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Background The cause of kidney failure is unknown in approximately 10% of patients with stage 5 chronic kidney disease (CKD). For those who first present to nephrology care with kidney failure, standard investigations of serology, imaging, urinalysis and kidney biopsy are limited differentiators of etiology. We aimed to determine the diagnostic utility of whole-genome sequencing (WGS) with analysis of a broad kidney gene panel in patients with kidney failure of unknown cause. Methods We prospectively recruited 100 participants who reached CKD stage 5 at 50 years of age and had an unknown cause of kidney failure after standard investigation. Clinically-accredited WGS was performed in this national cohort after genetic counselling. The primary analysis was targeted to 388 kidney-related genes with second-tier genome-wide and mitochondrial analysis. Results The cohort was 61% male and the average age of participants at stage 5 CKD was 32 years (9 months to 50 years). A genetic diagnosis was made in 25% of participants. Disease-causing variants were identified across autosomal dominant tubulointerstitial kidney disease (6), glomerular disorders (4), ciliopathies (3), tubular disorders (2), Alport syndrome (4) and mitochondrial disease (1). Most diagnoses (80%) were in autosomal dominant, X-linked or mitochondrial conditions (UMOD; COL4A5; INF2; CLCN5; TRPC6; COL4A4; EYA1; HNF1B; WT1; NBEA; m.3243A>G). Patients with a family history of CKD were more likely to have a positive result (OR 3.29, 95% CI 1.10-11.29). Thirteen percent of participants without a CKD family history had a positive result. In those who first presented in stage 5 CKD, WGS with broad analysis of a curated kidney-disease gene panel was diagnostically more informative than kidney biopsy, with biopsy being inconclusive in 24 of 25 participants. Conclusions In this prospectively ascertained Australian cohort, we identified a genetic diagnosis in 25% of patients with kidney failure of unknown cause.

Objectives: To examine the association between type 2 diabetes mellitus, with and without diabetic nephropathy, and cardiovascular disease-related mortality in dialysis-dependent patients with end-stage kidney disease (ESKD); to determine whether this association is affected by the age of the patient. Design, setting, participants: Prospective population cohort analysis of Australia and New Zealand Dialysis and Transplant Registry data for all patients with incident ESKD who commenced dialysis in Australia or New Zealand during 1980e2014. Outcome measures: Primary outcome: Cardiovascular diseaserelated mortality; secondary outcome: All-cause mortality. Result(s): Of 56 552 patients followed for a median 2.5 years (total, 193 549 person-years), 15 829 (28.0%) had type 2 diabetes and diabetic nephropathy; 4993 (8.8%) had type 2 diabetes and non-diabetic nephropathy. Cardiovascular diseaserelated mortality during the first 10 years of dialysis was significantly higher for patients with diabetes/diabetic nephropathy (277 deaths per 1000 patients; 95% CI, 270e284) or diabetes/non-diabetic nephropathy (220 deaths per 1000 patients; 95% CI, 208e231) than for patients without type 2 diabetes (136 deaths per 1000 patients; 95% CI, 133e140). The risk of cardiovascular disease-related mortality was greater for patients with diabetes/diabetic nephropathy (adjusted hazard ratio [aHR], 1.63; 95% CI, 1.56e1.72) or diabetes/non-diabetic nephropathy (aHR, 1.31; 95% CI, 1.23e1.41) than for patients without diabetes. The excess risk associated with having diabetes was greater for younger than for older patients. Conclusion(s): Mortality risk is higher for patients with incident ESKD commencing dialysis who also have type 2 diabetes than for patients without diabetes, particularly among patients under 50 years of age, and the risk was more pronounced in patients for whom ESKD was attributed to diabetic nephropathy.Copyright © 2018 AMPCo Pty Ltd. Produced with Elsevier B.V. All rights r

Purpose: Risk scores may aid risk quantification and decision-making in kidney transplantation. The Living Kidney Donor Profile Index (LKDPI) was developed to choose between living donors. The original LKDPI is moderately discriminatory (Harrel's C Statistic=0.59,95% CI 0.55-0.61) but poorly calibrated in Australia/New Zealand. We developed a risk prediction score for overall graft survival in adult recipients of a living kidney donor transplant in an Australian and New Zealand population. Method(s): Using data from the Australia and New Zealand Dialysis and Transplant Registry, we included adult recipients of living kidney donor transplants over 2004-2018. We constructed Cox models for overall graft survival. We refit the original USA variables and then constructed a new model (ANZ LKDPI) considering all available potential covariates. Model performance was validated by assessing discrimination and calibration. Result(s): 4049 living donors were included. The C-statistic for the re-fit model was 0.57(95%CI 0.54-0.59). The remodeled score included the new variables history of hypertension and HLA-A mismatches. Variables excluded were donor:recipient weight ratio, HLA-B, both male, and ABO incompatibility. The ANZ LKDPI had similar discrimination (C=0.56,95%CI 0.54-0.58). The model fit and calibration was better. Conclusion(s): The ANZ LKDPI had similar discrimination to the original and the refitted LKDPI. The discrimination was low for both scores and so should be used with caution to decide between donors. The new score is better calibrated for our population so could be used to predict individual graft prognosis. (Figure Presented).

Aim: We developed a risk prediction score for overall graft survival in adult recipients of a living kidney donor transplant in an Australian and New Zealand population. Background(s): Risk scores may aid risk quantification and decision-making in kidney transplantation. The Living Kidney Donor Profile Index (LKDPI) was developed to choose between living donors. The original LKDPI is not discriminatory (C = 0.59, 95% CI 0.55-0.62) or well calibrated in Australia/New Zealand. Method(s): Using data from the Australia and New Zealand Dialysis and Transplant Registry, we included adult recipients of living kidney donor transplants over 2004-2018. We constructed Cox models for overall graft survival. We refit the original USA variables and constructed a new model considering all available potential covariates. Model performance was examined by partial validation, bootstrapping, Harrell's C-statistic (C) and Akaike information criterion (AIC). Result(s): 4049 living donors were included; 58.2% were female, 10.4% had hypertension and 18.7% were obese. For the original USA LKDPI the variables of both male and donor: recipient weight ratio were mis-specified. The C-statistic for the re-fit model was 0.57 (95%CI 0.54-0.59). When remodelling the score, the new variables included were history of hypertension and HLA-A mismatches. Variables excluded were donor: recipient weight ratio, HLA-B, both male, and ABO incompatibility. The Aus/NZ LKDPIC-statistic was 0.56 (95%CI 0.54-0.58). Calibration was similar but the Aus/NZ LKDPI had better model fit (AIC: 10402 vs. 11 023). Conclusion(s): The Aus/NZ LKDPI had similar discrimination to the original LKDPI and the LKDPI with adjusted coefficients. The discrimination was low for both scores and so should be used with caution to decide between donors. The new score is better calibrated for our population so could be used to predict graft prognosis.

Rationale & Objective: Mortality is an important outcome for all dialysis stakeholders. We examined associations between dialysis modality and mortality in the modern era. Study Design: Observational study comparing dialysis inception cohorts 1998-2002, 2003-2007, 2008-2012, and 2013-2017. Setting & Participants: Australia and New Zealand (ANZ) dialysis population. Exposure: The primary exposure was dialysis modality: facility hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), automated PD (APD), or home HD. Outcome(s): The main outcome was death. Analytical Methods: Cause-specific proportional hazards models with shared frailty and subdistribution proportional hazards (Fine and Gray) models, adjusting for available confounding covariates. Result(s): In 52,097 patients, the overall death rate improved from ~15 deaths per 100 patient-years in 1998-2002 to ~11 in 2013-2017, with the largest cause-specific contribution from decreased infectious death. Relative to facility HD, mortality with CAPD and APD has improved over the years, with adjusted hazard ratios in 2013-2017 of 0.88 (95% CI, 0.78-0.99) and 0.91 (95% CI, 0.82-1.00), respectively. Increasingly, patients with lower clinical risk have been adopting APD, and to a lesser extent CAPD. Relative to facility HD, mortality with home HD was lower throughout the entire period of observation, despite increasing adoption by older patients and those with more comorbidities. All effects were generally insensitive to the modeling approach (initial vs time-varying modality, cause-specific versus subdistribution regression), different follow-up time intervals (5 year vs 7 year vs 10 year). There was no effect modification by diabetes, comorbidity, or sex. Limitation(s): Potential for residual confounding, limited generalizability. Conclusion(s): The survival of patients on PD in 2013-2017 appears greater than the survival for patients on facility HD in ANZ. Additional research is needed to assess whether ch

Background: The Peritoneal Dialysis Outcomes and Practice Patterns Study (PDOPPS) is an international, prospective study following persons treated by peritoneal dialysis (PD) to identify modifiable practices associated with improvements in PD technique and person survival. The aim of this study was to assess the representativeness of the Australian cohort included in PDOPPS compared to the complete Australian PD population, as reported to the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry. Method(s): Adults with at least one PD treatment reported to ANZDATA Registry during the census period of PDOPPS Phase I (November 2014 to April 2018) were compared to the Australian PDOPPS cohort. The primary outcomes were the representativeness of centres and persons. Secondary outcomes explored the association of person characteristics with consent to study participation. Result(s): After data linkage, 511 PDOPPS participants were compared to 5616 Australians treated with PD. Within centres eligible for PDOPPS, selected centres were similar to other Australian centres. The PDOPPS participants' cohort tended to include older persons, more males, a higher proportion of Caucasians and more persons with higher socioeconomic advantage compared to the Australian PD population. Differences in distribution across sex and ethnicities between the PDOPPS cohort and the overall PD population were in part due to the selection and consent processes, during which females and non-Caucasians were more likely to not consent to PDOPPS participation. Conclusion(s): Sampling methods used in PDOPPS allowed for good national representativeness of the included centres. However, representativeness of the unweighted PDOPPS sample was suboptimal in regard to some participant characteristics.Copyright © The Author(s) 2021.

Social disparity is a major impediment to optimal health outcomes after kidney transplantation. In this study, we aimed to define the association between socio-economic status (SES) disparities and patient-relevant outcomes after kidney allograft failure. Using data from the Australia and New Zealand Dialysis and Transplant registry, we included patients with failed first-kidney allografts in Australia between 2005 and 2017. The association between residential postcode-derived SES in quintiles (quintile 1-most disadvantaged areas, quintile 5-most advantaged areas) with uptake of home dialysis (peritoneal or home haemodialysis) within the first 12-months post-allograft failure, repeat transplantation and death on dialysis were examined using competing-risk analysis. Of 2175 patients who had experienced first allograft failure, 417(19%) and 505(23%) patients were of SES quintiles 1 and 5, respectively. Compared to patients of quintile 5, quintile 1 patients were less likely to receive repeat transplants (adjusted subdistributional hazard ratio [SHR] 0.70,95%CI 0.55-0.89) and were more likely to die on dialysis (1.37 [1.04-1.81]), but there was no association with the uptake of home dialysis (1.02 [0.77-1.35]). Low SES may have a negative effect on outcomes post-allograft failure and further research is required into how best to mitigate this. However, small-scale variation within SES cannot be accounted for in this study.Copyright © 2021 Steunstichting ESOT. Published by John Wiley & Sons Ltd

BACKGROUND: Elevated serum urate levels are associated with progression of chronic kidney disease. Whether urate-lowering treatment with allopurinol can attenuate the decline of the estimated glomerular filtration rate (eGFR) in patients with chronic kidney disease who are at risk for progression is not known. METHODS: In this randomized, controlled trial, we randomly assigned adults with stage 3 or 4 chronic kidney disease and no history of gout who had a urinary albumin: creatinine ratio of 265 or higher (with albumin measured in milligrams and creatinine in grams) or an eGFR decrease of at least 3.0 ml per minute per 1.73 m2 of body-surface area in the preceding year to receive allopurinol (100 to 300 mg daily) or placebo. The primary outcome was the change in eGFR from randomization to week 104, calculated with the Chronic Kidney Disease Epidemiology Collaboration creatinine equation. RESULTS: Enrollment was stopped because of slow recruitment after 369 of 620 intended patients were randomly assigned to receive allopurinol (185 patients) or placebo (184 patients). Three patients per group withdrew immediately after randomization. The remaining 363 patients (mean eGFR, 31.7 ml per minute per 1.73 m2; median urine albumin: creatinine ratio, 716.9; mean serum urate level, 8.2 mg per deciliter) were included in the assessment of the primary outcome. The change in eGFR did not differ significantly between the allopurinol group and the placebo group (-3.33 ml per minute per 1.73 m2 per year [95% confidence interval {CI}, -4.11 to -2.55] and -3.23 ml per minute per 1.73 m2 per year [95% CI, -3.98 to -2.47], respectively; mean difference, -0.10 ml per minute per 1.73 m2 per year [95% CI, -1.18 to 0.97]; P = 0.85). Serious adverse events were reported in 84 of 182 patients (46%) in the allopurinol group and in 79 of 181 patients (44%) in the placebo group. CONCLUSIONS: In patients with chronic kidney disease and a high risk of progression, urate-lowering treatment with a

Background Hyperphosphatemia is associated with increased fibroblast growth factor 23 (FGF23), arterial calcification, and cardiovascular mortality. Effects of phosphate-lowering medication on vascular calcification and arterial stiffness in CKD remain uncertain. Methods To assess the effects of non-calcium-based phosphate binders on intermediate cardiovascular markers, we conducted a multicenter, double-blind trial, randomizing 278 participants with stage 3b or 4 CKD and serum phosphate.1.00 mmol/L (3.10 mg/dl) to 500 mg lanthanum carbonate or matched placebo thrice daily for 96 weeks. We analyzed the primary outcome, carotid-femoral pulse wave velocity, using a linear mixed effects model for repeated measures. Secondary outcomes included abdominal aortic calcification and serum and urine markers of mineral metabolism. Results A total of 138 participants received lanthanum and 140 received placebo (mean age 63.1 years; 69% male, 64% White). Mean eGFR was 26.6 ml/min per 1.73 m2; 45% of participants had diabetes and 32% had cardiovascular disease. Mean serum phosphate was 1.25 mmol/L (3.87 mg/dl), mean pulse wave velocity was 10.8 m/s, and 81.3% had abdominal aortic calcification at baseline. At 96 weeks, pulse wave velocity did not differ significantly between groups, nor did abdominal aortic calcification, serum phosphate, parathyroid hormone, FGF23, and 24-hour urinary phosphate. Serious adverse events occurred in 63 (46%) participants prescribed lanthanum and 66 (47%) prescribed placebo. Although recruitment to target was not achieved, additional analysis suggested this was unlikely to have significantly affected the principle findings. Conclusions In patients with stage 3b/4 CKD, treatment with lanthanum over 96 weeks did not affect arterial stiffness or aortic calcification compared with placebo. These findings do not support the role of intestinal phosphate binders to reduce cardiovascular risk in patients with CKD who have normophosphatemia. Clinical Trial r

BACKGROUND: Elevated serum urate levels are associated with progression of chronic kidney disease. Whether urate-lowering treatment with allopurinol can attenuate the decline of the estimated glomerular filtration rate (eGFR) in patients with chronic kidney disease who are at risk for progression is not known. METHOD(S): In this randomized, controlled trial, we randomly assigned adults with stage 3 or 4 chronic kidney disease and no history of gout who had a urinary albumin: creatinine ratio of 265 or higher (with albumin measured in milligrams and creatinine in grams) or an eGFR decrease of at least 3.0 ml per minute per 1.73 m2 of body-surface area in the preceding year to receive allopurinol (100 to 300 mg daily) or placebo. The primary outcome was the change in eGFR from randomization to week 104, calculated with the Chronic Kidney Disease Epidemiology Collaboration creatinine equation. RESULT(S): Enrollment was stopped because of slow recruitment after 369 of 620 intended patients were randomly assigned to receive allopurinol (185 patients) or placebo (184 patients). Three patients per group withdrew immediately after randomization. The remaining 363 patients (mean eGFR, 31.7 ml per minute per 1.73 m2; median urine albumin: creatinine ratio, 716.9; mean serum urate level, 8.2 mg per deciliter) were included in the assessment of the primary outcome. The change in eGFR did not differ significantly between the allopurinol group and the placebo group (-3.33 ml per minute per 1.73 m2 per year [95% confidence interval {CI}, -4.11 to -2.55] and -3.23 ml per minute per 1.73 m2 per year [95% CI, -3.98 to -2.47], respectively; mean difference, -0.10 ml per minute per 1.73 m2 per year [95% CI, -1.18 to 0.97]; P = 0.85). Serious adverse events were reported in 84 of 182 patients (46%) in the allopurinol group and in 79 of 181 patients (44%) in the placebo group. CONCLUSION(S): In patients with chronic kidney disease and a high risk of progression, urate-lowering treatment

BACKGROUND: Peritoneal dialysis (PD)-related infections lead to significant morbidity. The International Society for Peritoneal Dialysis (ISPD) guidelines for the prevention and treatment of PD-related infections are based on variable evidence. We describe practice patterns across facilities participating in the Peritoneal Dialysis Outcomes and Practice Patterns Study (PDOPPS). METHOD(S): PDOPPS, a prospective cohort study, enrolled nationally representative samples of PD patients in Australia/New Zealand (ANZ), Canada, Thailand, Japan, the UK and the USA. Data on PD-related infection prevention and treatment practices across facilities were obtained from a survey of medical directors'. RESULT(S): A total of 170 centers, caring for >11000 patients, were included. The proportion of facilities reporting antibiotic administration at the time of PD catheter insertion was lowest in the USA (63%) and highest in Canada and the UK (100%). Exit-site antimicrobial prophylaxis was variably used across countries, with Japan (4%) and Thailand (28%) having the lowest proportions. Exit-site mupirocin was the predominant exit-site prophylactic strategy in ANZ (56%), Canada (50%) and the UK (47%), while exit-site aminoglycosides were more common in the USA (72%). Empiric Gram-positive peritonitis treatment with vancomycin was most common in the UK (88%) and USA (83%) compared with 10-45% elsewhere. Empiric Gram-negative peritonitis treatment with aminoglycoside therapy was highest in ANZ (72%) and the UK (77%) compared with 10-45% elsewhere. CONCLUSION(S): Variation in PD-related infection prevention and treatment strategies exist across countries with limited uptake of ISPD guideline recommendations. Further work will aim to understand the impact these differences have on the wide variation in infection risk between facilities and other clinically relevant PD outcomes.Copyright © The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

OBJECTIVES: To examine the association between type 2 diabetes mellitus, with and without diabetic nephropathy, and cardiovascular disease-related mortality in dialysis-dependent patients with end-stage kidney disease (ESKD); to determine whether this association is affected by the age of the patient. DESIGN, SETTING, PARTICIPANTS: Prospective population cohort analysis of Australia and New Zealand Dialysis and Transplant Registry data for all patients with incident ESKD who commenced dialysis in Australia or New Zealand during 1980-2014. OUTCOME MEASURES: Primary outcome: cardiovascular disease-related mortality; secondary outcome: all-cause mortality. RESULT(S): Of 56 552 patients followed for a median 2.5 years (total, 193 549 person-years), 15 829 (28.0%) had type 2 diabetes and diabetic nephropathy; 4993 (8.8%) had type 2 diabetes and non-diabetic nephropathy. Cardiovascular disease-related mortality during the first 10 years of dialysis was significantly higher for patients with diabetes/diabetic nephropathy (277 deaths per 1000 patients; 95% CI, 270-284) or diabetes/non-diabetic nephropathy (220 deaths per 1000 patients; 95% CI, 208-231) than for patients without type 2 diabetes (136 deaths per 1000 patients; 95% CI, 133-140). The risk of cardiovascular disease-related mortality was greater for patients with diabetes/diabetic nephropathy (adjusted hazard ratio [aHR], 1.63; 95% CI, 1.56-1.72) or diabetes/non-diabetic nephropathy (aHR, 1.31; 95% CI, 1.23-1.41) than for patients without diabetes. The excess risk associated with having diabetes was greater for younger than for older patients. CONCLUSION(S): Mortality risk is higher for patients with incident ESKD commencing dialysis who also have type 2 diabetes than for patients without diabetes, particularly among patients under 50 years of age, and the risk was more pronounced in patients for whom ESKD was attributed to diabetic nephropathy.

Introduction: The living kidney donor profile index (LKDPI), developed using US data, has been proposed as a risk score to assist clinicians and recipients in choosing between potential living kidney donors. To do this successfully it must be able to discriminate graft survival. It has not been validated outside the US. We therefore examined the association between LKDPI and living kidney donor transplant outcomes in the Australian and New Zealand population. Method(s): Using data from the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry, we included adult recipients of a living kidney donor transplant in Australia or New Zealand over 2004-2017. We examined the associations between LKDPI and (1) death-censored graft survival, (2) overall graft survival, and (3) patient survival using Cox models with and without adjustment for recipient factors and ischaemic time. The primary outcome was the Harrell's C statistic, indicating the ability of each Cox model to discriminate between those with and without graft failure or death. Result(s): 4,287 transplants met inclusion criteria, of which 3,826 (89%) had enough data to calculate the LKDPI. Median follow-up was 6.7 years, during which 396 grafts failed, 340 recipients died and 83 recipients were lost to follow-up. Recipients of higher risk kidneys (LKDPI >40%, vs <0%) were older, less likely to be male, more likely to be Caucasian, more likely to have coronary disease, cerebrovascular disease and peripheral vascular disease, were more poorly HLA matched and were less likely to have been transplanted previously. On unadjusted analyses the LKDPI demonstrated poor discrimination in predicting death-censored graft survival (C 0.54, figure), overall graft survival (C 0.54) and patient survival (C 0.55). In adjusted models the LKDPI provided no meaningful increase in discrimination compared with models including only recipient factors (table). [Figure presented] [Figure presented] Conclusion(s): The LKDPI de

Introduction Maintaining fluid intake sufficient to reduce arginine vasopressin (AVP) secretion has been hypothesised to slow kidney cyst growth in autosomal dominant polycystic kidney disease (ADPKD). However, evidence to support this as a clinical practice recommendation is of poor quality. The aim of the present study is to determine the long-term efficacy and safety of prescribed water intake to prevent the progression of height-adjusted total kidney volume (ht-TKV) in patients with chronic kidney disease (stages 1-3) due to ADPKD. Methods and analysis A multicentre, prospective, parallel-group, open-label, randomised controlled trial will be conducted. Patients with ADPKD (n=180; age ≤65 years, estimated glomerular filtration rate (eGFR) ≥30 mL/min/1.73 m 2) will be randomised (1:1) to either the control (standard treatment+usual fluid intake) or intervention (standard treatment+prescribed fluid intake) group. Participants in the intervention arm will be prescribed an individualised daily fluid intake to reduce urine osmolality to ≤270 mOsmol/kg, and supported with structured clinic and telephonic dietetic review, self-monitoring of urine-specific gravity, short message service text reminders and internet-based tools. All participants will have 6-monthly follow-up visits, and ht-TKV will be measured by MRI at 0, 18 and 36 months. The primary end point is the annual rate of change in ht-TKV as determined by serial renal MRI in control vs intervention groups, from baseline to 3 years. The secondary end points are differences between the two groups in systemic AVP activity, renal disease (eGFR, blood pressure, renal pain), patient adherence, acceptability and safety. Ethics and dissemination The trial was approved by the Human Research Ethics Committee, Western Sydney Local Health District. The results will inform clinicians, patients and policy-makers regarding the long-term safety, efficacy and feasibility of prescribed fluid intake as an approach to reduce kidn

Aim: To describe the direct and indirect costs incurred by Australian living kidney donors. Method(s): A total of 55 living kidney donors from three centres in Perth, Australia and one centre in Melbourne, Australia (2010-2014) was studied. Forty-nine donors provided information on expenses incurred during the donor evaluation period and up to 3 months after donation. A micro-costing approach was used to measure and value the units of resources consumed. Expenses were grouped as direct costs (ground and air travel, accommodation, and prescription medications) and indirect costs (lost wages and lost productivity). Costs were standardized to the year 2016 in Australian dollars. Result(s): The most common direct costs were for ground travel (100%), parking (76%), and post-donation pain medications or antibiotics (73%). The highest direct costs were for air travel (median $1986 [three donors]) and ground travel (median $459 [49 donors]). Donors also reported lost wages (median $9891 [37 donors]). The inability to perform household activities or care for dependants were reported by 32 (65%) and 23 (47%) donors. Total direct costs averaged $1682 per donor (median $806 among 49 donors). Total indirect costs averaged $7249 per donor (median $7273 among 49 donors). Total direct and indirect costs averaged $8932 per donor (median $7963 among 49 donors). Conclusion(s): Many Australian living kidney donors incur substantial costs during the donation process. Our findings inform the continued development of policies and programmes designed to minimize costs incurred by living kidney donors.Copyright © 2017 Asian Pacific Society of Nephrology

Aim: To examine the association between T2DM with and without diabetic nephropathy and CVD mortality in incident dialysis patients and to determine whether this association was modified by age. Background(s): The overall survival of dialysis-dependent end-stage kidney disease (ESKD) patients with T2DM may be different for those with diabetic nephropathy than those with ESKD attributed to another cause. Method(s): Using data from the ANZDATA Registry, all incident ESKD patients commencing dialysis in Australia and New Zealand between 1980- 2014 were included. The association between diabetes status (i.e. no diabetes, T2DM with ESKD attributed to diabetic nephropathy or T2DM with ESKD attributed to non-diabetic nephropathy) and CVD mortality was examined using adjusted Cox regression and competing risk analyses. Result(s): Of 56,552 patients followed for a median of 2.5 years (193,549 person- years), 15,829 (30.0%) and 4993 (8.8%) had T2DM with diabetic nephropathy and non-diabetic nephropathy, respectively. Compared to patients without diabetes, the adjusted hazard ratio (HR) for CVD mortality was 1.63 (95%CI 1.55-1.71) for patients with T2DM and diabetic nephropathy, and 1.31 (1.22-1.40) for patients with T2DM and non-diabetic nephropathy. There was an interaction between age and CVD mortality (pinteraction<0.001), with the excess risk of CVD mortality being greater in younger patients with T2DM and diabetic nephropathy or T2DM and nondiabetic nephropathy (age <=30 years: 3.25 [1.87, 5.63] and 1.64 [0.71, 3.80]; >70 years: 1.24 [1.13, 1.35] and 1.21 [1.09, 1.34], respectively). Estimates from the competing risk models were similar. Conclusion(s): Prevalent T2DM is associated with a survival disadvantage in incident dialysis patients, particularly younger patients, with this disadvantage more pronounced when ESKD was attributed to diabetic nephropathy as opposed to another cause.

Introduction and Aims: Technique failure is a major complication of peritoneal dialysis (PD) treatment and is associated with significant risk to patients and health services. The first year has been recognised as a particularly vulnerable period, with studies estimating that just under one-half of patients who develop technique failure do so within this time. This study aimed to identify the key risk factors and risk periods for early transfer to haemodialysis or death in incident PD patients. Method(s): Using data from the ANZDATA Registry, this study included all adult patients who commenced PD in Australia and New Zealand between 2000 and 2014. Competing risk regression models were used to analyse the primary outcome, which was technique failure within the first year (kidney transplantation was the competing risk), as well as the secondary outcomes, which examined each cause of technique failure (kidney transplantation and other causes of technique failure were the competing risks). Patients were censored at the time of kidney transplantation, recovery of renal function, loss to follow up, or at 365.25 days after commencement of PD. Result(s): Of 16,748 patients who commenced PD during the study period, 4,389 patients reached the primary outcome. Factors associated with increased risk included age >70 years, diabetes or vascular disease, prior renal replacement therapy, late referral to a nephrology service, or management in a smaller centre. Asian or other race and use of continuous ambulatory PD were associated with reduced risk, as was commencement of PD between 2010 and 2014. Although the risk of technique failure due to death or infection was constant over the first year, mechanical and other causes accounted for a greater number of cases within the initial 9 months of treatment. [Figure Presented] Conclusion(s): Several modifiable and non-modifiable factors are associated with early technique failure. Variation in the principal cause of early technique fai

This is an 18-month prospective, randomized controlled trial (RCT) designed to compare the effect of early conversion from cyclosporin to everolimus/mycophenolic acid (E-MPA) between 3 and 4 months post-transplant to cyclosporin/mycophenolic acid (CsA-MPA) on left ventricular mass index (LVMI) at 3 and 18 months post-transplant (primary outcome). Secondary outcomes included estimated glomerular filtration rate (eGFR), viral infection, and adverse events. Twenty-four patients were randomized in a 1:1 ratio to E-MPA or CsA-MPA groups. There were no significant differences in mean (SD) LVMI at 3 (51.6±18.5 vs 53.7±15.7 g/m 2.7 ) and 18 months (52.7±16.3 vs 51.7±16.8 g/m 2.7 ) between CsA-MPA and E-MPA groups. The incidence of viral infections was reduced in E-MPA compared to CsA-MPA treatment groups (8% vs 50%, P=.02), but the incidences of acute rejection, adverse events, and drug discontinuation were similar between groups. There was an overall increase in eGFR with time (0.04 log- mL/min/1.73 m 2 per 6 months, P=.012) but no significant difference between the two groups across time (0.11 log- mL/min/1.73 m 2 , P=.311). Immunosuppressive regimen comprising early conversion from cyclosporine to everolimus was not associated with a regression of LVMI, but a lower risk of viral infections was observed.

Background: The aim of the present study was to evaluate the predictors of transfer to home hemodialysis (HHD) after peritoneal dialysis (PD) completion. Methods: All Australian and New Zealand patients treated with PD on day 90 after initiation of renal replacement therapy between 2000 and 2012 were included. Completion of PD was defined by death, transplantation, or hemodialysis (HD) for 180 days or more. Patients were categorized as "transferred to HHD" if they initiated HHD fewer than 180 days after PD had ended. Multivariable logistic regression was used to evaluate predictors of transfer to HHD in a restricted cohort experiencing PD technique failure; a competing-risks analysis was used in the unrestricted cohort. Results: Of 10 710 incident PD patients, 3752 died, 1549 underwent transplantation, and 2915 transferred to HD, among whom 156 (5.4%) started HHD. The positive predictors of transfer to HHD in the restricted cohort were male sex [odds ratio (OR): 2.81], obesity (OR: 2.20), and PD therapy duration (OR: 1.10 per year). Negative predictors included age (OR: 0.95 per year), infectious cause of technique failure (OR: 0.48), underweight (OR: 0.50), kidney disease resulting from hypertension (OR: 0.38) or diabetes (OR: 0.32), race being Maori (OR: 0.65) or Aboriginal and Torres Strait Islander (OR: 0.30). Comparable results were obtained with a competing-risks model. Conclusion(s): Transfer to HHD after completion of PD is rare and predicted by patient characteristics at baseline and at the time of PD end. Transition to HHD should be considered more often in patients using PD, especially when they fulfill the identified characteristics.Copyright © 2016 International Society for Peritoneal Dialysis.

Introduction and Aims: Long-term peritoneal dialysis (PD) is often limited by technique failure and a significant proportion of PD patients are eventually transferred to hemodialysis. In countries promoting home dialysis, home hemodialysis (HHD) has been identified as an attractive alternative for patients experiencing PD technique failure. Nonetheless, there is still a paucity of data regarding predictors of transfer to HHD after PD completion, which is the main objective of this study. Method(s): This registry study included all Australian and New Zealand patients treated with PD in the first 90 days after renal replacement therapy initiation, between 2000 and 2012. Definitive PD completion was defined by hemodialysis treatment for 180 days or more. Patients with definitive PD completion were further categorized as 'transferred to HHD' if they initiated HHD less than 180 days after PD ending (first day of hemodialysis). Predictors of transfer to HHD (versus chronic transfer to facility hemodialysis) were evaluated through a multivariable logistic regression. Result(s): The total cohort included 10 710 incident PD patients. Definitive PD completion was identified in 2915 patients, among which 156 (5.4%) were transferred to HHD while the other patients remained treated by facility hemodialysis. In the multivariable logistic regression model, male gender, obesity and longer duration of PD therapy were identified as positive predictors of transfer to HHD while increasing age, infectious cause of PD completion, underweight, hypertension and diabetes as cause of kidney disease and Indigenous races were found to be negative predictors. (Table 1) The predictive capacity of the model was overall good (area under receiving operator characteristics [ROC] 0.81). Conclusion(s): Only 5% of patients with definitive PD completion were transferred to HHD in less than 180 days after PD ending. Based registry data from Australia and New Zealand, predictors of transfer to HHD include

This paper updates a previous 'Call to Action' paper (Nephrology 2011; 16: 19-29) that reviewed key outcome data for Australian and New Zealand peritoneal dialysis patients and made recommendations to improve care. Since its publication, peritonitis rates have improved significantly, although they have plateaued more recently. Peritoneal dialysis patient and technique survival in Australian and New Zealand have also improved, with a reduction in the proportion of technique failures attributed to 'social reasons'. Despite these improvements, technique survival rates overall remain lower than in many other parts of the world. This update includes additional practical recommendations based on published evidence and emerging initiatives to further improve outcomes.Copyright © 2016 Asian Pacific Society of Nephrology

Introduction and Aims: The 'Integrated home dialysis' model involving initiation of peritoneal dialysis (PD) first followed by home hemodialysis (HHD) has previously been proposed as an optimal form of dialysis that maximises the advantages of both modalities. While this model has great potential, its clinical outcomes, especially compared to direct HHD initiation, remain uncertain. Hence, the aim of this study was to evaluate survival in patients treated with PD and subsequently HHD, compared to treatment with a single home dialysis modality. Method(s): This study included all incident home dialysis patients, defined as PD or HHD in the first 90 days after renal replacement therapy initiation, in Australia and New Zealand between 2000 and 2012. Propensity score matching was performed to evaluate patients initially treated with PD followed by HHD ('PD + HHD' group), PD without subsequent transition to HHD ('PD only' group) and HHD without subsequent transition to PD ('HHD only' group). The composite primary outcome was death and home dialysis technique failure (defined as transfer to facility hemodialysis for at least 90 days). The secondary outcome included death on home dialysis (censored for technique failure). For all time-to-event analyses, time zero was defined as the time when HHD was initiated for patients in the 'PD+HHD' group and matching time for the other groups. Groups were compared using Cox proportional hazards models. Result(s): The 2:1 matched cohort included 84 patients in the 'PD+HHD' group, 168 patients in the 'HHD only' group and 168 patients in the 'PD only' group. Baseline characteristics were similar across the three matched groups. Compared to the 'PD +HHD' group, death and home dialysis technique failure was similar for patients treated with 'HHD only' (hazard ratio [HR] 0.92, 95% confidence interval [CI] 0.52-1.62; p=0.77) and higher for those treated with 'PD only' (HR 3.22, 95% CI 1.97-5.25; p<0.001). Similar results were observed for mo

Background Recent literature suggests that living kidney donation may be associated with an excess risk of end-stage kidney disease and death. Efforts to maximize access to transplantation may result in acceptance of donors who do not fit within current guidelines, potentially placing them at risk of adverse long-Term outcomes. Methods We studied the risk profile of Australian and New Zealand living kidney donors using data from the Australia and New Zealand Dialysis and Transplant Living Kidney Donor Registry over 2004 to 2012. We compared their predonation profile against national guidelines for donor acceptance. Results The analysis included 2,932 donors (mean age 48.8 +/- 11.2 years, range 18-81), 58% female and 87% Caucasian. Forty (1%) had measured glomerular filtration rate less than 80 mL/min; 32 (1%) had proteinuria >300 mg/day; 589 (20%) were hypertensive; 495 (18%) obese; 9 (0.3%) were diabetic while a further 55 (2%) had impaired glucose tolerance; and 218 (7%) were current smokers. Overall 767 donors (26%) had at least one relative contraindication to donation and 268 (9%) had at least one absolute contraindication according to national guidelines. Conclusions Divergence of current clinical practice from national guidelines has occurred. In the context of recent evidence demonstrating elevated long-Term donor risk, rigorous follow-up and reporting of outcomes are now mandated to ensure safety and document any change in risk associated with such a divergence.Copyright © Wolters Kluwer Health, Inc. All rights reserved.

Background. Alport syndrome is a rare inheritable renal disease. Clinical outcomes for patients progressing to endstage kidney disease (ESKD) are not well described. Methods. This study aimed to investigate the characteristics and clinical outcomes of patients from Australia and New Zealand commencing renal replacement therapy (RRT) for ESKD due to Alport syndrome between 1965 and 1995 (early cohort) and between 1996 and 2010 (contemporary cohort) compared with propensity score-matched, RRT-treated, non-Alport ESKD controls. Results. A total of 58 422 patients started RRT during this period of which 296 (0.5%) patients had Alport ESKD. In the Conclusion. Alport syndrome patients experienced comparable dialysis and renal transplant outcomes to matched non-Alport ESKD controls in the contemporary cohort due to relatively greater improvements in outcomes for non-Alport ESKD patients over time. Post-transplant anti-GBM disease was rare.