AN ATYPICAL CASE: POST-PARTUM AHUS

S SO1,2, E FISCHER1, B BOSE1,3
1Department of Renal Medicine, Nepean Hospital, Kingswood, Australia, 2Department of Renal Medicine, Westmead Hospital, Westmead, Australia, 3University of Sydney, Nepean Clinical School, Kingswood, Australia

Background: Hypertensive complications of pregnancy, such as pre-eclampsia, are the leading cause of AKI in pregnancy globally. However, features of these syndromes can overlap with thrombotic microangiopathies (TMAs). Delayed treatment of TMAs correlate with worse renal outcomes
Case Report: A 27-year-old primigravida presented at 36 weeks gestation, with abdominal discomfort and hypertension. This is on a background of spina bifida with associated paraplegia. On Day 2, she had an emergency caesarean section for obstructed labour, complicated by postpartum haemorrhage, requiring blood transfusion. Coagulation profile was unremarkable.Immediately post-operatively, she developed oliguric acute kidney injury and haemolysis as demonstrated by reduced haptoglobin, elevated lactate dehydrogenase (LDH), fragmented red cells and raised reticulocyte count. She also had deranged liver function tests (LFTs). It was thought her presentation was due to severe pre-eclampsia/HELLP syndrome.She was commenced on dialysis. Although LFTs normalised within days, she remained dialysis-dependent with ongoing haemolysis. Vasculitic and autoimmune screen was unremarkable and direct antiglobulin test was negative. ADAMTS13 activity was normal. Ongoing haemolysis and renal impairment was considered more consistent with aHUS. She commenced Eculizumab on Day 10. By Day 28, she had ceased haemodialysis and haemolytic markers had normalised. Two years post-discharge, her renal function stabilised with a creatinine of 95 umol/L and there is no evidence of haemolysis.As she did not have risk factors for relapse and negative genetic testing for aHUS mutations, eculizumab was ceased after two years, without any evidence of relapse thus far.
Conclusions: Due to clinical overlap, hypertensive complications of pregnancy can be difficult to differentiate from TMAs. This differential should not be overlooked in patients who have ongoing haemolysis or end-organ dysfunction post-partum.


Biography:
Dr So is a second-year renal advanced trainee in the Western Sydney renal network.

MICROALBUMINURIA AS AN EARLY PREDICTOR OF PREECLAMPSIA IN THE PRE-GESTATIONAL DIABETIC POPULATION

M ZEN1,2, S PADMANABHAN1,  W CHEUNG1,2,  A KIRBY1, S JESUDASON 4, T  ALAHAKOON1,3, V LEE1,2
1Westmead Hospital, Westmead, Australia, 2University of Sydney, Sydney, Australia, 3Westmead Institute for Maternal & Fetal Medicine, Westmead, Australia, 4Central and Northern Adelaide Renal and Transplantation Service, Royal Adelaide Hospital, Adelaide, Australia

Background: Microalbuminuria is an established marker of endothelial cell dysfunction and micro-vascular disease, and a hallmark of diabetic nephropathy. Outside of pregnancy, uACR is a well-validated tool in the diagnosis and prognosis of renal disease. In contrast, little is known about the utility of uACR in predicting adverse pregnancy outcomes within the obstetric population.
Aim: To determine if microalbuminuria can be used as a predictive marker of preeclampsia (PE) and adverse pregnancy and neonatal outcomes in women with pre-existing diabetes and to compare the prognostic utility of urinary albumin to creatinine ratio (uACR) and urinary protein to creatinine ratio (uPCR) and their ability to predict PE.
Methods: This is a multicentre prospective cohort study of 158 women with pre-existing diabetes. A spot uPCR and uACR was performed in each trimester and pregnancy and fetal outcomes were investigated using linear and logistic regression models and receiver operating characteristic (ROC) curves.
Results: Increasing levels of both uPCR and uACR in trimester 3 were associated with the occurrence of PE (p = 0.007, 0.010 respectively). In the 113 patients with normal pregnancy uPCR (<30mg/mmol) in trimester 1, microalbuminuria was found to be predictive of PE (p = 0.01) and need for operative delivery (p = 0.03).
Conclusions: In women with pre-existing diabetes, uPCR and uACR have similar ability to diagnose PE, but microalbuminuria demonstrates prognostic ability at a much earlier gestation, prior to the onset of other signs or symptoms of PE. We therefore suggest that assessing microalbuminuria rather than overt proteinuria in trimester 1 provides prognostic information in women with pre-existing diabetes and that early diabetic nephropathy confers a worse prognosis compared to diabetes without nephropathy.


Biography:
Dr Zen is an obstetric fellow at Westmead Hospital. Her current research interest is in prediction, pathogenesis and outcomes of preeclampsia.

IDENTIFYING BABIES BORN TO MOTHERS RECEIVING RENAL REPLACEMENT THERAPY IN SOUTH AUSTRALIA (SA) 1991-2013: AN ANZDATA AND PERINATAL DATA LINKAGE STUDY

G AARTI1, S MCDONALD1,2, S JESUDASON2
1Australian and New Zealand Dialysis and Transplant Registry, Adelaide, Australia, 2Central and Northern Adelaide Renal and Transplantation Service (CNARTS),  Royal Adelaide Hospital, Adelaide, Australia

Aim: To explore the birth rates of babies born to mothers requiring renal replacement therapy (RRT).
Background: Pregnancy in women receiving Renal Replacement Therapy (RRT) is uncommon but potentially high-risk. Accurate prevalence rates in the Australian population are unknown. ANZDATA collects parenthood data but we suspect it is potentially under-reported.
Methods: We linked SA mandatory perinatal data collection records for births > 20 weeks gestation or 400g birth weight occurring in 1991-2013, with ANZDATA (1978-2015) to identify babies born to mothers within the ANZDATA cohort. RRT modality at conception was calculated from gestational age.
Results: Of 440863 births in SA during the study period, 299 babies were born to 192 women who received RRT at any time in their life to 2015 at a rate of 0.68 births /1000 births. Of these, 162 women had a pregnancy only before starting RRT; 33 had a Pregnancy after starting RRT; and 3 had pregnancies both before and after. Overall there were 49 babies born,10 babies were born to women receiving chronic dialysis at conception (0.02 /1000 births); 2 women started dialysis during pregnancy and 39 were born to mothers who had functioning transplant at conception ( 0.09 /1000 births). During 1991-2013, Only 38 births in SA with gestational age > 20 weeks were reported to ANZDATA (3 to dialysed mothers, 33 to transplanted mothers; 2 women commenced chronic dialysis during pregnancy).
Conclusions: Linking ANZDATA with mandatory perinatal data records identifies more births than those reported to ANZDATA directly. Having identified these births, detailed perinatal data that is not captured by ANZDATA can be analysed to better understand the impact of RRT on pregnancy outcomes.


Biography:
Dr Shilpa Jesudason, MBBS, PhD, FRACP, is a Staff Specialist Nephrologist and Chair of the Clinical Research Group at the Royal Adelaide Hospital’s Central Northern Adelaide Renal and Transplant Service (CNARTS). Her clinical and research interests include Parenthood in Patients with Kidney Disease. She runs a Renal Pregnancy Clinic for preconception counselling, antenatal and postnatal care, and her research program employs a broad array of methodologies (population data linkage, registry, cohort studies, qualitative, systematic reviews, basic science) to investigate parenthood outcomes for women and men with renal disease. She is also the Clinical Director of Kidney Health Australia

SAFETY OF RENIN-ANGIOTENSIN SYSTEM BLOCKERS IN EARLY PREGNANCY: A POPULATION-BASED STUDY

B AHMED1, D TRAN1, H ZOEGA3, S KENNEDY2, L JORM1, A HAVARD1
1Centre for Big Data Research in Health, University of New South Wales, Sydney, Australia, 2School of Women’s & Children’s Health, University of New South Wales , Sydney, Australia, 3Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland

Aims: To explore whether use of renin-angiotensin system (RAS) blockers in early pregnancy is associated with adverse perinatal outcomes.
Background: Previous research that reported adverse perinatal outcomes following first trimester exposure to angiotensin converting enzyme inhibitors (ACEIs), was limited by the use of non-hypertensive women as controls. We examined outcomes of pregnancies with first trimester exposure to RAS blockers, whilst controlling for underlying hypertension.
Methods: Perinatal data for all deliveries in New South Wales, between 2005 and 2012 were linked to hospital discharge and pharmaceutical dispensing records. Analyses were restricted to women who were concessional beneficiaries and had chronic hypertension. Outcomes of interest were preterm delivery, caesarean section, low birth weight (LBW) and small for gestational age (SGA). We used multivariable logistic regression, adjusting for demographics and comorbidity. Pregnancies exposed to ACEIs and angiotensin receptor blockers (ARBs), were compared with pregnancies exposed to methyldopa. We excluded pregnancies if RAS blockers were used beyond first trimester.
Results: There were 456 births to women with chronic hypertension, who received either ACEIs (n=67), ARBs (n=73) or methyldopa (n=316) during first trimester. Compared with pregnancies exposed to methyldopa, the adjusted odds ratio (aOR) for ACEI exposure was 0.5 (95% CI: 0.2 – 1.1) for preterm delivery, 0.6 (0.2 – 1.3) for LBW, 0.8 (0.4 – 1.9) for SGA, and 1.6 (0.8 – 3.1) for caesarean section. The corresponding aORs for ARB exposure were 0.7 (0.3 – 1.5), 1.3 (0.7 – 2.6), 1.2 (0.6-2.6) and 1.2 (0.6 – 2.4).
Conclusion: Adverse perinatal outcomes related to RAS blocker use restricted to first trimester were not observed, however the possibility of an association cannot be ruled out due to limited power.


Biography:
Sean is a Head of Nephrology at Sydney Children’s Hospital Randwick and senior lecturer in the School of Women’s & Children’s Health,University of New South Wales.

SIRT1 ATTENUATES KIDNEY DISORDERS IN OFFSPRING DUE TO MATERNAL HIGH-FAT FEEDING

L NGUYEN1, C MAK2,  H CHEN2, A ZAKY1, C POLLOCK1, S SAAD1
1KOLLING INSTITUTE, ST. LEONARDS, AUSTRALIA, 2UNIVERSITY OF TECHNOLOGY, SYDNEY, ULTIMO, AUSTRALIA

Background: Maternal high-fat feeding (MHF) has been associated with kidney damage and dysfunction in male offspring. Our previous study suggested that the downregulation of Sirtuin (SIRT)1, an essential regulator of metabolic stress responses, might underline the effect.
Aim: We aimed to test the hypothesis that SIRT1 overexpression or activation in the offspring early in life can attenuate kidney disorders due to MHF.
Methods: Diet-induced obese female C57BL/6 mice were crossed with heterozygous SIRT1-transgenic (Tg) male mice to produce both Wild-type (WT) and Tg offspring. Alternatively, SIRT1 activator SRT1720 (25mg/kg/2days i.p) was administrated in WT offspring from week 3 to week 9 of age. Offspring mice were studied at weaning or postnatal week 9 and examined for metabolic and kidney disorders.
Results: Perinatal SIRT1 overexpression improved MHF offspring’s metabolic profiles and kidney antioxidant capacity, while suppressing inflammation and fibrotic markers. SRT1720 administration in MHF offspring weaned on the high-fat diet also improved glucose homeostasis and attenuated renal lipotoxicity, oxidative stress, and fibrogenesis markers, suggesting attenuated kidney disorders in the animals. Urinary albumin creatinine ratio, however, was not improved.
Conclusion: The findings support the important roles of SIRT1 in fetal programming and suggest that SIRT1 therapy can mitigate the development of chronic kidney diseases early in life due to maternal obesity.


Biography:
Long Nguyen recently completed his PhD in Prof. Carol Pollock’s lab at the Kolling Institute. He is interested in studying the etiology of metabolic disorders, especially in regard to fetal programming. His current research focuses on Sirt1, a metabolic sensor involved in caloric restriction and senescence.

INCREASED EXPRESSION OF 6-PHOSPHOFRUCTO-2-KINASE/FRUCTOSE-2,6-BISPHOSPHATASE ISOFORMS IN URINARY EXOSOMES IN PRE-ECLAMPSIA

R ELLIS1,2, M KATERELOS2,4, N COOK2, K PAIZIS2, S WALKER3, S CHOY2,  G PELL3, P MOUNT1,2,4,5, D POWER1,2,4,5
1The University of Melbourne, Parkville, Australia, 2Austin Health, Heidelberg, Australia, 3Mercy Hospital for Women, Heidelberg, Australia, 4Institute for Breathing and Sleep Kidney Laboratory, Heidelberg, Australia, 5Equal senior authors

Aim: To detect and characterise the expression and phosphorylation of glycolytic regulatory proteins in urinary exosomes of normotensive non-pregnant (NC), normotensive pregnant (NP) and pre-eclamptic (PE) subjects.
Background: Some kidney diseases are characterised by a switch in energy metabolism from predominant fatty acid oxidation to aerobic glycolysis, where glycolysis without mitochondrial oxidation becomes the preferred energy source. The principal regulator of glycolysis in cells is 6-phosphofructokinase-2-kinase/fructose-2,6-bisphosphatase (PFK2). To determine whether there may be a switch to aerobic glycolysis in the kidney in women with pre-eclampsia, we studied expression and phosphorylation of PFK2 isozymes in urinary exosomes.
Methods: A cross sectional study of NC (n=19), NP (n=23) and PE (n=33) subjects was performed. Exosomes were isolated from urine samples using differential ultracentrifugation techniques. Exosomal content was analysed by Western blot and computer densitometry for expression and phosphorylation levels of three PFK2 isozymes (PFKFB2, PFKFB3 and PFKFB4).
Results: There was a 9.9-fold increase in PFKFB2 phosphorylated at Ser483 in PE compared to NP (p<0.0001). Expression of phosphorylated PFKFB2 at Ser466 was more common with PE, present in 72.72% (95% CI=55.6-85.1%) of PE and 8.70% (95% CI=1.3-28.0%) of NP samples (p<0.0001). PFKFB3 expression was more frequent with PE, detected in 93.9% (95% CI=79.4-99.3%) of PE and 8.70% (95% CI=1.3-28.0%) of NP samples (p<0.0001). PFKFB4 expression was increased 6.5-fold in PE compared to NP (p=0.0003). No significant differences between NP and NC groups were observed.
Conclusions: Renal expression and activating phosphorylation of PFK2 isoforms is increased in women with pre-eclampsia. Activity of these enzymes is predicted to increase glycolysis, suggesting that there may be a switch in metabolism in the kidneys of women with pre-eclampsia to aerobic glycolysis.


Biography:
Rachael Ellis is a final year Doctor of Medicine student at The University of Melbourne, where she also obtained her Bachelor of Science in 2014. She has recently completed her project with the Nephrology Department at Austin Health and the Institute for Breathing and Sleep (Kidney Laboratory), looking into changes in renal metabolism that can be detected in urinary exosomes of patients with pre-eclampsia.

THROMBOTIC MICROANGIOPATHY IN PREGNANCY WITH TYPE 1 DIABETES MELLITUS: A CASE REPORT

B LAZARUS1, A LU1, M TEE1
1Monash Health, Clayton, Australia

A 26-year-old primiparous female was referred at 20 weeks gestation with a thrombotic microangiopathy (TMA) of unclear cause in the setting of poorly controlled type 1 diabetes mellitus. She reported fatigue and mild pedal oedema, but was otherwise asymptomatic and normotensive. Routine investigations demonstrated a microangiopathic haemolytic anemia (haemoglobin [Hb] 70 g/L, moderate schistocytes, haptoglobin <0.06 g/L, LDH 747 U/L) and new thrombocytopenia (platelets 98×10^9/L from 273×10^9/L in early pregnancy). Her renal function was preserved (serum creatinine [sCr] 50 micromol/L, urea 6.6 mmol/L), but there was microscopic hematuria (370 x10^6 cells/L) with glomerular morphology, and heavy proteinuria (urine protein:creatinine ratio 0.5g/mmol) in the setting of baseline macroalbuminuria (pre-pregnancy urine albumin:creatinine ratio 132mg/mmol). Foetal morphology and Doppler studies were normal. Thrombotic thrombocytopenic purpura was excluded (ADAMTS13 activity 95%). Regular blood transfusions were required to maintain a Hb > 80 g/L. Renal function worsened slightly (sCr 85umol/L, urea 14mmol/L) over a period of two weeks, and kidney biopsy demonstrated moderately advanced diabetic nephropathy and TMA without glomerular endotheliosis. Genetic testing for a panel of atypical haemolytic uraemic syndrome (aHUS) genes returned a heterozygous mutation of unknown significance in exon 2 of the CFI gene (c.292A>G, p.Thr98Ala). Eculizumab was commenced for presumed aHUS, however there was minimal improvement in platelet count, renal function and blood transfusion frequency. Over the subsequent 5 weeks she developed hypertension, hyperreflexia, and increased proteinuria. Caesarean section was successfully performed at 27+4 weeks for pre-eclampsia. Within 48 hours her platelet count normalised, haemolysis substantially improved and renal function stabilized (sCr 96 micromol/L, eGFR 71 ml/min), however hypertension persisted. We discuss our approach to distinguishing the cause of TMA in this challenging case.


Biography:
Ben is a renal registrar at Monash Health.

A COHORT STUDY UTILISING BIOCHEMICAL ASSESSMENT OF ASPIRIN RESISTANCE VS NON-COMPLIANCE IN HIGH-RISK PREGNANT WOMEN

R SHANMUGALINGAM1,2,3, XS WANG6, K CHAU3,4, B XU3, G LEE1, R KUMAR, A HENNESSY1,2,3, A MAKRIS1,2,3,5
1South Western Sydney Local Health District, Liverpool, Australia, 2Western Sydney University, , Australia, 3Heart Research Institute, , Australia, 4University of Sydney, , Australia, 5University of New South Wales, , Australia, 6Bosch Mass Spectrometry Facility, Bosch Institute, Sydney Medical School, University of Sydney, SYDNEY, Australia

Aim: To examine the incidence of aspirin non-compliance and resistance and compare this against self-reported compliance. To examine clinical outcomes against biochemical compliance.
Background: Benefit of low-dose aspirin in preventing preeclampsia is well established. Despite prescription of aspirin, 30-40% of women develop preeclampsia. Aspirin-resistance and non-compliance has not been examined in high-risk pregnant women and could, in-part, explain the lack of clinical response.
Methods: Sequential recruitment of high-risk pregnant women was undertaken in metropolitan hospitals. Clinical data with a 3-point questionnaire and plasma collection was undertaken at 8 time-points (12,16,20,24,28,32,36,38 weeks gestation). Blood samples were assessed for PFA 100 (platelet function analyser) and plasma salicylate acid (SA) detection through liquid-chromatography, mass-spectrometry (LCMS). Non-compliance was defined as normal PFA100 and non-detectable plasma SA in <90% timepoints. Resistance was defined as a normal PFA100 but detectable plasma SA. Clinical outcomes were compared between compliant and non-compliant women prescribed aspirin <16 weeks of gestation. Statistical analysis utilised chi-squared analysis and linear regression(SPSSv24).
Results: Seventy-one women completed the protocol. Biochemical non-compliance was identified in 22(31%) women and only 45(63%) of women’s self-reported compliance corresponded biochemically (kappa coefficient=0.65)). No women were aspirin resistant. Clinical outcomes of women compliant and non-compliant with aspirin were significantly different. Compliant women had a lower incidence of late-onset preeclampsia (4.1% vs 59% %,p<0.001), lower blood pressure (p=0.01) and were more than 34 weeks of gestation at delivery (96% vs 81%,p=0.02). Incidence of early-onset preeclampsia (2% vs 18%, p=0.001) and IUGR was lower (4.1% vs 23% p=0.003), favouring > 90% compliance.
Conclusion: Aspirin non-compliance is more likely than aspirin resistance and self-reporting is not a reliable measure. Women who are non-compliant have worse clinical outcomes.


Biography:
Dr.Shanmugalingam is a Nephrologist with an interest in obstetric medicine. She is currently undertaking her PhD in examining the role of aspirin in preventing preeclampsia

EFFECT OF PREVENTATIVE LOW-DOSE ASPIRIN TREATMENT ON EXPERIMENTAL PREECLAMPSIA INDUCED BY TNF-α IN PREGNANT MICE

K CHAU1,2, B XU1, A HENNESSY1,2,3, A MAKRIS1,4
1Heart Research Institute, Newtown, Australia, 2Sydney Medical School, University of Sydney, Sydney, Australia, 3School of Medicine, Western Sydney University , Campbelltown, Australia, 4The Renal Unit, Liverpool Hospital, Liverpool, Australia

Aim: To evaluate the effect of preventative treatment with low-dose aspirin (LDA) in a mouse model of experimental preeclampsia (EPE) induced by tumour necrosis factor-α (TNF-α) infusion.
Background: LDA is prescribed as a preventative treatment for women at risk of preeclampsia but its mechanism of action is uncertain. Treatment with LDA is effective when commenced prior to 16 weeks’ gestation suggesting a potential effect of LDA on placental development but this remains unproven.
Methods: Pregnant C57/BL6 mice were treated from gestational day (gd) 10 daily with oral LDA plus intraperitoneal 100 µL of phosphate buffered saline (PBS) or PBS only. Mice were allocated to one of 3 experimental arms: 1) Animals (n=5 per group) were euthanised on gd13 to assess the effect of LDA in early pregnancy; 2) Animals had continuous blood pressure (BP) measurement by intra-arterial radio-telemetry (n=5 per group) and had EPE induced by continuous TNF-α (500 ng/kg/day) infusion from gd13; 3) Animals (n=3 per group) had EPE induced as above and live placenta magnetic resonance imaging (MRI) in an 11.74 Tesla spectrometer on gd17. Animals in arms 2 and 3 were euthanized at gd17 and blood, urine and tissue samples were collected. Data was analysed with GraphPad Prism 7.
Results: LDA animals euthanised at gd13 demonstrated increased placenta PlGF (p=0.02) mRNA expression as compared with controls. In animals with EPE there was no difference in BP (p=1), proteinuria (p>0.9) or T2 labyrinthine/junctional zone ratio (p=1) at gd17 between control and LDA treated animals.
Conclusions: LDA administered in early pregnancy increases placenta PlGF mRNA expression but this does not influence the subsequent development of EPE features induced by TNF-α infusion.


Biography:
Dr Katrina Chau is a renal physician at Blacktown Hospital and is completing a PhD in preeclampsia under the supervision of A/Prof Angela Makris and Prof Annemarie Hennessy.

MITOCHONDRIAL ANTIOXIDANT PREVENTS METABOLIC AND RENAL DYSFUNCTION INDUCED BY MATERNAL SMOKING

G LI1,2,3, C LUNG2, S SUKJAMNONG1, B OLIVER1,2, S SAAD1,3, H CHEN1
1University Of Technology Sydney, Sydney, Australia, 2Woolcock Institute of Medical Research, Sydney, Australia, 3Kolling Institute of Medical Research, Sydney, Australia

Background: Maternal smoking during pregnancy leads to range of health complications in the offspring including type 2 diabetes and chronic kidney disease. Previous studies from our team suggest that the development of these conditions are closely related to tissue mitochondrial damage induced by maternal smoking. MitoQ is a mitochondrial targeted antioxidant, with the potential in treating mitochondrial dysfunction related disorders. However, the impacts of maternal MitoQ supplementation during gestation on metabolic and renal outcomes in offspring from the smoking mothers are unknown.
Aim: To investigate the impacts of maternal MitoQ supplementation on the metabolic and renal disorders induced by maternal smoking in a mouse model.
Methods:Female Balb/c mice were either exposed to air or cigarette smoke for six weeks prior to mating and throughout gestation and lactation. A subset of the cigarette exposed mice were supplemented with MitoQ during gestation and lactation. Male offspring underwent intraperitoneal glucose tolerance test at 12 weeks and kidneys and livers were collected at 13 weeks for further analysis.
Results: Maternal smoking reduced birth weight, kidney weight and liver weight in the offspring. Offspring from smoke exposed mothers also had impaired glucose tolerance, renal pathology combined with abnormal hepatic lipid metabolic markers. Maternal MitoQ supplementation was able to restore birth weight, glucose metabolic disorders, renal pathology and hepatic lipid metabolic markers. Maternal MitoQ supplementation also restored renal and hepatic mitochondrial density and oxidative stress.
Conclusions: Maternal MitoQ supplementation can reverse mitochondrial dysfunction and associated disorders induced by maternal smoking in offspring mice, suggesting a potential therapeutic role of mitochondrial targeted antioxidants in the development of metabolic and renal disease.


Biography:
I am a PhD candidate at the University of Technology Sydney where I am investigating the impacts of maternal cigarette smoke exposure on mitochondrial dysfunction and the related metabolic and renal disorders.

About ANZSN

The ASM is hosted by Australian and New Zealand Society of Nephrology.

The aims of the Society are to promote and support the study of the kidney and urinary tract in health and disease, and to ensure the highest professional standards for the practice of nephrology in Australia and New Zealand.

Conference Managers

Please contact the team at Conference Design with any questions regarding the Annual Scientific Meeting

© 2015 - 2016 Conference Design Pty Ltd