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For the segmentation of magnetic resonance brain images into anatomical regions, numerous fully automated methods have been proposed and compared to reference segmentations obtained manually. However, systematic differences might exist between the resulting segmentations, depending on the segmentation method and underlying brain atlas. This potentially results in sensitivity differences to disease and can further complicate the comparison of individual patients to normative data. In this study, we aim to answer two research questions: 1) to what extent are methods interchangeable, as long as the same method is being used for computing normative volume distributions and patient-specific volumes? and 2) can different methods be used for computing normative volume distributions and assessing patient-specific volumes? To answer these questions, we compared volumes of six brain regions calculated by five state-of-the-art segmentation methods: Erasmus MC (EMC), FreeSurfer (FS), geodesic information flows (GIF), multi-atlas label propagation with expectation–maximization (MALP-EM), and model-based brain segmentation (MBS). We applied the methods on 988 non-demented (ND) subjects and computed the correlation (PCC-v) and absolute agreement (ICC-v) on the volumes. For most regions, the PCC-v was good ((Formula presented.)), indicating that volume differences between methods in ND subjects are mainly due to systematic differences. The ICC-v was generally lower, especially for the smaller regions, indicating that it is essential that the same method is used to generate normative and patient data. To evaluate the impact on single-subject analysis, we also applied the methods to 42 patients with Alzheimer’s disease (AD). In the case where the normative distributions and the patient-specific volumes were calculated by the same method, the patient’s distance to the normative distribution was assessed with the z-score. We determined the diagnostic value of this z-score, which sho

Introduction In the USA, transgender women are among the most vulnerable to HIV. In particular, transgender women of colour face high rates of infection and low uptake of important HIV prevention tools, including pre-exposure prophylaxis (PrEP). This paper describes the design, sampling methods, data collection and analyses of the TURNNT ('Trying to Understand Relationships, Networks and Neighbourhoods among Transgender women of colour') study. In collaboration with communities of transgender women of colour, TURNNT aims to explore the complex social and environmental (ie, neighbourhood) structures that affect HIV prevention and other aspects of health in order to identify avenues for intervention. Methods and analyses TURNNT is a prospective cohort study, which will recruit 300 transgender women of colour (150 Black/African American, 100 Latina and 50 Asian/Pacific Islander participants) in New York City. There will be three waves of data collection separated by 6 months. At each wave, participants will provide information on their relationships, social and sexual networks, and neighbourhoods. Global position system technology will be used to generate individual daily path areas in order to estimate neighbourhood-level exposures. Multivariate analyses will be conducted to assess cross-sectional and longitudinal, independent and synergistic associations of personal relationships (notably individual social capital), social and sexual networks, and neighbourhood factors (notably neighbourhood-level social cohesion) with PrEP uptake and discontinuation. Ethics and dissemination The TURNNT protocol was approved by the Columbia University Institutional Review Board (reference no. AAAS8164). This study will provide novel insights into the relationship, network and neighbourhood factors that influence HIV prevention behaviours among transgender women of colour and facilitate exploration of this population's health and well-being more broadly. Through community-based dissem

BACKGROUND: Survivors of acute kidney injury (AKI) are at increased risk of major adverse kidney events and international guidelines recommend individuals be evaluated 3 months following AKI. AIMS: We describe practice patterns and predictors of post-AKI care in an Australian tertiary hospital. METHOD(S): A retrospective analysis was undertaken of adults with AKI (defined by KDIGO criteria) admitted to a single centre between 2012 and 2016. The primary outcome was outpatient nephrology review at 3 months. Secondary outcomes included inpatient nephrology review, and outpatient serum creatinine and urinary protein measurements. Data were analysed using multivariable logistic and competing risk regression. RESULT(S): Only 117 of 2111 patients with AKI (6%) were reviewed by a nephrologist at 3 months. Reviewed patients were more likely to have a higher discharge serum creatinine (OR 1.20 per 10 mumol/L increase, 95% CI 1.16-1.25) or a history of peripheral vascular disease (OR 1.77, 95% CI 1.00-3.14). They were less likely to be older (OR 0.66 per decade, 95% CI 0.57-0.76), or to have a history of liver (OR 0.47, 95% CI 0.26-0.87) or ischaemic heart disease (OR 0.50, 95% CI 0.27-0.94). AKI stage did not predict follow up. The median time from discharge to outpatient serum creatinine testing was 12days (IQR 4-47) and proteinuria was measured in 538 patients (25%). CONCLUSION(S): A minority of admitted AKI patients receive recommended post-AKI care. Studies in other Australian institutions are required to confirm or refute these concerning findings. This article is protected by copyright. All rights reserved.

BACKGROUND: Survivors of acute kidney injury (AKI) are at increased risk of major adverse kidney events and international guidelines recommend individuals be evaluated 3 months following AKI. AIMS: We describe practice patterns and predictors of post-AKI care in an Australian tertiary hospital. METHOD(S): A retrospective analysis was undertaken of adults with AKI (defined by KDIGO criteria) admitted to a single centre between 2012 and 2016. The primary outcome was outpatient nephrology review at 3 months. Secondary outcomes included inpatient nephrology review, and outpatient serum creatinine and urinary protein measurements. Data were analysed using multivariable logistic and competing risk regression. RESULT(S): Only 117 of 2111 patients with AKI (6%) were reviewed by a nephrologist at 3 months. Reviewed patients were more likely to have a higher discharge serum creatinine (OR 1.20 per 10 mumol/L increase, 95% CI 1.16-1.25) or a history of peripheral vascular disease (OR 1.77, 95% CI 1.00-3.14). They were less likely to be older (OR 0.66 per decade, 95% CI 0.57-0.76), or to have a history of liver (OR 0.47, 95% CI 0.26-0.87) or ischaemic heart disease (OR 0.50, 95% CI 0.27-0.94). AKI stage did not predict follow up. The median time from discharge to outpatient serum creatinine testing was 12days (IQR 4-47) and proteinuria was measured in 538 patients (25%). CONCLUSION(S): A minority of admitted AKI patients receive recommended post-AKI care. Studies in other Australian institutions are required to confirm or refute these concerning findings. This article is protected by copyright. All rights reserved.

Introduction and Aims: Robust estimatesof the long-term outcomesof acute kidney injury are needed to inform clinical practice and guide optimal allocation of healthcare resources. This systematic review and meta-analysis aimed to quantify the association between acute kidney injury and chronic kidney disease, end stage kidney disease, and death, using consensus definitions of exposure. Method(s): Systematic searches were performed through EMBASE, MEDLINE, and grey literature sources to identify cohort studies reporting an association between acute kidney injury and at least one of the outcomes of interest. All studies in adults published after 2004, using standardised definitions for acute kidney injury (Risk, Injury, Failure, Loss, and End-stage kidney disease; Acute Kidney Injury Network; or Kidney Disease Improving Global Outcomes), which included a non-acute kidney injury control arm, and followed patients for at least 1 year were considered eligible. A modified Newcastle-Ottawa Scale was used to assess risk of bias, random effects meta-analysis was performed to estimate the pooled risk, and meta-regression was completed to identify potential sources of heterogeneity. Result(s): The search retrieved 3435 unique citations, of which 30 cohort studies (comprising 1,012,627 participants) were eligible for inclusion. The most frequent sources of bias related to inadequate follow up and variable adjustment for potential confounders. Compared to those without acute kidney injury, individuals with acute kidney injury were at significantly increased risk of chronic kidney disease (6 studies; 15,925 participants; hazard ratio [HR] 3.71, 95% CI 2.35-5.86; I2 93.1% p<0.001), end stage kidney disease (5 studies; 45,365 participants; HR 4.18, 95% CI 1.93-9.08; I2 88.8% p<0.001), and death (16 studies; 913,682 participants; HR 1.54, 95% CI 1.40-1.71; I2 85.6% p<0.001). The risk of death increased with greater acute kidney injury severity, and was highest in intensive care and

Introduction and Aims: Robust estimatesof the long-term outcomesof acute kidney injury are needed to inform clinical practice and guide optimal allocation of healthcare resources. This systematic review and meta-analysis aimed to quantify the association between acute kidney injury and chronic kidney disease, end stage kidney disease, and death, using consensus definitions of exposure. Method(s): Systematic searches were performed through EMBASE, MEDLINE, and grey literature sources to identify cohort studies reporting an association between acute kidney injury and at least one of the outcomes of interest. All studies in adults published after 2004, using standardised definitions for acute kidney injury (Risk, Injury, Failure, Loss, and End-stage kidney disease; Acute Kidney Injury Network; or Kidney Disease Improving Global Outcomes), which included a non-acute kidney injury control arm, and followed patients for at least 1 year were considered eligible. A modified Newcastle-Ottawa Scale was used to assess risk of bias, random effects meta-analysis was performed to estimate the pooled risk, and meta-regression was completed to identify potential sources of heterogeneity. Result(s): The search retrieved 3435 unique citations, of which 30 cohort studies (comprising 1,012,627 participants) were eligible for inclusion. The most frequent sources of bias related to inadequate follow up and variable adjustment for potential confounders. Compared to those without acute kidney injury, individuals with acute kidney injury were at significantly increased risk of chronic kidney disease (6 studies; 15,925 participants; hazard ratio [HR] 3.71, 95% CI 2.35-5.86; I2 93.1% p<0.001), end stage kidney disease (5 studies; 45,365 participants; HR 4.18, 95% CI 1.93-9.08; I2 88.8% p<0.001), and death (16 studies; 913,682 participants; HR 1.54, 95% CI 1.40-1.71; I2 85.6% p<0.001). The risk of death increased with greater acute kidney injury severity, and was highest in intensive care and

Aims: To evaluate erythropoietic response rates to oral iron over time in iron-deficient anemic patients with nondialysis- dependent chronic kidney disease (NDCKD). Materials and methods: FIND-CKD was a 1-year, randomized, multicenter trial of iron therapy in patients with ND-CKD, anemia, and iron deficiency, without erythropoiesis- stimulating agent (ESA) therapy. Patients with active infection or C-reactive protein > 20 mg/L were excluded. In this post-hoc analysis, response was defined as ≥ 1 g/dL increase in hemoglobin (Hb) from baseline, before initiation of alternative anemia therapy (i.e., ESA, transfusion, or intravenous iron). Results: 308 patients received oral iron (200 mg elemental iron/day). Mean (SD) Hb at baseline was 10.4 (0.7) g/dL. At week 4, Hb data were available from 292 patients without alternative anemia therapy: 63/292 (21.6%) showed a response. Among the 229 nonresponders at week 4, 48.8% showed a cumulative response on ≥1 occasion by week 52 (11.1%, 19.9%, 25.9%, and 28.7% had a response at weeks 8, 12, 24, and 52, respectively), and 27.9% had received alternative iron therapy by week 52. Baseline levels of Hb, ferritin, and transferrin saturation were lower in responders than in nonresponders. Neither concomitant medication nor adherence (as assessed by medication count) was substantially different between early responders and nonresponders. Conclusion: Four weeks after starting oral iron therapy, only 21.6% of anemic patients with ND-CKD and iron deficiency showed an Hb increase of at least 1 g/dL. Among early nonresponders, < 30% responded at any subsequent time point. Earlier consideration of alternative therapy could improve anemia management in this population.

Aim: To validate high-resolution magnetic resonance imaging (HR-MRI) assessment of bone microstructure compared to histomorphometry and micro-CT of bone biopsies from renal transplant recipients. Background(s): Renal osteodystrophy (ROD) affects bone quantity and quality and is associated with increased fractures in chronic kidney disease. Screening for ROD is hindered by complex pathophysiology and inadequacy of current diagnostic methods. Bone biopsy is invasive and infrequently performed in routine practice. HR-MRI is a new imaging technique to assess trabecular and cortical microarchitecture. Method(s): Distal tibia HR-MRI scans (Siemens Trio, 3 T) and iliac crest bone biopsies were performed in 10 transplant recipients at transplantation. Structural parameters of biopsies were analysed by histomorphometry and 3D micro-CT. Structural measures included trabecular bone volume (TV/ BV), thickness (TbTh), number (TbN), separation (TbS), mean cortical thickness (CtTh) and porosity (Po.%). Bone mineral density (BMD) was measured by peripheral quantitative computed tomography (pQCT, radius) and dual energy x-ray absorptiometry (DXA, hip). Associations were determined by analysis with Spearman's rank correlation coefficients. Result(s): HR-MRI (tibia) and micro-CT (iliac crest) indices correlated positively for TbN and TbS (r = 0.52, p = 0.12 and 0.56, p = 0.09 respectively) and TV/BV, with no significant correlation for CtTh at these differing sites. HR-MRI (tibia) CtTh correlated to CtTh and BMD measured by pQCT (radius) (r = 0.65, p = 0.06 and 0.78, p = 0.008 respectively). Micro-CT (iliac) CtTh correlated to BMD by DXA (hip), and cortical porosity by micro-CT correlated negatively to BMD by DXA (r = -0.65, p = 0.04). Conclusion(s): Micro-CT histomorphometry correlates to tibial HR-MRI for important trabecular indices and to hip DXA for cortical indices. Non-invasive HR-MRI and DXA combined with biochemical turnover markers may provide rapid, accessible information t

Aim: To validate high-resolution magnetic resonance imaging (HR-MRI) assessment of bone microstructure compared to histomorphometry and micro-CT of bone biopsies from renal transplant recipients. Background(s): Renal osteodystrophy (ROD) affects bone quantity and quality and is associated with increased fractures in chronic kidney disease. Screening for ROD is hindered by complex pathophysiology and inadequacy of current diagnostic methods. Bone biopsy is invasive and infrequently performed in routine practice. HR-MRI is a new imaging technique to assess trabecular and cortical microarchitecture. Method(s): Distal tibia HR-MRI scans (Siemens Trio, 3 T) and iliac crest bone biopsies were performed in 10 transplant recipients at transplantation. Structural parameters of biopsies were analysed by histomorphometry and 3D micro-CT. Structural measures included trabecular bone volume (TV/ BV), thickness (TbTh), number (TbN), separation (TbS), mean cortical thickness (CtTh) and porosity (Po.%). Bone mineral density (BMD) was measured by peripheral quantitative computed tomography (pQCT, radius) and dual energy x-ray absorptiometry (DXA, hip). Associations were determined by analysis with Spearman's rank correlation coefficients. Result(s): HR-MRI (tibia) and micro-CT (iliac crest) indices correlated positively for TbN and TbS (r = 0.52, p = 0.12 and 0.56, p = 0.09 respectively) and TV/BV, with no significant correlation for CtTh at these differing sites. HR-MRI (tibia) CtTh correlated to CtTh and BMD measured by pQCT (radius) (r = 0.65, p = 0.06 and 0.78, p = 0.008 respectively). Micro-CT (iliac) CtTh correlated to BMD by DXA (hip), and cortical porosity by micro-CT correlated negatively to BMD by DXA (r = -0.65, p = 0.04). Conclusion(s): Micro-CT histomorphometry correlates to tibial HR-MRI for important trabecular indices and to hip DXA for cortical indices. Non-invasive HR-MRI and DXA combined with biochemical turnover markers may provide rapid, accessible information t

The aim of this cross-sectional study was to assess the association of olfactory function and nutritional status in vital older adults and geriatric patients. Three hundred forty-five vital (mean age 67.1 years) and 138 geriatric older adults (mean age 80.9 years) were included. Nutritional status was assessed using the mini nutritional assessment-short form. The Sniffin’ Sticks was used to measure olfactory function. Eleven percentage of the vital older adults were at risk of malnutrition, whereas 60% of the geriatric participants were malnourished or at risk. Only 2% of the vital older adults were anosmic, compared with 46% of the geriatric participants. Linear regression demonstrated a significant association (P = 0.015) between olfactory function and nutritional status in the geriatric subjects. However, this association became insignificant after adjustment for confounders. Both crude and adjusted analysis in the vital older adults did not show a significant association. The results indicate that, in both groups of elderly, there is no direct relation between olfactory function and nutritional status. We suggest that a decline in olfactory function may still be considered as one of the risk-factors for malnutrition in geriatric patients—once co-occurring with other mental and/or physical problems that are more likely to occur in those patients experience.

Aim: To assess the association between urinary phosphate excretion and outcomes in a large population-based cohort. Background(s): Serum phosphate is associated with cardiovascular disease (CVD) and mortality in the general population. Greater dietary phosphorus intake may lead to higher serum phosphate and adverse outcomes. Urinary phosphate excretion is a marker of intestinal phosphorus absorption and may be a more reliable marker of phosphate homeostasis. Studies report good correlation between urine phosphate-creatinine ratio (uPiCr) and 24-hour urinary phosphate excretion, but whether uPiCr is associated with risk of CVD or mortality is uncertain. Method(s): Using the nationally representative AusDiab cohort, uPiCr was determined from available urine samples (n = 11,116). Participant baseline characteristics were compared across quartiles of uPiCr and regression analysis was used to determine associations. Relationships between uPiCr and all-cause mortality were determined using Cox proportion hazards regression with uPiCr modelled using fractional polynomials. Result(s): Mean age 51+/-14 y, 45% males and 9.6% chronic kidney disease (CKD-Epi equation). During a median follow-up 12.1 years there were 1265 deaths. Mean uPiCr was 1.45+/-0.7 mmol/mmol. Participants with higher uPiCr were older, more likely female, had higher albuminuria, lower GFR, greater prevalence of CVD and hypertension (all p < 0.001) and higher BMI (p = 0.002). With increasing quartiles of uPiCr the hazard ratios (HR) for all-cause mortality were 1.27 [95%CI 1.07,1.52], 1.54 [1.30,1.83], and 2.07 [1.76,2.44] (compared to the lowest quartile). When modelled as fractional polynomial, both low and high urine phosphate were independently associated with an increased risk of mortality. Conclusion(s): Low and high uPiCr is associated with increased all-cause mortality in a general population cohort and may serve as a useful marker for interventions aimed at improving phosphate balance.

Aim: To assess the association between urinary phosphate excretion and outcomes in a large population-based cohort. Background(s): Serum phosphate is associated with cardiovascular disease (CVD) and mortality in the general population. Greater dietary phosphorus intake may lead to higher serum phosphate and adverse outcomes. Urinary phosphate excretion is a marker of intestinal phosphorus absorption and may be a more reliable marker of phosphate homeostasis. Studies report good correlation between urine phosphate-creatinine ratio (uPiCr) and 24-hour urinary phosphate excretion, but whether uPiCr is associated with risk of CVD or mortality is uncertain. Method(s): Using the nationally representative AusDiab cohort, uPiCr was determined from available urine samples (n = 11,116). Participant baseline characteristics were compared across quartiles of uPiCr and regression analysis was used to determine associations. Relationships between uPiCr and all-cause mortality were determined using Cox proportion hazards regression with uPiCr modelled using fractional polynomials. Result(s): Mean age 51+/-14 y, 45% males and 9.6% chronic kidney disease (CKD-Epi equation). During a median follow-up 12.1 years there were 1265 deaths. Mean uPiCr was 1.45+/-0.7 mmol/mmol. Participants with higher uPiCr were older, more likely female, had higher albuminuria, lower GFR, greater prevalence of CVD and hypertension (all p < 0.001) and higher BMI (p = 0.002). With increasing quartiles of uPiCr the hazard ratios (HR) for all-cause mortality were 1.27 [95%CI 1.07,1.52], 1.54 [1.30,1.83], and 2.07 [1.76,2.44] (compared to the lowest quartile). When modelled as fractional polynomial, both low and high urine phosphate were independently associated with an increased risk of mortality. Conclusion(s): Low and high uPiCr is associated with increased all-cause mortality in a general population cohort and may serve as a useful marker for interventions aimed at improving phosphate balance.

The dialysate calcium (Ca) concentration for hemodialysis (HD) patients can be adjusted to manage more optimally the body's Ca and phosphate balance, and thus improve bone metabolism as well as reduce accelerated arteriosclerosis and cardiovascular mortality. The appropriate dialysate Ca concentration allowing this balance should be prescribed to each individual patient depending on a multitude of variable factors relating to Ca load. A lower dialysate Ca concentration of 1.25 to 1.3 mmol/L will permit the use of vitamin D supplements and Ca-based phosphate binders in clinical practice, with much less risk of Ca loading and resultant hypercalcemia and calcification. Low Ca baths are useful in the setting of adynamic bone disease where an increase in bone turnover is required. However, low Ca levels in the dialysate may also predispose to cardiac arrhythmias and hemodynamically unstable dialysis sessions with intradialytic hypotension. Higher Ca dialysate is useful to sustain normal serum Ca levels where patients are not taking Ca-based binders or if Ca supplements are not able to normalize serum levels. Suppression of hyperparathyroidism is also effective with dialysate Ca of 1.75 mmol/L, but hypercalcemia, metastatic calcification, and oversuppression of parathyroid hormone are risks. Dialysate Ca of 1.5 mmol/L may be a compromise between bone protection and reduction in cardiovascular risk for conventional HD and is a common concentration used throughout the world. The increase in longer, more frequent dialysis such as short-daily and nocturnal HD, however, provides another challenge with regard to optimal dialysate Ca levels and higher levels of 1.75 mmol/L are probably indicated in this setting. Difficulties in determining the ideal dialysate Ca occur because of the complex pathophysiology of bone and mineral metabolism in HD patients and there needs to be a balance between dialysis prescription and other treatment modalities. To optimize management of the abnor

The dialysate calcium (Ca) concentration for hemodialysis (HD) patients can be adjusted to manage more optimally the body's Ca and phosphate balance, and thus improve bone metabolism as well as reduce accelerated arteriosclerosis and cardiovascular mortality. The appropriate dialysate Ca concentration allowing this balance should be prescribed to each individual patient depending on a multitude of variable factors relating to Ca load. A lower dialysate Ca concentration of 1.25 to 1.3 mmol/L will permit the use of vitamin D supplements and Ca-based phosphate binders in clinical practice, with much less risk of Ca loading and resultant hypercalcemia and calcification. Low Ca baths are useful in the setting of adynamic bone disease where an increase in bone turnover is required. However, low Ca levels in the dialysate may also predispose to cardiac arrhythmias and hemodynamically unstable dialysis sessions with intradialytic hypotension. Higher Ca dialysate is useful to sustain normal serum Ca levels where patients are not taking Ca-based binders or if Ca supplements are not able to normalize serum levels. Suppression of hyperparathyroidism is also effective with dialysate Ca of 1.75 mmol/L, but hypercalcemia, metastatic calcification, and oversuppression of parathyroid hormone are risks. Dialysate Ca of 1.5 mmol/L may be a compromise between bone protection and reduction in cardiovascular risk for conventional HD and is a common concentration used throughout the world. The increase in longer, more frequent dialysis such as short-daily and nocturnal HD, however, provides another challenge with regard to optimal dialysate Ca levels and higher levels of 1.75 mmol/L are probably indicated in this setting. Difficulties in determining the ideal dialysate Ca occur because of the complex pathophysiology of bone and mineral metabolism in HD patients and there needs to be a balance between dialysis prescription and other treatment modalities. To optimize management of the abnor

Aim: To determine barriers towards an evidence-practice gap by surveying haemodialysis (HD) patients and staff about awareness and management of chronic kidney disease mineral and bone disorder (CKD-MBD). Background(s): Although guidelines exist for optimal levels of serum markers of CKD-MBD, target parameters are not achieved in many HD patients. The reason for this evidence-practice gap is unclear and more information from patients and healthcare professionals is required to improve knowledge transfer. Method(s): 136 prevalent HD patients, 25 nephrologists and 58 dialysis nurses/ technicians were surveyed. Three separate questionnaires included issues of knowledge and awareness of CKD-MBD and factors limiting management (including compliance, medications and general understanding). Result(s): 1. HD patients: 84% had heard about phosphate, 24% aware of normal levels; 54% were aware of consequences of elevated phosphate; 42% were unsure of high phosphate foods; 27% had difficulty taking and 35% admitted to forgetting to take phosphate binders; and 74% wanted to know more about CKD-MBD (40% via written material). 2. Nephrologists: 52% were aware of a CKD-MBD protocol in their unit and 60% were satisfied with CKD-MBD management; 76% thought non-compliance with binders was the main reason for poor control of phosphate (predominantly related to insufficient understanding of phosphate, binders and consequences of elevated levels); 84% thought patients wanted to know more but only 7% provided written material on CKD-MBD. 3. Dialysis nurses/technicians: 63% thought non-compliance with binders was the predominant reason for poor control, main reasons again being lack of patient understanding; 88% thought patients would want to know more but only 17% provided written education. Conclusion(s): Implementation of an intensive educational program, with a multi-faceted approach, for HD patients may promote better control CKD-MBD and improve achievement of target levels.

Aim: To determine the effect of lanthanum carbonate compared to calcium-containing phosphate binders on vascular calcification (VC) in a randomized controlled trial. Background(s): VC contributes to cardiovascular disease in haemodialysis (HD) patients. Few controlled studies have addressed interventions to reduce VC but non-calcium-based phosphate binders may be beneficial. No published randomized study to date has assessed the effect of lanthanum carbonate on VC progression. Method(s): Forty-five HD patients were randomized to either lanthanum carbonate (LC) or calcium carbonate (CC). Primary outcome was change in aortic VC after 18 months. Secondary outcomes included superficial femoral artery (SFA) VC, bone mineral density (BMD) of lumbar spine and serum markers of mineral metabolism. At baseline, 6 and 18 months computed tomography (CT) was performed to measure VC and BMD. Analysis was by intention-to-treat, with ANCOVA to assess differences. Result(s): 30 patients completed the study (17 LC, 13 CC); baseline median age 58 yrs, 38% diabetic, 64% male. 93% had aortic VC at commencement and 87% showed progression. At 18 months, there was significantly less aortic VC progression with LC than CC (adjusted difference-98.1 [-149.4, -46.8] Hounsfield Units, p < 0.001). There was also a non-significant reduction in those on LC in left SFA VC (-25.8 [-67.7, 16.1] HU, p = 0.2) and right SFA VC (-35.9 [-77.8, 5.9] HU, p = 0.09). There was no difference in lumbar spine BMD and serum phosphate, calcium and parathyroid hormone levels between groups. Limitations to the study include small sample size and loss to follow-up. Conclusion(s): Lanthanum carbonate was associated with reduced progression of aortic calcification compared to calcium carbonate in HD patients over 18 months.

Aim: To assess the changes in nephrology advanced training in Australia with respect to trainee numbers and exposure to patients and procedures over 10 years. Background(s): Advanced training in nephrology should provide broad experience in all aspects of nephrology. Recent increases in trainee numbers leads to concern about dilution of nephrology training. The Nephrology Specialist Advisory Committee (SAC) oversees trainees and final supervisor's reports (end of year of training) may provide important information about differences in experience over time. Method(s): A retrospective study using supervisor reports was performed to determine changes in patient exposure and trainee procedures from 2000 to 2010. Result(s): 542 reports were reviewed involving 208 trainees across 53 different training sites in Australia. Trainee numbers have steadily risen since 2004 increasing from 24 to 82 in 2010. The greatest increases have occurred in NSW, Victoria and Queensland (6-fold, 3-fold and 5-fold respectively). Trainee exposure to dialysis patients has gradually decreased in the last 10 yrs, with average number per trainee in 2000 compared to 2010 being 66 vs 43 (p = 0.02) and 28 vs 16 (p = 0.01) for HD and PD respectively. With exposure to acute kidney injury cases per trainee there was a gradual non-significant reduction over time. Average procedural numbers per trainee decreased significantly with less temporary dialysis catheters inserted (39 vs 10, p < 0.01) and less renal biopsies (65 vs 41, p < 0.01) in 2000 compared to 2010. The proportion of trainees not working in a hospital that provides exposure to acute transplantation has steadily increased from 15% in 2003 to 44% in 2010. Conclusion(s): There has been a dramatic increase in nephrology advanced trainee numbers over the last decade, at a relatively more rapid rate than dialysis and transplant patient numbers, potentially restricting adequate training experience.

Aim: Examine agreement between various indicators of dialysis 'quality'. Background(s): There has been considerable discussion about markers of dialysis 'quality'. The extent of agreement between these in Australian units in not known. Method(s): From the ANZDATA Registry, units were ranked (in a deidentified fashion) by a number of criteria including size, achievement of various dialysis parameters including HD access, peritonitis rates, biochemical parameters etc. Consistency among rankings from various markers was then compared internally between various markers. Markers were also a compared with achieved unit mortality (adjusted for covariates) as the 'gold standard'. The consistency of unit rankings over time was also examined. Result(s): Overall, there was poor agreement between rankings derived from various measures. Specifically, rankings derived from peritonitis rate did not statistically correlate with those of use of central venous catheters (CVC) at first haemodialysis (r = 0.14, p = 0.28); neither peritonitis rate (r = 0.05, p = 0.7) nor CVC ranking (r = 0.10, p = 0.42) correlated with that based on longer term mortality. There was also little indicators of agreement with rankings based on achievement of phosphate or haemoglobin targets, unit size or number of preemptive kidney transplants. Within units, peritonitis rates and CVC rates (and therefore) rankings did fluctuate from year to year especially for smaller units. Among 74 units, the overall standard deviation (over 5 years) for rankings for peritonitis was 17 and for CVC use 13. Conclusion(s): There is poor agreement among markers proposed for measurement of dialysis 'quality'. This underlines the complexity of assessment of performance of dialysis units. Rates of line use and peritonitis (and therefore rankings) fluctuate over time; this will reflect components of statistical variation (especially for smaller units and real changes in practice).

Aim: To assess the prevalence of abdominal aortic calcification (ACC) using simple radiological imaging in dialysis patients. Background(s): Vascular calcification is highly prevalent in patients with chronic kidney disease on dialysis. Plain X-rays can detect AAC, although AAC is less well documented in anatomical distribution and severity compared to coronary calcification. This study is an analysis of AAC in prevalent Australian haemodialysis (HD) patients. Method(s): Lateral lumbar X-ray of the abdominal aorta was used to determine the overall AAC score, which is related to the severity of calcific deposits at lumbar vertebral segments L1 to L4. Semi-quantitative measurement, using a validated 24-point scale, was determined by two radiologists on HD patients from 7 satellite dialysis centres. Result(s): A lateral lumbar X-ray was obtained in 134 patients. Patients were aged 67 +/- 12 years, 67% were male, 36% diabetic with mean duration of HD 54 +/- 48 months. Calcification (AAC score >= 1) was present in 94.4% of patients. The mean AAC score was 11.0 +/- 6.4 (median 12). Independent predictors for the presence and severity of calcification were age (P < 0.0001) and duration of dialysis (P = 0.003). There was no significant association between AAC and time-averaged serum markers of mineral metabolism, lipid status, CRP levels or the presence of diabetes. Vertebral fractures were noted on 7% of X-rays. Conclusion(s): AAC detected by lateral lumbar X-ray is associated with increasing age and duration of HD. This semi-quantitative method of determining vascular calcification is more widely available and less expensive than current procedures and could form part of cardiovascular risk stratification.

Aim: To assess an extended and broadened regimen of CMV prophylaxis in renal transplantation. Background(s): Cytomegalovirus (CMV) poses a mortality and morbidity risk in transplant recipients. Prophylaxis against CMV reduces mortality, but recent studies suggest that prophylaxis regimens delay rather than prevent disease. In 2004 we introduced a regimen in which CMV negative recipients (R-) receiving kidneys from CMV positive donors (D+) receive six months of valganciclovir, while D+/R+ and D-/R- receive three months. D-/R- were not routinely administered prophylaxis. Method(s): Data from all kidney transplantations at the Royal Melbourne Hospital between November 2004 and December 2009 were analysed, with a minimum of 180 days follow up post-prophylaxis. Result(s): 521 patient transplants were eligible for analysis; 64 D+/R-, 221 D+/ R+, 90 D-/R+, 75 D-/R- and 26 of unknown CMV status. CMV disease was reported in 7/476 patients, with 6/64 (9.4%) D+/R- and 1/221 (0.5%) D+/R+. In three cases CMV disease occurred greater than six months post-transplant. This compares with an incidence of 21.4% in D+/R- using our previous regimen of valacyclovir and CMVIg. At that time the incidence of CMV was 8.7% in D+/R- was 3% in D-/R+, who did not receive prophylaxis. Conclusion(s): Extending the duration of prophylaxis for D+/R- and broadening the regimen to include D+/R+, D-/R+ has had a significant effect in reducing the incidence of CMV disease. CMV prophylaxis for 90 days in D+/R+ and D-/ R+ is sufficient to prevent CMV disease and is well tolerated. In the higher risk D+/R- group CMV disease affected 9.4% of patients despite 180 days of prophylaxis. Although this prophylaxis regimen appears to delay CMV infection in some cases, it does not exclude it in high risk groups.

Aim: To determine barriers towards an evidence-practice gap by surveying haemodialysis (HD) patients and staff about awareness and management of chronic kidney disease mineral and bone disorder (CKD-MBD). Background(s): Although guidelines exist for optimal levels of serum markers of CKD-MBD, target parameters are not achieved in many HD patients. The reason for this evidence-practice gap is unclear and more information from patients and healthcare professionals is required to improve knowledge transfer. Method(s): 136 prevalent HD patients, 25 nephrologists and 58 dialysis nurses/ technicians were surveyed. Three separate questionnaires included issues of knowledge and awareness of CKD-MBD and factors limiting management (including compliance, medications and general understanding). Result(s): 1. HD patients: 84% had heard about phosphate, 24% aware of normal levels; 54% were aware of consequences of elevated phosphate; 42% were unsure of high phosphate foods; 27% had difficulty taking and 35% admitted to forgetting to take phosphate binders; and 74% wanted to know more about CKD-MBD (40% via written material). 2. Nephrologists: 52% were aware of a CKD-MBD protocol in their unit and 60% were satisfied with CKD-MBD management; 76% thought non-compliance with binders was the main reason for poor control of phosphate (predominantly related to insufficient understanding of phosphate, binders and consequences of elevated levels); 84% thought patients wanted to know more but only 7% provided written material on CKD-MBD. 3. Dialysis nurses/technicians: 63% thought non-compliance with binders was the predominant reason for poor control, main reasons again being lack of patient understanding; 88% thought patients would want to know more but only 17% provided written education. Conclusion(s): Implementation of an intensive educational program, with a multi-faceted approach, for HD patients may promote better control CKD-MBD and improve achievement of target levels.

Aim: To determine the effect of lanthanum carbonate compared to calcium-containing phosphate binders on vascular calcification (VC) in a randomized controlled trial. Background(s): VC contributes to cardiovascular disease in haemodialysis (HD) patients. Few controlled studies have addressed interventions to reduce VC but non-calcium-based phosphate binders may be beneficial. No published randomized study to date has assessed the effect of lanthanum carbonate on VC progression. Method(s): Forty-five HD patients were randomized to either lanthanum carbonate (LC) or calcium carbonate (CC). Primary outcome was change in aortic VC after 18 months. Secondary outcomes included superficial femoral artery (SFA) VC, bone mineral density (BMD) of lumbar spine and serum markers of mineral metabolism. At baseline, 6 and 18 months computed tomography (CT) was performed to measure VC and BMD. Analysis was by intention-to-treat, with ANCOVA to assess differences. Result(s): 30 patients completed the study (17 LC, 13 CC); baseline median age 58 yrs, 38% diabetic, 64% male. 93% had aortic VC at commencement and 87% showed progression. At 18 months, there was significantly less aortic VC progression with LC than CC (adjusted difference-98.1 [-149.4, -46.8] Hounsfield Units, p < 0.001). There was also a non-significant reduction in those on LC in left SFA VC (-25.8 [-67.7, 16.1] HU, p = 0.2) and right SFA VC (-35.9 [-77.8, 5.9] HU, p = 0.09). There was no difference in lumbar spine BMD and serum phosphate, calcium and parathyroid hormone levels between groups. Limitations to the study include small sample size and loss to follow-up. Conclusion(s): Lanthanum carbonate was associated with reduced progression of aortic calcification compared to calcium carbonate in HD patients over 18 months.

Aim: To assess the changes in nephrology advanced training in Australia with respect to trainee numbers and exposure to patients and procedures over 10 years. Background(s): Advanced training in nephrology should provide broad experience in all aspects of nephrology. Recent increases in trainee numbers leads to concern about dilution of nephrology training. The Nephrology Specialist Advisory Committee (SAC) oversees trainees and final supervisor's reports (end of year of training) may provide important information about differences in experience over time. Method(s): A retrospective study using supervisor reports was performed to determine changes in patient exposure and trainee procedures from 2000 to 2010. Result(s): 542 reports were reviewed involving 208 trainees across 53 different training sites in Australia. Trainee numbers have steadily risen since 2004 increasing from 24 to 82 in 2010. The greatest increases have occurred in NSW, Victoria and Queensland (6-fold, 3-fold and 5-fold respectively). Trainee exposure to dialysis patients has gradually decreased in the last 10 yrs, with average number per trainee in 2000 compared to 2010 being 66 vs 43 (p = 0.02) and 28 vs 16 (p = 0.01) for HD and PD respectively. With exposure to acute kidney injury cases per trainee there was a gradual non-significant reduction over time. Average procedural numbers per trainee decreased significantly with less temporary dialysis catheters inserted (39 vs 10, p < 0.01) and less renal biopsies (65 vs 41, p < 0.01) in 2000 compared to 2010. The proportion of trainees not working in a hospital that provides exposure to acute transplantation has steadily increased from 15% in 2003 to 44% in 2010. Conclusion(s): There has been a dramatic increase in nephrology advanced trainee numbers over the last decade, at a relatively more rapid rate than dialysis and transplant patient numbers, potentially restricting adequate training experience.

Aim: Examine agreement between various indicators of dialysis 'quality'. Background(s): There has been considerable discussion about markers of dialysis 'quality'. The extent of agreement between these in Australian units in not known. Method(s): From the ANZDATA Registry, units were ranked (in a deidentified fashion) by a number of criteria including size, achievement of various dialysis parameters including HD access, peritonitis rates, biochemical parameters etc. Consistency among rankings from various markers was then compared internally between various markers. Markers were also a compared with achieved unit mortality (adjusted for covariates) as the 'gold standard'. The consistency of unit rankings over time was also examined. Result(s): Overall, there was poor agreement between rankings derived from various measures. Specifically, rankings derived from peritonitis rate did not statistically correlate with those of use of central venous catheters (CVC) at first haemodialysis (r = 0.14, p = 0.28); neither peritonitis rate (r = 0.05, p = 0.7) nor CVC ranking (r = 0.10, p = 0.42) correlated with that based on longer term mortality. There was also little indicators of agreement with rankings based on achievement of phosphate or haemoglobin targets, unit size or number of preemptive kidney transplants. Within units, peritonitis rates and CVC rates (and therefore) rankings did fluctuate from year to year especially for smaller units. Among 74 units, the overall standard deviation (over 5 years) for rankings for peritonitis was 17 and for CVC use 13. Conclusion(s): There is poor agreement among markers proposed for measurement of dialysis 'quality'. This underlines the complexity of assessment of performance of dialysis units. Rates of line use and peritonitis (and therefore rankings) fluctuate over time; this will reflect components of statistical variation (especially for smaller units and real changes in practice).

Aim: To assess the prevalence of abdominal aortic calcification (ACC) using simple radiological imaging in dialysis patients. Background(s): Vascular calcification is highly prevalent in patients with chronic kidney disease on dialysis. Plain X-rays can detect AAC, although AAC is less well documented in anatomical distribution and severity compared to coronary calcification. This study is an analysis of AAC in prevalent Australian haemodialysis (HD) patients. Method(s): Lateral lumbar X-ray of the abdominal aorta was used to determine the overall AAC score, which is related to the severity of calcific deposits at lumbar vertebral segments L1 to L4. Semi-quantitative measurement, using a validated 24-point scale, was determined by two radiologists on HD patients from 7 satellite dialysis centres. Result(s): A lateral lumbar X-ray was obtained in 134 patients. Patients were aged 67 +/- 12 years, 67% were male, 36% diabetic with mean duration of HD 54 +/- 48 months. Calcification (AAC score >= 1) was present in 94.4% of patients. The mean AAC score was 11.0 +/- 6.4 (median 12). Independent predictors for the presence and severity of calcification were age (P < 0.0001) and duration of dialysis (P = 0.003). There was no significant association between AAC and time-averaged serum markers of mineral metabolism, lipid status, CRP levels or the presence of diabetes. Vertebral fractures were noted on 7% of X-rays. Conclusion(s): AAC detected by lateral lumbar X-ray is associated with increasing age and duration of HD. This semi-quantitative method of determining vascular calcification is more widely available and less expensive than current procedures and could form part of cardiovascular risk stratification.

Aim: To assess an extended and broadened regimen of CMV prophylaxis in renal transplantation. Background(s): Cytomegalovirus (CMV) poses a mortality and morbidity risk in transplant recipients. Prophylaxis against CMV reduces mortality, but recent studies suggest that prophylaxis regimens delay rather than prevent disease. In 2004 we introduced a regimen in which CMV negative recipients (R-) receiving kidneys from CMV positive donors (D+) receive six months of valganciclovir, while D+/R+ and D-/R- receive three months. D-/R- were not routinely administered prophylaxis. Method(s): Data from all kidney transplantations at the Royal Melbourne Hospital between November 2004 and December 2009 were analysed, with a minimum of 180 days follow up post-prophylaxis. Result(s): 521 patient transplants were eligible for analysis; 64 D+/R-, 221 D+/ R+, 90 D-/R+, 75 D-/R- and 26 of unknown CMV status. CMV disease was reported in 7/476 patients, with 6/64 (9.4%) D+/R- and 1/221 (0.5%) D+/R+. In three cases CMV disease occurred greater than six months post-transplant. This compares with an incidence of 21.4% in D+/R- using our previous regimen of valacyclovir and CMVIg. At that time the incidence of CMV was 8.7% in D+/R- was 3% in D-/R+, who did not receive prophylaxis. Conclusion(s): Extending the duration of prophylaxis for D+/R- and broadening the regimen to include D+/R+, D-/R+ has had a significant effect in reducing the incidence of CMV disease. CMV prophylaxis for 90 days in D+/R+ and D-/ R+ is sufficient to prevent CMV disease and is well tolerated. In the higher risk D+/R- group CMV disease affected 9.4% of patients despite 180 days of prophylaxis. Although this prophylaxis regimen appears to delay CMV infection in some cases, it does not exclude it in high risk groups.

This manual brings together the experiences of an Internet outreach project conducted by theWestern Australian AIDS Council (WAAC) and the Western Australian Centre for Health PromotionResearch (WACHPR) at Curtin University of Technology along with other selected research. It presents guidelines on the development and implementation of Internet outreach programs for health promotion practitioners and peer education workers.It is divided into sections for ease of navigation, including an overview of Internet outreach as a health promotion strategy and the CyberReach project (through the implementation of which the contents were produced). There are additional components to support agencies interested in learning more about whether Internet outreach may be a useful strategy for them in expanding the range of their current services.Who this manual is for: Anyone working in health service delivery with an interest in developing Internet-based health promotion outreach programs. Although based on a project targeting same sex attracted youth (SSAY) and men who have sex with men (MSM), we believe there are aspects applicable to health practitioners working with other groups in a range of health and human services areas.

Cardiovascular disease is highly prevalent in chronic kidney disease (CKD) and is often associated with increased vascular stiffness and calcification. Recent studies have suggested a complex interaction between vascular calcification and abnormalities of bone and mineral metabolism, with an inverse relationship between arterial calcification and bone mineral density (BMD). Although osteoporosis is recognized and treated in CKD 1 to 3, the interpretation of BMD levels in the osteoporotic range is controversial in CKD 4, 5, and 5D when renal osteodystrophy is generally present. In addition, there is a paucity of data for patients with CKD mineral and bone disorder (MBD), because studies using bisphosphonates in postmenopausal and glucocorticoid- induced osteoporosis have generally excluded patients with significant CKD. For these patients, treatment of low BMD using standard therapies for osteoporosis is not without potential for harm due to the possibility of worsening low bone turnover, osteomalacia, mixed uraemic osteodystrophy, and of exacerbated hyperparathyroidism; and bisphosphonates should only be used selectively and with caution. Some experimental and clinical studies have also suggested that bisphosphonates may reduce progression of extra-osseous calcification and inhibit the development of atherosclerosis. The authors review the potential benefits and risks associated with bisphosphonate use for bone protection in CKD, and assess their effect on vascular calcification and atherosclerosis. Copyright © 2009 by the American Society of Nephrology.

Cardiovascular disease is the commonest cause of mortality in people with chronic kidney disease (CKD), precipitated by many highly prevalent traditional and non-traditional cardiovascular risk factors. Vascular calcification, induced by calcium and phosphate excess and uraemia, is a major risk factor. A mediated complex of factors are involved in the pathogenesis of vascular calcification, including calcium-regulatory proteins and inhibitory extra-cellular factors such as fetuin-A, but the normal balance becomes dysregulated in CKD towards the development of vascular calcification. This leads to vascular smooth muscle cell apoptosis and differentiation into phenotypically distinct osteoblast-like cells with subsequent ossification of the arterial wall. Arterial stiffness represents the functional disturbance of vascular calcification and comprises non-occlusive arterial remodelling (arteriosclerosis), different from atherosclerosis.Vascular calcification has intimate interactions with bone mineralization and, as a result of imbalances in mineral metabolism in CKD, is associated with enhanced bone resorption. Reflecting an increased recognition of the close relationship of mineral metabolism to bone abnormalities, vascular calcification and the consequences of fracture, cardiovascular disease and increased mortality, the term 'Chronic Kidney Disease-Mineral and Bone Disorder' (CKD-MBD) was recently introduced to encompass one or more combinations of these abnormalities. Vascular calcification and arterial stiffness can be measured and monitored with X-ray and CT imaging, echocardiography, and pulse wave velocity. Management in CKD is difficult but detection, prevention and treatment is crucial to reduce cardiovascular mortality. The optimal control of mineral metabolism, especially hyperphosphatemia, with the use of non-calcium based phosphate binders has been shown to be effective to reduce vascular calcification. The use of bisphosphonates, calcimimetics, vitamin

Cardiovascular disease is highly prevalent in chronic kidney disease (CKD) and is often associated with increased vascular stiffness and calcification. Recent studies have suggested a complex interaction between vascular calcification and abnormalities of bone and mineral metabolism, with an inverse relationship between arterial calcification and bone mineral density (BMD). Although osteoporosis is recognized and treated in CKD 1 to 3, the interpretation of BMD levels in the osteoporotic range is controversial in CKD 4, 5, and 5D when renal osteodystrophy is generally present. In addition, there is a paucity of data for patients with CKD mineral and bone disorder (MBD), because studies using bisphosphonates in postmenopausal and glucocorticoid- induced osteoporosis have generally excluded patients with significant CKD. For these patients, treatment of low BMD using standard therapies for osteoporosis is not without potential for harm due to the possibility of worsening low bone turnover, osteomalacia, mixed uraemic osteodystrophy, and of exacerbated hyperparathyroidism; and bisphosphonates should only be used selectively and with caution. Some experimental and clinical studies have also suggested that bisphosphonates may reduce progression of extra-osseous calcification and inhibit the development of atherosclerosis. The authors review the potential benefits and risks associated with bisphosphonate use for bone protection in CKD, and assess their effect on vascular calcification and atherosclerosis. Copyright © 2009 by the American Society of Nephrology.

Cardiovascular disease is the commonest cause of mortality in people with chronic kidney disease (CKD), precipitated by many highly prevalent traditional and non-traditional cardiovascular risk factors. Vascular calcification, induced by calcium and phosphate excess and uraemia, is a major risk factor. A mediated complex of factors are involved in the pathogenesis of vascular calcification, including calcium-regulatory proteins and inhibitory extra-cellular factors such as fetuin-A, but the normal balance becomes dysregulated in CKD towards the development of vascular calcification. This leads to vascular smooth muscle cell apoptosis and differentiation into phenotypically distinct osteoblast-like cells with subsequent ossification of the arterial wall. Arterial stiffness represents the functional disturbance of vascular calcification and comprises non-occlusive arterial remodelling (arteriosclerosis), different from atherosclerosis.Vascular calcification has intimate interactions with bone mineralization and, as a result of imbalances in mineral metabolism in CKD, is associated with enhanced bone resorption. Reflecting an increased recognition of the close relationship of mineral metabolism to bone abnormalities, vascular calcification and the consequences of fracture, cardiovascular disease and increased mortality, the term 'Chronic Kidney Disease-Mineral and Bone Disorder' (CKD-MBD) was recently introduced to encompass one or more combinations of these abnormalities. Vascular calcification and arterial stiffness can be measured and monitored with X-ray and CT imaging, echocardiography, and pulse wave velocity. Management in CKD is difficult but detection, prevention and treatment is crucial to reduce cardiovascular mortality. The optimal control of mineral metabolism, especially hyperphosphatemia, with the use of non-calcium based phosphate binders has been shown to be effective to reduce vascular calcification. The use of bisphosphonates, calcimimetics, vitamin

In vivo imaging of the cardiac 3D fibre architecture is still a challenge, but it would have many clinical applications, for instance to better understand pathologies and to follow up remodelling after therapy. Recently, cardiac MRI enabled the acquisition of Diffusion Tensor images (DTI) of 2D slices. We propose a method for the complete 3D reconstruction of cardiac fibre architecture in the left ventricular myocardium from sparse in vivo DTI slices. This is achieved in two steps. First we map non-linearly the left ventricular geometry to a truncated ellipsoid. Second, we express coordinates and tensor components in Prolate Spheroidal System, where an anisotropic Gaussian kernel regression interpolation is performed. The framework is initially applied to a statistical cardiac DTI atlas in order to estimate the optimal anisotropic bandwidths. Then, it is applied to in vivo beating heart DTI data sparsely acquired on a healthy subject. Resulting in vivo tensor field shows good correlation with literature, especially the elevation (helix) angle transmural variation. To our knowledge, this is the first reconstruction of in vivo human 3D cardiac fibre structure. Such approach opens up possibilities in terms of analysis of the fibre architecture in patients.

In vivo imaging of the cardiac 3D fibre architecture is still a challenge, but it would have many clinical applications, for instance to better understand pathologies and to follow up remodelling after therapy. Recently, cardiac MRI enabled the acquisition of Diffusion Tensor images (DTI) of 2D slices. We propose a method for the complete 3D reconstruction of cardiac fibre architecture in the left ventricular myocardium from sparse in vivo DTI slices. This is achieved in two steps. First we map non-linearly the left ventricular geometry to a truncated ellipsoid. Second, we express coordinates and tensor components in Prolate Spheroidal System, where an anisotropic Gaussian kernel regression interpolation is performed. The framework is initially applied to a statistical cardiac DTI atlas in order to estimate the optimal anisotropic bandwidths. Then, it is applied to in vivo beating heart DTI data sparsely acquired on a healthy subject. Resulting in vivo tensor field shows good correlation with literature, especially the elevation (helix) angle transmural variation. To our knowledge, this is the first reconstruction of in vivo human 3D cardiac fibre structure. Such approach opens up possibilities in terms of analysis of the fibre architecture in patients.

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