Interprofessional Differences in Multidimensional Self-Efficacy Associated With Professional Performance in Nephrology During Case-Based Learning.

Introduction: Postgraduate medical education assumes rising importance in the rapidly advancing field of medicine. Case-based learning (CBL), a learner-centered pedagogy employing clinical cases to improve decision-making, is widely embraced in postgraduate medical education, including nephrology. Studies suggest that learning self-efficacy (SE) was closely associated with learning motivation and academic performance; however, very few studies examined this association in postgraduate nephrology education. None evaluated whether there were interprofessional differences concerning such association. Methods: In 2022, we prospectively enrolled physicians and nurses participating in chronic kidney disease (CKD) care from institutions around Taiwan. They completed the Professional Medical Learning Self-efficacy (PMLS) questionnaire after attending >1 CBL session involving CKD care. We undertook confirmatory factor analysis (CFA), followed by structural equation modeling (SEM) to evaluate associations between 5 dimensions of learning SE (conceptual understanding [CU], higher-order cognitive skills [HC], practical work [PW], everyday application [EA], and medical science communication [MSC]) and their professional SE in nephrology according to participants' medical professions. Results: A total of 513 healthcare providers were surveyed. The convergent and construct validity of our questionnaire were satisfied after analyses. We found that better perceived professional performance in the form of higher professional SE in nephrology was significantly associated with all 5 dimensions of learning SE among physicians and nurses. Only CU and PW were significantly associated with physicians' professional performance; whereas among nurses, only HC and MSC were significantly associated. Conclusion: We showed that learning SE was an important determinant of nephrology professional performance. Different medical professions posed influences on major SE dimensions.

Vascular Calcification Heterogeneity from Bench to Bedside: Implications for Manifestations, Pathogenesis, and Treatment Considerations.

Vascular calcification (VC) is the ectopic deposition of calcium-containing apatite within vascular walls, exhibiting a high prevalence in older adults, and those with diabetes or chronic kidney disease. VC is a subclinical cardiovascular risk trait that increases mortality and functional deterioration. However, effective treatments for VC remain largely unavailable despite multiple attempts. Part of this therapeutic nihilism results from the failure to appreciate the diversity of VC as a pathological complex, with unforeseeable variations in morphology, risk associates, and anatomical and molecular pathogenesis, affecting clinical management strategies. VC should not be considered a homogeneous pathology because accumulating evidence refutes its conceptual and content uniformity. Here, we summarize the pathophysiological sources of VC heterogeneity from the intersecting pathways and networks of cellular, subcellular, and molecular crosstalk. Part of these pathological connections are synergistic or mutually antagonistic. We then introduce clinical implications related to the VC heterogeneity concept. Even within the same individual, a specific artery may exhibit the strongest tendency for calcification compared with other arteries. The prognostic value of VC may only be detectable with a detailed characterization of calcification morphology and features. VC heterogeneity is also evident, as VC risk factors vary between different arterial segments and layers. Therefore, diagnostic and screening strategies for VC may be improved based on VC heterogeneity, including the use of radiomics. Finally, pursuing a homogeneous treatment strategy is discouraged and we suggest a more rational approach by diversifying the treatment spectrum. This may greatly benefit subsequent efforts to identify effective VC therapeutics.

The screening, diagnosis, and management of patients with autosomal dominant polycystic kidney disease: A national consensus statement from Taiwan.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of end-stage kidney disease (ESKD) worldwide. Guidelines for the diagnosis and management of ADPKD in Taiwan remains unavailable. In this consensus statement, we summarize updated information on clinical features of international and domestic patients with ADPKD, followed by suggestions for optimal diagnosis and care in Taiwan. Specifically, counselling for at-risk minors and reproductive issues can be important, including ethical dilemmas surrounding prenatal diagnosis and pre-implantation genetic diagnosis. Studies reveal that ADPKD typically remains asymptomatic until the fourth decade of life, with symptoms resulting from cystic expansion with visceral compression, or rupture. The diagnosis can be made based on a detailed family history, followed by imaging studies (ultrasound, computed tomography, or magnetic resonance imaging). Genetic testing is reserved for atypical cases mostly. Common tools for prognosis prediction include total kidney volume, Mayo classification and PROPKD/genetic score. Screening and management of complications such as hypertension, proteinuria, urological infections, intracranial aneurysms, are also crucial for improving outcome. We suggest that the optimal management strategies of patients with ADPKD include general medical care, dietary recommendations and ADPKD-specific treatments. Key points include rigorous blood pressure control, dietary sodium restriction and Tolvaptan use, whereas the evidence for somatostatin analogues and mammalian target of rapamycin (mTOR) inhibitors remains limited. In summary, we outline an individualized care plan emphasizing careful monitoring of disease progression and highlight the need for shared decision-making among these patients.

A combined circulating microRNA panel predicts the risk of vascular calcification in community-dwelling older adults with age strata differences.

BACKGROUND: Older adults have a higher risk of developing vascular calcification (VC). Circulating miRNAs can be potential risk indicators. However, prior studies used single miRNA mostly, whereas miRNA panels were rarely evaluated. We aimed to examine whether a miRNA panel outperformed each miRNA alone, and analyzed whether advanced age affected VC risk predictive performance offered by the miRNA panel. METHODS: We prospectively enrolled older adults (age ≥65 years) during their annual health checkup in 2017, and examined their VC severity followed by analyzing sera for VC regulatory miRNAs (miR-125b-5p, miR-125b-3p, and miR-378a-3p). We used multiple regression analyses to determine associations between each miRNA or a 3-combind panel and VC risk, followed by area under the receiver-operating-characteristics curve (AUROC) analysis. Participants were further divided to those of 65-75 and ≥75 years for comparison. RESULTS: From 199 older adults screened, 169 (median age, 73.3 years) with available calcification assessment were analyzed, among whom 74.6 % having VC. Those with VC had significantly lower circulating miR-125b-5p, miR-125b-3p, and miR-378a-3p levels than those without. Regression analyses showed that the 3-combined miRNA panel exhibited significant associations with VC risk, with significantly higher AUROC than those of models based on individual miRNA. Importantly, in those ≥75 years, the miRNA-predicted risk of VC was more prominent than that in the 65-75 years group. CONCLUSION: A miRNA panel for VC risk prediction might outperform individual miRNA alone in older adults, and advanced age modified the association between circulating miRNAs and the risk of VC.

Aortic arch calcification increases major adverse cardiac event risk, modifiable by echocardiographic left ventricular hypertrophy, in end-stage kidney disease patients.

Background: The factors affecting cardiovascular risk associated with vascular calcification in patients with chronic kidney disease are less well addressed. Distinct risk factors may contribute synergistically to this elevated cardiovascular risk in this population. Objectives: We aimed to determine whether echocardiographic left ventricular hypertrophy (LVH) affects the risk of major adverse cardiac events (MACE) associated with vascular calcification in end-stage kidney disease (ESKD) patients. Methods: In this retrospective cohort study, ESKD patients underwent chest radiography and echocardiography to assess aortic arch calcification (AoAC) and LVH, respectively, and were classified into three groups accordingly: non-to-mild AoAC without LVH, non-to-mild AoAC with LVH, and moderate-to-severe AoAC. The risks of MACE, cardiovascular mortality, and overall mortality were assessed using Cox proportional hazard analysis. Results: Of the 283 enrolled ESKD patients, 44 (15.5%) had non-to-mild AoAC without LVH, 117 (41.3%) had non-to-mild AoAC with LVH, and 122 (43.1%) had moderate-to-severe AoAC. After 34.1 months, 107 (37.8%) participants developed MACE, including 6 (13.6%), 40 (34.2%), and 61 (50%) from each respective group. Those with moderate-to-severe AoAC (Hazard ratio, 3.72; 95% confidence interval, 1.58-8.73) had a significantly higher risk of MACE than did those with non-to-mild AoAC without LVH or with non-to-mild AoAC and LVH (Hazard ratio, 2.73; 95% confidence interval, 1.16-6.46). A similar trend was observed for cardiovascular and overall mortality. Conclusion: Echocardiographic LVH could modify the risk of adverse cardiovascular events associated with vascular calcification in ESKD patients. Interventions aiming to ameliorate both morbidities might be translated into a lower MACE risk in this population.

Literacy for Frailty among Undergraduate Medical Education: An Under-Recognized Opportunity to Improve Geriatric Care.

Our society is aging much faster than it was before, and this phenomenon demands concerted action to optimize geriatric care. Presentations, clinical features, and management decision making are distinct between older adults and general population, and to enhance care quality, there remains unmet needs for undergraduate geriatric education. Among all geriatric syndromes that clinically matter, frailty is particularly instrumental, serving as the overarching phenotype that connects other geriatric conditions and predisposes individuals to adverse outcomes. However, understandings for frailty, or "literacy for frailty" is often poor among healthcare professionals, and misidentification, terminology confusion, and uncertainty surrounding the care of frail older adults, are not uncommon. This lack of frailty literacy undoubtedly contributes to the suboptimal geriatric care patients receive. We therefore propose a rationally designed, concise, and structured program for eliciting medical students' motivation for understanding frailty during their undergraduate period. Our increasing-frailty-literacy program includes 7 modules, accommodating the terminology, integrative pathogenesis, epidemiology of frailty, appropriate screening and identification tool selection, prognostication and patient communication, and individualization of treatment strategies. In combination with digital technologies and hands-on practice opportunities, we believe that our curriculum can promote medical students' learning efficacy for frailty and improve geriatric care for the current generation.

Extracellular MicroRNAs as Potential Biomarkers for Frail Kidney Phenotype: Progresses and Precautions.

Frailty describes the cumulative subtle health deficits leading to an increased vulnerability to insults among older individuals or disease-laden ones. The prevalence of frailty increases substantially and relentlessly over declining renal function. Frailty in patients with chronic kidney disease (CKD) carries kidney-specific risk factors, clinical correlates and outcomes associations, hence alternatively termed frail kidney phenotype by researchers. Pathogenetically, miRNAs participate extensively in the development and aggravation of frailty, including the occurrence of frail kidney phenotype in CKD patients. These understandings spark profound interest in discovering biomarkers for identifying this detrimental phenotype, and extracellular miRNAs emerge as potentially useful ones. Pilot studies identify promising miRNA candidates for evaluating intermediates and surrogates of frail kidney phenotype, and more are underway. Several potential miRNA species in biologic fluids, such as circulating miR-29b and miR-223 (as inflammatory markers), exosomal miR-16-5p, miR-17/92 cluster members, and miR-106-5p (for uremic vasculopathy), serum exosomal miR-203a-3p (for uremic sarcopenia) have been examined and can be promising choices. Nonetheless, there remains research gap in affirming the direct connections between specific miRNAs and frail kidney phenotype. This stems partially from multiple limitations less well acknowledged before. From this perspective, we further outline the limitations and precautions prior to validating specific extracellular miRNA(s) for this purpose, from the definition of frailty definition, the functional and tissue specificity of miRNAs, the severity of CKD, and various technical considerations. It is expected that more affirmative studies can be produced for extending the utility of extracellular miRNAs in predicting frail kidney phenotype.

The Impact of Glucose-Lowering Strategy on the Risk of Increasing Frailty Severity among 49,519 Patients with Diabetes Mellitus: A Longitudinal Cohort Study.

Patients with diabetes mellitus (DM) have a higher risk of incident and aggravating frailty over time. Frailty-initiating risk factors have been identified, but modulators of frail severity over time remain poorly defined. We aimed to explore the influences of glucose-lowering drug (GLD) strategy on DM patients' risk of increasing frail severity. We retrospectively identified type 2 DM patients between 2008 and 2016, dividing them into "no GLD", oral GLD (oGLD) monotherapy, oGLD combination, and those receiving insulin without or with oGLD at baseline. Increasing frail severity, defined as ≥1 FRAIL component increase, was the outcome of interest. Cox proportional hazard regression was utilized to analyze the risk of increasing frail severity associated with GLD strategy, accounting for demographic, physical data, comorbidities, medication, and laboratory panel. After screening 82,208 patients with DM, 49,519 (no GLD, 42.7%; monotherapy, 24.0%; combination, 28.5%; and insulin user, 4.8%) were enrolled for analysis. After 4 years, 12,295 (24.8%) had increasing frail severity. After multivariate adjustment, oGLD combination group exhibited a significantly lower risk of increasing frail severity (hazard ratio (HR) 0.90, 95% confidence interval (CI) 0.86 - 0.94), while the risk of insulin users increased (HR 1.11, 95% CI 1.02 - 1.21) than no GLD group. Users receiving more oGLD exhibited a trend of less risk reduction relative to others. In conclusion, we discovered that the strategy of oral glucose lowering drugs combination might reduce the risk of frail severity increase. Accordingly, medication reconciliation in frail diabetic older adults should take into account their GLD regimens.