Purpose of the review: The Royal College of Physicians and Surgeons of Canada, with its Competence by Design initiative, is adopting the principles of competency-based medical education for residency training and continuing professional development. This initiative is being undertaken to meet the new standards of medical education in Canada, which include social accountability to meet performance-based outcomes of training. Nephrology is poised to implement Competence by Design into residency training in July 2018 and initiate a continuous quality improvement cycle to periodically renew and update the training requirements to be socially accountable and relevant in the modern age of medicine. The purpose of this review is to describe the process of entrustable professional activity and required training experience development and how they will affect subspecialty training in Canada. Sources of information: The construct of competency-based medical education was derived from existing literature searches of the medical education literature, including documentation provided by the Royal College of Physicians and Surgeons of Canada. The content for each entrustable professional activity and milestone was derived by consensus from the community expertise of the working group, existing speciality training requirements, and elements of training requirements that the Royal College has been mandated to superimpose on all training requirements to meet societal expectations. Methods: The Royal College Specialty Committee in Nephrology participated in 2 years of preparation for this implementation, which has included the creation of a new educational design for the discipline and the elucidation of entrustable professional activities to describe the scope of nephrology practice and to guide teaching, learning, and assessment in residency, and ultimately maintenance of competence in practice. Key findings: This article introduces the set of entrustable professional activities for adult and pediatric nephrology and describes the national consultation as part of an ongoing quality improvement of this work. Limitations: The implementation of Competence by Design will be tested by whether trainees embrace competency-based education by training to just entrustable professional activities, rather than the holistic model idealized in physician training. This is mitigated by the entrustable professional activity development incorporating multiple layers of competencies beyond a procedural skill. Time commitment for faculty will pose additional challenges in increasing the time for assessment of trainees, but is supported by electronic platforms at the Royal College to assist in data gathering and analysis. Implications: Competence by Design in nephrology is an outcomes-based curriculum and assessment platform that aims to train nephrologists to meet societal expectations in an ever-changing and complicated health care system. The goals are to increase safety and professional accountability to society and improve upon the already high standards of training within Canada.

BACKGROUND:The Centers for Disease Control and Prevention recommend immunizing susceptible high-risk groups, such as hemodialysis patients, against hepatitis B virus. However, hemodialysis patients may not develop seroprotective antibodies despite receiving high doses of the vaccine. Recent reports indicate that combined vaccination against hepatitis B and hepatitis A viruses may improve the immunogenicity of hepatitis B vaccine in healthy individuals, but the effectiveness of this strategy in hemodialysis patients is unknown.STUDY DESIGN:Prospective randomized controlled trial.SETTING & PARTICIPANTS:Hepatitis B virus-seronegative hemodialysis patients with undetectable antibody levels at baseline.INTERVENTION:Intramuscular administration of Twinrix (inactivated hepatitis A virus [720 ELISA units] and purified hepatitis B virus surface antigen [20 μg]; GlaxoSmithKline) and Engerix-B (purified hepatitis B virus surface antigen [20 μg]) at 0, 1, and 6 months plus Engerix-B, 40 μg, at month 2 (intervention arm) or Engerix-B, 40 μg, at 0, 1, 2, and 6 months (control arm). Both groups received a total dose of 160 μg of hepatitis B antigen.OUTCOMES:The primary outcome was the difference in seroprotection rates at 7 months, defined by antibody titers >10 mIU/mL. The secondary outcome was frequency of adverse events.MEASUREMENTS:Antibody response at months 3 and 7.RESULTS:96 patients were enrolled, and 73 completed the investigation. At 3 months, there was no difference in the groups' seroprotection rates (25% vs 27%; P = 0.4). At the completion of the vaccination series, using per-protocol analysis, 27 of 40 (68%) and 16 of 33 (49%) had antibody titers >10 mIU/mL in the treatment and control groups, respectively (P = 0.05; RR, 1.4; absolute abatement, 19%). Intention-to-treat analysis showed 58% and 38% seroprotection rates in the treatment and control groups, respectively (P = 0.02; RR, 1.5; absolute abatement, 20%). There was no difference in adverse events.LIMITATIONS:Lack of evidence of long-term protection.CONCLUSION:Vaccination of hemodialysis patients with a combined hepatitis A and hepatitis B regimen resulted in a statistically significant and clinically important improvement in seroprotection against hepatitis B virus compared with hepatitis B monovalent vaccine.

BACKGROUND AND OBJECTIVES:Cardiovascular events are 10 to 100 times more frequent in chronic kidney disease (CKD). We tested the hypothesis that the rate of atherosclerotic plaque growth is faster in severe versus moderate CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:We performed a prospective cohort study in 318 prevalent CKD patients with initial creatinine clearance (CCr) between 20 and 50 ml/min/1.73 m(2). Baseline clinical and laboratory data were obtained on all patients. Plaque area was determined every 6 mo using bilateral carotid ultrasonography. Plaque area distribution was normalized using a cube root transformation. Unadjusted and adjusted associations between CCr quintiles and rate of change in the transformed plaque area were assessed using multiple linear regression. RESULTS:The rate of plaque progression appeared lower in patients with the lowest CCr. Median rate of plaque growth was 0.4 mm(2)/yr in the lowest quintile of CCr (< 23 ml/min/1.73 m(2)) versus 5.0 mm(2)/yr in the highest quintile (> 43 ml/min/1.73 m(2)). This association remained significant after adjustment for potential confounders. A secondary analysis using quintiles of Modification of Diet in Renal Disease (MDRD) GFR confirmed the absence of increased plaque growth at low GFR, although a reduced rate of growth in the lowest quintile of MDRD GFR was not observed. CONCLUSION:We did not observe accelerated plaque growth at low levels of renal function. We suggest that mechanisms other than plaque growth are responsible for the observed excess of cardiovascular disease in CKD patients.

Purpose: Haemodialysis patients often have increased TnT concentrations in the absence of symptoms suggestive of acute coronary syndrome. To evaluate the potential usefulness of establishing patient specific baselines, we investigated intra-individual variability of TnT concentration in stable haemodialysis patients.Methods: We measured pre-dialysis troponin T concentrations weekly for 15 weeks in 61 stable haemodialysis patients.Results: Thirty two of 61 patients had at least one result greater than the diagnostic cut-off for significant myocardial damage of 0.04 mu g/L. The intra-individual variability was small; 99% of all the variance from each patient's median was <= 0.063 mu g/L.Conclusions: Intra-individual variability in TnT concentration is small enough to merit establishment a of baseline concentration for each haemodialysis patient. This baseline is stable over at least 15 weeks; samples need be collected no more frequently than this. A change in concentration of more than 0.06 mu g/L from the individual's baseline is significant. (c) 2009 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

Background This randomized clinical trial is designed to assess whether the prevention and/or correction of anemia, by immediate versus delayed treatment with erythropoietin alfa in patients with chronic kidney disease, would delay left ventricular (LV) growth. Study design and sample size calculations were based on previously published Canadian data. Methods: One hundred seventy-two patients were randomly assigned. The treatment group received therapy with erythropoietin alfa subcutaneously to maintain or achieve hemoglobin (Hgb) level targets of 12.0 to 14.0 g/dL (120 to 140 g/L). The control/delayed treatment group had Hgb levels of 9.0 +/- 0.5 g/dL (90 5 g/L) before therapy was started: target level was 9.0 to 10.5 g/dL (90 to 105 g/L). Optimal blood pressure and parathyroid hormone, calcium, and phosphate level targets were prescribed; all patients were iron replete. The primary end point is LV growth at 24 months. Results: One hundred fifty-two patients were eligible for the intention-to-treat analysis: mean age was 57 years, 30% were women, 38% had diabetes, and median glomerular filtration rate was 29 mL/min (0.48 mL/s; range, 12 to 55 mL/min [0.20 to 0.92 mL/s]). Blood pressure and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker use were similar in the control/delayed treatment and treatment groups at baseline. Erythropoietin therapy was administered to 77 of 78 patients in the treatment group, with a median final dose of 2,000 IU/wk. Sixteen patients in the control/delayed treatment group were administered erythropoietin at a median final dose of 3,000 IU/wk. There was no statistically significant difference between groups for the primary outcome of mean change in LV mass index (LVMI) from baseline to 24 months, which was 5.21 +/- 30.3 g/m(2) in the control/delayed treatment group versus 0.37 +/- 25.0 g/m(2) in the treatment group. Absolute mean difference between groups was 4.85 g/m(2) (95% confidence interval, -4.0 to 13.7; P = 0.28). Mean Hgb level was greater in the treatment group throughout the study and at study end was 12.75 g/dL (127.5 g/L in treatment group versus 11.46 g/dL [114.6 g/L] in control/delayed treatment group; P = 0.0001). LV growth occurred in 20.1% in the treatment group versus 31% in the control/delayed treatment group (P = 0.136). In patients with a stable Hgb level, mean LVMI did not change (-0.25 +/- 26.7 g/m(2)), but it increased in those with decreasing Hgb levels (19.3 +/- 28.2 g/m(2); P = 0.002). Conclusion: This trial describes disparity between observational and randomized controlled trial data: observed and randomly assigned Hgb level and LVMI are not linked; thus, there is strong evidence that the association between Hgb level and LVMI likely is not causal. Large randomized controlled trials with unselected patients, using morbidity and mortality as outcomes, are needed.

The high prevalence of cardiovascular disease (CVD) in patients with kidney disease is well described. This Canadian, multicenter, observational cohort study reports the prevalence and risk factors of CVD associated with kidney disease, in a cohort of patients with established chronic kidney disease (CKD), who are followed-up by nephrologists. This analysis sought to answer 2 questions: (1) in patients with established CKD, are the prevalence and progression of CVD accounted for by conventional or uremia-related risk factors, and (2) to what extent can progression to renal replacement therapy (RRT) be explained by CVD versus traditional risk factors for kidney disease? This study population consists of 313 patients (predominantly men) who had a mean age of 56 years and a mean creatinine clearance of 36 mL/min. Thirty percent were diabetic. The overall prevalence of CVD was 46%, and was independent of severity of kidney dysfunction (P = 0.700). The median follow-up time was 23 months, for a total of 462 patient years. We note the overall incidence of CVD events (new CVD or worsening of CVD) was 47/244 (20%). The best predictors of new CVD events among those without preexisting CVD were diabetes (odds ratio [OR] = 5.35, P = 0.018) and age (OR = 1.26, P = 0.08). In those with preexisting CVD, low diastolic pressure (DP) (OR = .72, P = 0.004) and high triglycerides (OR = 1.48, P = 0.019) at baseline were independent predictors of progression of CVD. We could not determine an independent impact of kidney function on CVD in the overall cohort. Furthermore, we determined that the presence of CVD itself confers an increased risk for progression to RRT (relative risk [RR] = 1.58, P = 0.047), adjusted for kidney function. This is the first in-depth analysis of CVD in a cohort of patients with established chronic kidney disease who are not on dialysis. The question regarding the impact of the altered biology of uremia in contributing to CVD progression remains unanswered, and clearly needs further study. However, the findings do raise the issue of whether aggressive treatment of CVD and risk factors might, in fact, reduce progression to RRT. Further large-scale, observational studies as well as interventional studies are needed to more clearly understand the complex biology of cardiovascular and kidney disease progression. © 2001 by the National Kidney Foundation, Inc.