Problem-based learning in the first or second language: Does it make a difference?

Problem-based learning (PBL) is the key didactic approach in the curriculum of the Stenden Hotel Management School. Real-world problems are used to activate prior knowledge and to trigger a learning process aimed at expanding and elaborating students’ understanding and competences. Since the hotel school accommodates an international student population, the entire programme uses English as the medium for communication. For approximately 90% of our students, English is a second language. This paper reports on the effectiveness of using the mother tongue (language 1) in collaborative learning, as opposed to using the student’s second language. We did so by asking a group of 12 students, who all have Dutch as their first language to perform all PBL activities in English as they usually do. At a later stage, the same group was asked to do a similar task in Dutch. PBL sessions were videotaped in our PBL lab, transcribed and analysed. Utterances of students were divided into the following categories: (1) statements, (2) constructive statements, (3) arguments, (4) questions, (5) confirmations, (6) negations, and (7) source utterances. The utterance analysis was limited to the first five steps in a seven-step approach. The findings in this small-scale pilot show – in line with earlier research – that students mainly communicate factual statements, hardly ask questions, and seldom confirm each other’s contributions when using their second language. However, when the first language was used, scores were more positive. Further research should show whether or not this is a structural finding. It was a surprise to notice that the English session contained nine minutes of “reading from paper” out of 32 minutes of reporting. In the Dutch session “reading from paper/tablet/phone” was absent.Keywords: problem-based learning, second language, collaborative learning, verbal interactions, utterance analysis, Englishmedium educatio

A Self-management Approach for Dietary Sodium Restriction in Patients With CKD:A Randomized Controlled Trial

Health and self-regulatio

Fibroblast growth factor 23 is related to profiles indicating volume overload, poor therapy optimization and prognosis in patients with new-onset and worsening heart failure

Background: Fibroblast growth factor (FGF) 23 is a hormone that increases urinary phosphate excretion and regulates renal sodium reabsorption and plasma volume. We studied the role of plasma FGF23 in therapy optimization and outcomes in patients with new-onset and worsening heart failure (HF). Methods: We measured plasma C-terminal FGF23 levels at baseline in 2399 of the 2516 patients included in the BIOlogy Study to Tailored Treatment in Chronic HF (BIOSTAT-CHF) trial. The association between FGF23 and outcome was evaluated by Cox regression analysis adjusted for potential confounders. Results: Median FGF23 was 218.0 [IQR: 117.1–579.3] RU/ml; patients with higher FGF23 levels had a worse NYHA class, more signs of congestion, and were less likely to use an ACE-inhibitor (ACEi) or angiotensin receptor blocker (ARBs) at baseline (all P < 0.01). Higher FGF23 levels were independently associated with higher BNP, lower eGFR, the presence of oedema and atrial fibrillation (all P < 0.001). In addition, higher FGF23 was independently associated with impaired uptitration of ACEi/ARBs after 3 months, but not of beta-blockers. In multivariable Cox regression analysis, FGF23 was independently associated with all-cause mortality (hazard ratio: 1.17 (1.09–1.26) per log increase, P < 0.001), and the combined endpoint of all-cause mortality and HF hospitalization (1.15 (1.08–1.22) per log increase, P < 0.001). Conclusions: In patients with new-onset and worsening HF, higher plasma FGF23 levels were independently associated with volume overload, less successful uptitration of ACEi/ARBs and an increased risk of all-cause mortality and HF hospitalization

Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study

CONTEXT: Although dietary potassium and sodium intake may influence calcium-phosphate metabolism and bone health, the effects on bone mineral parameters, including fibroblast growth factor 23 (FGF23), are unclear. OBJECTIVE: Here, we investigated the effects of potassium or sodium supplementation on bone mineral parameters. DESIGN, SETTING, PARTICIPANTS: We performed a post hoc analysis of a dietary controlled randomized, blinded, placebo-controlled crossover trial. Prehypertensive individuals not using antihypertensive medication (n = 36) received capsules containing potassium chloride (3 g/d), sodium chloride (3 g/d), or placebo. Linear mixed-effect models were used to estimate treatment effects. RESULTS: Potassium supplementation increased plasma phosphate (from 1.10 ± 0.19 to 1.15 ± 0.19 mmol/L, P = 0.004), in line with an increase in tubular maximum of phosphate reabsorption (from 0.93 ± 0.21 to 1.01 ± 0.20 mmol/L, P < 0.001). FGF23 decreased (114.3 [96.8-135.0] to 108.5 [93.5-125.9] RU/mL, P = 0.01), without change in parathyroid hormone and 25-hydroxy vitamin D3. Fractional calcium excretion decreased (from 1.25 ± 0.50 to 1.11 ± 0.46 %, P = 0.03) without change in plasma calcium. Sodium supplementation decreased both plasma phosphate (from 1.10 ± 0.19 to 1.06 ± 0.21 mmol/L, P = 0.03) and FGF23 (from 114.3 [96.8-135.0] to 108.7 [92.3-128.1] RU/mL, P = 0.02). Urinary and fractional calcium excretion increased (from 4.28 ± 1.91 to 5.45 ± 2.51 mmol/24 hours, P < 0.001, and from 1.25 ± 0.50 to 1.44 ± 0.54 %, P = 0.004, respectively). CONCLUSIONS: Potassium supplementation led to a decrease in FGF23, which was accompanied by increase in plasma phosphate and decreased calcium excretion. Sodium supplementation reduced FGF23, but this was accompanied by dec

Fibroblast Growth Factor 23: a Bridge Between Bone Minerals and Renal Volume Handling

The work in this thesis addresses the interaction between the phosphate-regulating hormone Fibroblast Growth Factor 23 (FGF-23) as key player in bone-mineral homeostasis and renal volume handling, mainly in the context of the renin-angiotensin-aldosterone system (RAAS). First, we elaborate on the role of vitamin D in chronic kidney disease (CKD) and its potential to increase effectiveness of RAAS-blockade. Next, we review the role of (excessive) sodium intake and why patients with CKD are particularly susceptible to the effects of sodium. Consecutively, we found that high FGF-23 levels are associated with an impaired antiproteinuric response to RAAS-blockade combined with a low sodium diet in patients with CKD. High FGF-23 concentrations are strongly associated with a high risk of cardiovascular mortality in CKD and hemodialysis patients. We add to this that also in renal transplant recipients high FGF-23 concentrations are correlated with adverse cardiovascular events, independent of existing, established risk factors. Moreover, FGF-23 levels correlated with markers of high volume status as NT-proBNP and copeptin. FGF-23 levels are extremely high in end stage renal disease. We found that part of the variance in these levels can be explained by ultrafiltration volume: patients who need more fluid withdrawal in dialysis, have far higher FGF-23 levels. The aforementioned chapters strongly suggest a link between volume status and FGF-23. We tested whether volume interventions, i.e. infusion of 2L saline or a 6-week sodium restriction, could in turn affect FGF-23 levels, this seems not to be the case. Although sodium interventions do not change FGF-23 concentrations, interventions aimed at phosphate intake do. Therefore, we examined the relation between these two minerals. Sodium intake and phosphate intake, as assessed by 24h-excretion, are strongly and robustly correlated across different populations: in renal transplant recipients, but also in diabetes patients and healthy volunteers. We interpret these findings in line with the observation that food products rich in sodium are also rich in phosphate. For example, processed-foods are notorious for their high sodium content, but they also contain a lot of phosphate-based additives which is far less commonly known. Expanding on healthy components of a healthy diet, we next investigate potassium. Healthy food choices as fruits and vegetables are rich in potassium. Following the observation that potassium supplementation appears to increase serum phosphate level, we hypothesized that potassium may lower FGF-23 levels. We confirmed this in the KaNa trial, where participants received potassium supplements or placebo combined with a fully-controlled diet. Several of our findings advocate changes in dietary intake, however this is difficult to achieve. In the multicenter, randomized controlled trial SUBLIME we deployed an approach that combined E-health technology based on self-regulation (behavioral change) theory, group meetings and individual coaching and we discuss the first results and feedback from participants in this thesis. In conclusion, this thesis places FGF-23 firmly as a bridge between sodium-volume and bone-mineral (phosphate) homeostasis

Dietary sodium restriction:a neglected therapeutic opportunity in chronic kidney disease

PURPOSE OF REVIEW: Restriction of dietary sodium is recommended at a population level as well as for groups at high cardiovascular risk, and chronic kidney disease (CKD). This review addresses recent evidence for the protective effect of dietary sodium restriction in CKD patients specifically. RECENT FINDINGS: Sodium intake in CKD populations is generally high, and often above population average. Recent data demonstrated that moderately lower sodium intake in CKD patients is associated with substantially better long-term outcome of renin–angiotensin–aldosterone system (RAAS)-blockade, in diabetic and nondiabetic CKD, related to better effects of RAAS-blockade on proteinuria, independent of blood pressure. This is in line with better short-term efficacy of RAAS-blockade during moderate sodium restriction in diabetic and nondiabetic CKD. This effect of sodium restriction is likely mediated by its effects on volume status. Sustainable sodium restriction can be achieved by approaches on the basis of behavioral sciences. SUMMARY: Moderate restriction of dietary sodium can substantially improve the protective effects of RAAS-blockade in CKD, by specific renal effects apparent from proteinuria reduction. The latter precludes straightforward extrapolation of data from nonrenal populations to CKD. Concerns regarding the adverse effects of a very low sodium intake should not distract from the protective effects of moderate sodium restriction. Prospective studies should assess the efficacy and sustainability of different strategies to target high sodium intake in CKD, along with measures at population level. VIDEO ABSTRACT: http://links.lww.com/CONH/A1