HYPONATREMIA FOLLOWING ADMINISTRATION OF CANDESARTAN

G MAULANA1, R PRASANTO2, I KUSWADI3
1Renal and Hypertension Division, Internal Medicine Department,  Sardjito Hospital, Yogyakarta, Indonesia, 2Renal and Hypertension Division, Internal Medicine Department,  Sardjito Hospital, Yogyakarta, Indonesia, 3Renal and Hypertension Division, Internal Medicine Department,  Sardjito Hospital, Yogyakarta, Indonesia

Background: Hyperpotassemia is a common side effect of inhibitors of the renin–angiotensin–aldosterone system, but however hyponatremia is rarely case. We report a case of hyponatremia attributable to angiotensin II receptor blocker (ARB) therapy.
Case Report:  A 66-year-old man with nausea, vertigo, and loss of appetite presented to a hospital because of hyponatremia after administration of 16 mg candesartan once daily for 3 weeks. Three weeks after withdrawal of candesartan, serum Na concentrations improved. Diagnoses of hyponatremia caused by candesartan were made.
Conclusion: ARBs are useful antihypertensive drugs, their administration may cause both hyperpotassemia and hyponatremia.


Biography:
Gusti Hariyadi Maulana is a internist from Banjarbaru, South Kalimantan who currently studying Nephrology in Yogyakarta. He got Young Investigator Award in PIT PERNERI 2017 (2017 Annual Indonesia Nephrology Congres)

CORONARY ARTERY DISEASE IN END STAGE KIDNEY DISEASE, A DIAGNOSTIC CHALLENGE

A ELFORD1, E LUTTRELL2, M  MATHEW2
1Royal Hobart Hospital, Hobart, Australia, 2Launceston General Hospital, Launceston, Australia

Background: Cardiovascular disease is the leading cause of death amongst the end stage kidney disease (ESKD) population in Australia. Despite this high prevalence, it remains a diagnostic challenge to identify significant coronary artery disease (CAD). This population group establish CAD more rapidly, progress faster than the normal population and are more likely to present with atypical symptoms.
Case Report: To review two cases of symptomatic CAD  emphasising the diagnostic challenges to clinicians and importance for high clinical suspicion of CAD in ESKD patients.
First case: 74 year old female with ESKD presented with atypical central chest pain. This was on the background of shortness of breath on exertion and a normal echocardiogram 10 days prior. Serial troponins were mildly elevated. A clinical diagnosis of  costochondritis was made. Subsequent coronary angiogram showed a 90% lesion in the mid left anterior descending artery (LAD). Angioplasty and stenting of this lesion relieved her symptoms.
Second case: 85 year old female with ESKD presented with one week of intermittent shortness of breath on exertion. She never had typical chest pain. A coronary angiogram 9 months earlier showed 30-40% disease in major vessels. She was discharged home and booked for an urgent outpatient echocardiogram. She presented within 48 hours with severe shortness of breath. Echocardiogram revealed new inferolateral regional wall motion abnormality. Angiogram showed 80% culprit lesions in the mid LAD and ostial branch of the LAD.
Conclusion: These two cases expose the complexity of CAD in the ESKD population. Our cases demonstrate how much faster CAD can progress in ESKD patients, the tendency to present atypically and the need to investigate and treat with urgency to avoid adverse outcomes.


Biography:
I am a second year basic physician trainee from Tasmania. My previous research projects have included the successful implementation of a Rapid Access Chest Pain Assessment Clinic at the Royal Hobart Hospital. My research passions include improving clinical service as well as well as improving diagnostic recognition. As well as medicine, I love getting out and about in beautiful Tasmania

MAGNESIUM CITRATE REDUCES OXIDATIVE STRESS IN UREMIA-RELATED VASCULAR CALCIFICATION RATS

Z YAO1
1Nephrology Department, The Second Affiliated Hospital Of Xi’an Jiaotong University, Xi’an, China

Background and Aim: Oxidative stress (OS) is an important risk factor for vascular calcification (VC). Magnesium citrate (MgCit) had proven effective at preventing VC in uremic rats in our previous study. Conclusions about the relationships between magnesium (Mg) supplementation and OS levels varied among laboratories. The objective of this research was to investigate the effects of MgCit on OS in uremia-related VC rats.
Methods: Rats were divided into five groups: the control group (normal diet); the MgCit control group (normal diet with MgCit); the model group (0.75% adenine and 0.9% phosphorus diet); model rats with low dose MgCit (375mg/kg) and model rats with high dose MgCit (750 mg/kg). All rats were sacrificed at day 43 with blood and aortas. VC-related staining, levels of superoxide dismutase (SOD) and malonaldehyde (MDA) in serum and aorta, aorta dihydroethidium staining and mitochondria morphology of vascular smooth muscle cells (VSMCs) were detected.
Results: Uremia model group had extensive VC and highly increased OS compared with control group, including the increased MDA and reduced SOD levels in serum and aortas, increased superoxide anion contents in aortas and mitochondria morphology damage of VSMCs. Treatment with MgCit reduced the extent of VC, reduced MDA and increased SOD levels in serum and aortas, reduced superoxide anion contents in aortas and improved mitochondrial damage of VSMCs.
Conclusions: MgCit reduces the extent of OS and VC in uremic rats, so its protective effects on uremia-related VC may be associated with reducing OS.


Biography:
Zhihui Yao is a Ph.D student in Nephrology Department from the Second Hospital of Xi’an Jiaotong University (Xi’an, China). Now she is pursuing a year abroad study to further enrich her PhD training in University of California, Irvine. Zhihui Yao has been studying vascular calcification in vascular smooth muscle cells and rats model with chronic renal failure for 3 years. In previous study, she focused on how deficiency of the Nrf2 transcription factor may impact vascular health and liver expression of blood anti-calcification factors. She published 2 English papers as the first author in this field.

DIETHYL CITRATE ATTENUATES VASCULAR CALCIFICATION IN AN ADENINE-INDUCED CHRONIC RENAL FAILURE RAT MODEL

Z YAO1, B GUI1, X MA1, S MA1
1Nephrology Department, The Second Affiliated Hospital Of Xi’an Jiaotong University, Xi’an, China

Background and Aim: Diethyl citrate (Et2Cit) is a new anticoagulant drug synthesized by our team. We verified its inhibitory effects on vascular smooth muscle cells (VSMCs) calcification induced by high phosphorus in our previous study. This research aimed to investigate the inhibitory effects of Et2Cit on vascular calcification (VC) in adenine-induced chronic renal failure (CRF) rats and to determine an anticoagulant drug that also inhibits VC in vivo.
Methods: Rats were divided into 4 groups: the control group (normal diet); the model group (0.75% adenine and 0.9% high phosphorus diet from day 1 to 28); the low-dose Et2Cit group (model rats with 750 mg/kg Et2Cit from day 1 to 42); and the high-dose Et2Cit group (model rats with 1500 mg/kg Et2Cit from day 1 to 42). The rats were euthanized at day 43 with blood and aortas collections. Then biochemical indices in serum, von-Kossa staining, calcium and phosphorus contents, alkaline phosphatase (ALP) activity, alpha smooth muscle actin (α-SMA) protein and runt-related transcription factor 2 (RUNX2) protein expressions in aortas were assessed.
Results: CRF model group had extensive VC compared with control group. Compared to CRF model group, treatment with Et2Cit dose-dependently reduced the area of VC, reduced phosphorus and calcium contents in serum and aortas (P < 0.05) without reducing blood urea nitrogen (BUN) and creatinine (Cr) levels (P > 0.05). Also, Et2Cit treatment group had lower ALP activity, lower RUNX2 protein expressions and higher α-SMA protein expressions than model group.
Conclusions: Et2Cit prevented VC in adenine-induced CRF rats, thus may be a potential drug for both anticoagulation and VC prevention in CRF patients.


Biography:
Professor Gui is the director of Nephrology Department from the Second Hospital of Xi’an Jiaotong University (Xi’an, China). He has been doing research in anticoagulation therapy in hemodialysis patients for more than 10 years. Considering the inevitable side effects of sodium citrate during the anticoagulation process, he designed and synthesized diethyl citrate and verified its anticoagulation effects. He published 20 English papers as the first or the correspondence author in nephrology field.

IMPACT OF DIETARY SODIUM REDUCTION ON ESTIMATED GLOMERULAR FILTRATION RATE IN CHRONIC KIDNEY DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS

A KANG1, F NERBASS2,3, R PECOITS-FILHO1,2,3, B NEAL1, M JARDINE1
1The George Institute for Global Health, University Of New South Wales, Sydney, Newtown, Australia, 2Pro-Rim Foundation, Joinville, Brazil, 3Pontificia Universidade Catolica do Parana, , Curitiba, Brazil

Aim: Determine the short and long-term impact of dietary sodium reduction on estimated glomerular filtration rate (eGFR) in chronic kidney disease (CKD).
Background: Dietary sodium reduction improves blood pressure (BP), an important predictor of CKD progression. In healthy subjects, sodium restriction leads to a short-term reduction in eGFR. The long-term effects of dietary sodium reduction have greater clinical importance.
Methods: We performed a systematic review of randomised controlled trials of higher versus lower sodium consumption in people with CKD (eGFR<60ml/min or as defined by study authors). We searched the Cochrane central register of controlled trials, MEDLINE, EMBASE, and clinicaltrials.gov with a pre-specified strategy. Two reviewers independently assessed studies and extracted data. Outcomes included eGFR, albuminuria and BP. Prespecified subgroups were short- and long-term (<3 months, ≥3 months) study duration. The effect on outcomes was meta-analysed using random effects models.
Results: From 2245 references, 20 trials were identified reporting outcomes of interest representing 1038 people with CKD. Mean follow-up was 8.1[range:1-24] weeks with only 3 trials ≥3 months. Separation in dietary sodium was achieved through either dietary (15) or combined sodium supplementation +/- dietary-based (5) interventions. Lower dietary sodium improved BP (SBP-5.83[-7.78 to -3.88]/ DBP-2.92[-3.88 to -1.95]mmHg). There was no overall difference in eGFR (-0.39[-3.13 to 2.35]ml/min/1.73m2, heterogeneity I² 55%) or albuminuria (1.13[-1.42 to 1.12] mg/day I² 0%). Trial duration made no difference to the impact of lower dietary sodium on eGFR (short-term -3.40[-8.12 to 1.31]; long-term 1.69[-0.58 to 3.96]ml/min/1.73m2, p 0.06.
Conclusion: In CKD, dietary sodium reduction improves BP but not albuminuria. With few longer term studies, there is currently insufficient evidence to determine the long-term effect of sodium reduction on renal function.


Biography:
Amy Kang is nephrologist and PhD student at the George Institute for Global Health, UNSW, Sydney.

PROFILING CARDIAC BIOMARKERS PREDICTS CARDIAC PATHOPHYSIOLOGY IN URAEMIC CARDIOMYOPATHY.

A CROSTHWAITE1,2,  R LIM3, R MASTERSON4, E VELCOSKA2, A HEDLEY1, L BURRELL2,  M ROBERTS6, O FAROUQUE1,2, F IERINO7,2
1Department of Nephrology, Austin Health, Heidelberg, Australia, 2Department of Medicine, University of Melbourne, , Australia, 3Department of Radiology, Austin Health, Heidelberg, Australia, 4Department of Nephrology, Melbourne Health, Parkville, Australia, 5Department of Cardiology, Austin Health, Heidelberg, Australia, 6Department of Renal Medicine, Eastern Health Clinical School, Monash University, Box Hill, Australia, 7Department of Nephrology, St. Vincent’s Hospital Melbourne, Fitzroy, Australia

Aim: Define cardiac structural and functional changes and serum cardiac biomarker profile in end-stage kidney disease (ESKD).
Background: “Uraemic Cardiomyopathy” describes various cardiac structural and functional abnormalities in chronic and ESKD. Cardiac biomarkers predict clinical outcomes and represent surrogate markers of pathophysiological processes defined by cardiac magnetic resonance imaging (cMRI).
Method: Baseline data from two prospective observational cohort studies in adults with ESKD. All patients underwent transthoracic echocardiography (TTE), cMRI, stress nuclear cardiac perfusion imaging (rNPI) and measurement of cardiac biomarkers (angiotensin converting enzyme 2 (ACE2) activity, high-sensitivity cardiac troponin T (hscTnT) and N-terminal proBNP (NT-proBNP).
Results: Patient characteristics (n=65) were: mean age 52.6±14.0 years, 74% male, 83% requiring dialysis with median cumulative dialysis vintage 1.92 (0.59,4.79) years and previous renal transplant recipients (22%). Cardiovascular risk factors were prevalent: Hypertension (92%), Dyslipidaemia (72%), Diabetes (22%), Smoking (46%) and known cardiovascular disease (34%).26(44%) and 30(47%) had LV hypertrophy and 14(23%) and 7(11%) had LV systolic dysfunction by cMRI and TTE criteria respectively. 30(48%) had diastolic dysfunction. Baseline mean cMRI LVMI (80g/m2, 95%CI 74-85) and median LVEF 64%(57,67) were normal. 11(18%) demonstrated perfusion defects (rNPI).Geometric mean hs-cTnT (41.7ng/L 95%CI 33.8-51.9), NT-proBNP (608ng/L 95%CI 407-898) and median ACE2 activity (19.5pmol/mL/min IQR 10.4,25.3) were elevated.Hs-cTnT (r=0.71 p<0.001)  and ACE2 (r=0.61 p<0.001) correlated with LVMI(cMRI). Hs-cTnT predicted LVH(cMRI) (ROC AUC 0.84 95%CI 0.73-0.94) and diastolic dysfunction (TTE) (ROC AUC 0.75 95%CI 0.62–0.87). NT-proBNP predicted systolic dysfunction (cMRI) (ROC AUC 0.75 95%CI 0.62-0.88). ACE2 predicted diastolic dysfunction (TTE) (ROC AUC 0.67 95%CI 0.54-0.82).
Conclusion: Elevated cardiac biomarkers are common in ESKD and highly predictive of cardiac structural/functional changes. Further work defining profiles for clinical application are in progress.


Biography:
Amy Crosthwaite is a Nephrologist, General and Obstetric Physician and PhD candidate at the University of Melbourne. Her research examines the cardiac structural and functional changes associated with chronic and end-stage kidney disease and the impact of renal transplantation and extended hours haemodialysis.

MULTIFACTORIAL INTRADIALYSIS PULMONARY OEDEMA. REAL TIME MEASUREMENT DURING DIALYSIS USING SWAN GANZ CATHETER TO EVALUATE CAUSES OF THE PULMONARY OEDEMA

R SHETTIGAR1
1Dunedin Public Hospital, New Zealand, Dunedin, New Zealand

Background: Intradialytic pulmonary oedema is associated with hypotension and hypoxaemia and leads to difficult to manage haemodialysis sessions. We believe this is the first reported case where Swan Ganz catheter measurements were undertaken during dialysis to evaluate this phenomenon.
Case report: A 71 year old woman presented with dysponea and progressive kidney injury requiring dialysis. Four months prior she underwent an open AAA repair complicated by intraoperative hypotension requiring a single haemodialysis session.   Echocardiogram showed moderate mitral stenosis, Atrial Fibrillation with preserved ejection fraction.She was commenced on dialysis with rate control for resistant tachycardia. Severe acute pulmonary oedema developed soon after the commencement of each dialysis session with hypoxia and hypotension. A coronary angiogram revealed LAD and RCA lesions treated with PCI.  Unfortunately intradialytic pulmonary oedema continued. Right heart catheterization with continuous measurements of right and left sided pressures was then performed during dialysis. This showed diastolic dysfunction with pulmonary capillary wedge pressure 29mmHg (<12) prior to commencing dialysis. Thirty minutes into dialysis there was an acute elevation in the pulmonary arterial pressure (from 35 to 58mmHg) and pulmonary capillary wedge pressures increased to 48mmHg.  The impression was this signified severe diastolic dysfunction with moderate mitral stenosis – not amenable for operative intervention.Due to these events the decision was made to cease further attempts at haemodialysis and a PD catheter was inserted.
Conclusions: Mitral stenosis with severe diastolic dysfunction triggered rapid elevations in left and right sided heart pressures during dialysis led to recurrent severe intradialytic pulmonary oedema which rendered ongoing haemodialysis impossible.


Biography:
I am first year nephrology advance trainee at Dunedin Hospital. I graduated from Mumbai, India before moving to Dunedin 5 years ago. Before taking up full time clinical role, I worked as a Teaching fellow at Medical schools both in Otago and Auckland. I have a huge interest in Transplant medicine and would like to pursue in career in the same.

HYPERTENSION AND DIABETES DIFFERENTIALLY AFFECT RENAL REACTIVE OXYGEN SPECIES AND CATECHOLAMINE CONTENT

A WATSON1, P PRATAMA1,  S PENFOLD1,  E GOULD2,  S GRAY2, G LAMBERT3, G HEAD2, K JANDELEIT-DAHM1
1Department Of Diabetes, Monash University, Melbourne, Australia, 2Baker Heart and Diabetes Institute, Melbourne, Australia, 3Swinburne University of Technology, Melbourne, Australia

Aims: To examine changes in renal function, sympathetic nerves and the oxidative status of the kidney in diabetic mice with and without concomitant hypertension.
Background: Patients with both diabetes and hypertension develop nephropathy at an accelerated rate. Using the hypertensive Schlager mouse as a model, we examined changes in the kidney from diabetic mice with and without concomitant hypertension.
Methods: After 10 weeks of study, hypertensive BPH/2J and normotensive BPN/3J Schlager mice with and without concomitant streptozotocin induced diabetes (5x 55 mg/kg i.p.) were placed in metabolic cages (24hr) before kidneys were harvested; alternatively BP telemetry probes were implanted.
Results: Induction of diabetes did not change the hypertensive status of BPH mice (MAP 131±4 vs. 129±4 mmHg for non-diabetic vs. diabetic BPH, n=5 &6). Diabetes induced albuminuria in both strains however diabetic BPH showed significantly greater albuminuria than diabetic BPN (1205±196 vs. 439±73 μg/24hr, n=8, 7). Plasma cystatin C was significantly lower in diabetic animals with no difference between strains. HPLC measurement of cortical noradrenaline showed significantly greater levels in BPH mice. Diabetic mice of both strains had significantly less renal noradrenaline. Renal cortical hydrogen peroxide formation was increased in non-diabetic BPH mice. While activity of catalase was increased in non-diabetic BPH mice it was significantly less in diabetic BPH animals (non-diabetic vs. diabetic BPH 104±8 vs. 63±6 nmol/min/ml, n=8/gp).
Conclusions: Hypertensive mice show greater renal oxidative stress than normotensive mice however diabetic hypertensive animals also demonstrated lower catalase activity, indicating a compromised ability to deal with hypertensive lead increases in oxidative stress. This could contribute to greater renal neuropathy and which may underlie the poor outcome for patients with hypertensive diabetic nephropathy.


Biography:
After working in autonomic neurobiology at the Florey Institute (Melbourne) and at the German Institute for Human Nutrition (Potsdam, German) Anna Watson completed her PhD at the Florey Institute investigating neural and humoral control of the heart. She then moved into the field of diabetic cardiovascular and renal complications (Baker Institute, Melbourne) before moving to the newly formed Department of Diabetes (Monash University). She is currently investigating the role of neural signalling in the development of diabetic nephropathy and hypertension.

 

CARDIOVASCULAR MORTALITY RATES IN PEOPLE WITH END-STAGE KIDNEY DISEASE WITH PRE-EXISTING CARDIOVASCULAR DISEASE

N DE LA MATA1 P KELLY1, A WEBSTER1,2
1Sydney School Of Public Health, The University Of Syd, Camperdown, Australia, 2Centre for Renal and Transplant Research, Westmead Hospital, Westmead, Australia

Aim:To estimate cardiovascular mortality rates and graft failure rates for people receiving dialysis and kidney transplant recipients in Australia and New Zealand, stratified by pre-existing cardiovascular disease (CVD).
Background:People with ESKD have a high burden of cardiovascular deaths.
Methods:We included incident ESKD patients in Australia,1980-2013 and New Zealand,1988-2012 from ANZDATA. We ascertained primary cause of death from data linkage with national death registries and patient related data from ANZDATA. Age-specific mortality rates were estimated by dividing the number of deaths by person-years (pys) of follow-up, stratified by age at ESKD treatment initiation, ESKD treatment (dialysis or transplant) and pre-existing CVD.
Results:Our analysis included 60,823 ESKD patients, with 8,223 cardiovascular deaths and 26,094 other deaths over 381,878pys. Of the 17,415 kidney transplant recipients, there were 4,145 graft failures over 136,930pys. The prevalence of CVD was 34.8% (95%CI:34.4-35.2%) in dialysis patients and 8.4% (95%CI:8.0-8.8%) in transplant recipients. Among dialysis patients, the cardiovascular mortality rate was almost double in those with CVD compared to without CVD in all ages, at 45.7 (95%CI:43.4-48.2)/1000pys versus 23.5 (95%CI:22.3-24.7)/1000pys in people aged 45-64yrs. Non-cardiovascular mortality rates were also higher among those with CVD compared to without CVD in all ages, at 116.9 (95%CI:113.1-120.8)/1000pys versus 82.8 (95%CI:80.7-85.0)/1000pys in people aged 45-64yrs. Mortality rates were similar in kidney transplant recipients with or without CVD, at 10.7 (95%CI:8.3-13.7)/1000pys and 8.0 (95%CI:7.3-8.8)/1000pys for cardiovascular deaths, and at 30.7 (95%CI:26.5-35.5)/1000pys and 23.4 (95%CI:22.1-24.8) for other deaths in recipients aged 45-64yrs. Graft failure rates did not differ by pre-existing CVD.
Conclusions:Dialysis patients with CVD experienced higher cardiovascular and non-cardiovascular mortality rates. While kidney transplant recipients with CVD had similar mortality and graft failure rates to those without CVD.


Biography:
Nicole De La Mata is an early career researcher and biostatistician working with Sydney School of Public Health, The University of Sydney. She has previous experience in managing and utilizing large observational cohorts to evaluate patient outcomes and influence health  policy. Her interests include cohort studies, data linkage and survival analysis. Her current research focuses on health outcomes in people with end-stage kidney disease (ESKD), living kidney donors and organ transplant recipients.

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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