland, Woolloongabba, Australia, 8Australasian Kidney Trials Network, Brisbane, Australia, 9Princess Alexandra Hospital, Woolloongabba, Australia

Background: Hyperparathyroidism, hyperphosphataemia and progression of chronic kidney disease (CKD) have been associated with worsening vascular calcification and an increase in cardiovascular morbidity and mortality. Few placebo-controlled studies involving the management of Chronic Kidney Disease-Mineral Bone Disorder (CKD-MBD) have assessed effects on arterial compliance, vascular calcification and mitigation of cardiovascular risk in CKD.
Methods: The IMPROVE-CKD study is a multi-centre, placebo-controlled, randomised trial assessing the effects of lanthanum carbonate, a non-calcium-based phosphate binder, on surrogate markers of cardiovascular disease in patients with CKD over a 96-week period. Inclusion criteria are patients with CKD stages 3b-4 with serum phosphate >1.00mmol/L. The primary outcome is change in pulse wave velocity (PWV), and secondary outcomes include changes in aortic calcification (computed tomography), left ventricular mass index (MRI), serum phosphate, parathyroid hormone (PTH) and FGF-23, and bone mineral density.
Results: 278 patients were recruited in total across 17 sites (Australia 206; New Zealand 31; Malaysia 41), 33% with CKD3b and 67% CKD4. Baseline demographics of participants included mean age 62.7+/-12.5 years, 69.4% male, 64.6% Caucasian, and mean BMI 29.9+/-6.0kg/m2. 45% were diabetic, 89.9% had hypertension, and 32.1% had known cardiovascular disease. Primary cause of CKD was diabetic nephropathy (30.3%) followed by renovascular disease (16.2%). Mean (+/-SD) serum phosphate was 1.25+/-0.2mmol/L, calcium 2.32+/-0.13mmol/L, and creatinine 221.4+/-59.4µmol/L (eGFR 26.6+/-8.3ml/min/1.73m2). Median (IQR) PTH was 13.0(7.7-20.6)pmol/L and median proteinuria was 0.79(0.18-1.7)g/day. Mean PWV was 10.6+/-3.5m/s and augmentation index 27.9+/-10.1%. Baseline CT scans showed 82.3% of participants had aortic calcification.
Conclusion: The IMPROVE-CKD study will be the largest and longest placebo-controlled trial to date assessing phosphate control in pre-dialysis CKD, with important end-points of arterial compliance and vascular calcification.


Biography:
Dr Nicole Lioufas has recently completed her FRACP as a nephrologist and is currently undertaking a PhD at The Royal Melbourne Hospital in the area of CKD-MBD.

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