Durable efficacy of liraglutide in patients with type 2 diabetes and pronounced insulin-associated weight gain: 52-week results from the Effect of Liraglutide on insulin-associated wEight GAiN in patients with Type 2 diabetes' (ELEGANT) randomized controlled trial.

BACKGROUND: Pronounced weight gain frequently complicates insulin therapy in patients with type 2 diabetes (T2DM). We have previously reported that addition of liraglutide for 26 weeks can reverse insulin-associated weight gain, decrease insulin dose and improve glycaemic control, as compared with continuation of standard insulin treatment. OBJECTIVES: To investigate whether the beneficial effects of liraglutide are sustained up to 52 weeks and whether similar effects could be obtained when liraglutide is added 6 months later. METHODS: Adult T2DM patients with ≥ 4% weight gain within 16 months of insulin therapy completing the first 26-week trial period of open-label addition of liraglutide 1.8 mg day(-1) (n = 26) versus continuation of standard insulin therapy (n = 24) were all treated with liraglutide for another 26 weeks. Results were analysed according to the intention-to-treat principle. RESULTS: Overall, 24 (92%) and 18 (75%) patients originally assigned to liraglutide and standard therapy, respectively, completed the study. Addition of liraglutide decreased body weight to a similar extend when given in the first 26 weeks (liraglutide group) or second 26 weeks (original standard therapy group): -4.4 vs. -4.3 kg (difference -0.32 kg, 95% confidence interval -2.2 to 1.6 kg; P = 0.74). Similar results were also seen in the two groups with regard to decrease in haemoglobin A1c (HbA1c ) (-0.77 vs. -0.66%; P = 0.23) and insulin dose (-28 vs. -26 U day(-1) ; P = 0.32). In both groups, 22% of patients could discontinue insulin. Continuation of liraglutide until 52 weeks led to sustained effects on body weight, HbA1c and insulin-dose requirements. CONCLUSION: In T2DM patients with pronounced insulin-associated weight gain, addition of liraglutide within 2 years leads to sustained reversal of body weight, improved glycaemic control and decrease in insulin dose. Thus, liraglutide offers a valuable therapeutic option.

Start of insulin therapy in patients with type 2 diabetes mellitus promotes the influx of macrophages into subcutaneous adipose tissue.

AIMS/HYPOTHESIS: Insulin therapy in patients with type 2 diabetes mellitus is accompanied by weight gain characterised by an increase in abdominal fat mass. The expansion of adipose tissue mass is generally paralleled by profound morphological and inflammatory changes. We hypothesised that the insulin-associated increase in fat mass would also result in changes in the morphology of human subcutaneous adipose tissue and in increased inflammation, especially when weight gain was excessive. METHODS: We investigated the effects of weight gain on adipocyte size, macrophage influx, and mRNA expression and protein levels of key inflammatory markers within the adipose tissue in patients with type 2 diabetes mellitus before and 6 months after starting insulin therapy. RESULTS: As expected, insulin therapy significantly increased body weight. At the level of the subcutaneous adipose tissue, insulin treatment led to an influx of macrophages. When comparing patients gaining no or little weight with patients gaining >4% body weight after 6 months of insulin therapy, both subgroups displayed an increase in macrophage influx. However, individuals who had gained weight had higher protein levels of monocyte chemoattractant protein-1, TNF-α and IL-1ß after 6 months of insulin therapy compared with those who had not gained weight. CONCLUSIONS/INTERPRETATION: We conclude that insulin therapy in patients with type 2 diabetes mellitus improved glycaemic control but also induced body weight gain and an influx of macrophages into the subcutaneous adipose tissue. In patients characterised by a pronounced insulin-associated weight gain, the influx of macrophages into the adipose tissue was accompanied by a more pronounced inflammatory status. TRIAL REGISTRATION: ClinicalTrials.gov: NCT00781495. FUNDING: The study was funded by European Foundation for the Study of Diabetes and the Dutch Diabetes Research Foundation.

Progressive renal disease despite immunosuppressive therapy in a patient with Wegener s granulomatosis.

We present a patient with Morbus Wegener and crescentic glomerulonephritis. Treatment with cyclophosphamide and prednisolone resulted in the disappearance of signs and symptoms of systemic inflammation. However, renal function deteriorated. Renal biopsy showed evidence of continuing capillary necrosis. Renal function improved with added plasmapheresis treatment. This case report illustrates that in patients with vasculitis necrotizing glomerulonephritis may remain active despite immunosuppressive therapy, even in the absence of extrarenal disease activity.

A cost-controlling treatment strategy of adding liraglutide to insulin in type 2 diabetes.

BACKGROUND: Addition of the GLP-1 receptor agonist liraglutide to insulin can reverse insulin-associated weight gain, improve HbA1c and decrease the need for insulin, but is expensive. From a cost perspective, such treatment should be discontinued when it is clear that treatment targets will not be achieved. Our aim was to find the best cost-controlling treatment strategy: the shortest possible trial period needed to discriminate successfully treated patients from those failing to achieve predefined targets of treatment success. METHODS: We used data from the 'Effect of Liraglutide on insulin-associated wEight GAiN in patients with Type 2 diabetes' (ELEGANT) trial, comparing additional liraglutide (n = 47) and standard insulin therapy (n = 24) during 26 weeks, to calculate the costs associated with different trial periods. Treatment success after 26 weeks was defined by having achieved ≥ 2 of the following: ≥ 4% weight loss, HbA1c ≤ 53 mmol/mol (7%), and/or discontinuation of insulin. RESULTS: The additional direct costs of adding liraglutide for 26 weeks were € 699 per patient, or € 137 per 1 kg weight loss, compared with standard therapy. The best cost-controlling treatment strategy (identifying 21 of 23 responders, treating four non-responders) was to continue treatment in patients showing ≥ 3% weight loss or ≥ 60% decrease in insulin dose at 8 weeks, with a total cost of € 246 for this t rial period, saving € 453 in case of early discontinuation. CONCLUSION: An 8-week trial period of adding liraglutide to insulin in patients with insulin-associated weight gain is an effective cost-controlling treatment strategy if the liraglutide is discontinued in patients not showing an early response regarding weight loss or insulin reduction.

[Hyponatremia: effective treatment based on calculated outcomes]. / Hyponatriëmie: adequate behandeling op geleide van te berekenen uitkomsten.

A 78-year-old man was treated for symptomatic hyponatremia. Despite administration of an isotonic NaCl 0.9% solution, plasma sodium remained unchanged due to high concentrations of sodium and potassium in the urine. After infusion of a hypertonic NaCl solution, a satisfactory increase in plasma sodium was reached and symptoms resolved gradually. The hyponatremia was found to be caused by hypothyroidism, which was treated. A 70-year-old female was admitted to the hospital with loss of consciousness and hyponatremia. She was treated initially with a hypertonic NaCl 2.5% solution, which resulted in a steady increase in plasma sodium and a resolution of symptoms. Treatment was changed to an isotonic NaCl 0.9% infusion to attenuate the rise of serum sodium. Nevertheless plasma sodium increased too rapidly due to increased diuresis and reduced urinary sodium and potassium excretion. A slower increase in plasma sodium was achieved by administering a glucose 5% infusion. Hyponatremia is frequently observed in hospitalised patients. It should be treated effectively, and the rate of correction should be adapted to the clinical situation. Effective treatment is determined by calculating changes in effective osmoles and the resulting changes in the distribution of water over extra- and intracellular spaces. Changes in urine production and urinary excretion of sodium and potassium should be taken into account.

[A young man with a painful knee]. / Een jongeman met een pijnlijke knie.

A 23-year-old man injured his left knee. A CT scan showed a dislocation of the proximal tibiofibular joint. Closed reduction of the dislocation was done successfully under procedural sedation and analgesia. Afterwards he was treated with a pressure bandage and immobilisation of the knee for 2 weeks.

Center of mass trajectories during turning in patients with Parkinson's disease with and without freezing of gait.

BACKGROUND: Despite the strong relationship between freezing of gait (FOG) and turning in Parkinson's disease (PD), few studies have addressed specific postural characteristics during turning that might contribute to freezing. METHODS: Thirty participants with PD (16 freezers, 14 non-freezers) (all tested OFF medication) and 14 healthy controls walked 5 meters and turned 180° in a 3D gait laboratory. COM behavior was analyzed during four turning quadrants of 40° between 10° and 170° pelvic rotation and during 40° before actual FOG episodes. These pre-FOG segments were compared with similar turning sections in turns of freezers without FOG. Outcome parameters were turn time, COM distance, COM velocity, step width and the medial- and anterior COM position. RESULTS: Turn time was increased in freezers compared to non-freezers (p=.000). No differences were found regarding COM distance and velocity during turning quadrants between groups and between freezers' pre-FOG segments and similar turning segments without FOG. Medial COM deviation was reduced in PD patients compared to controls (p=.004), but no differences were found between freezers and non-freezers. In turns with freezing, turn time increased (p=.005) and step width decreased (p=.025) pre-FOG. Freezers also showed a less medial (p=.020) and more anterior (p=.016) COM position pre-FOG compared to turning sections without FOG. CONCLUSIONS: Our results revealed no subgroup differences in COM behavior during uninterrupted turning. However, we found a reduced medial deviation, a forward COM shift and a decreased step width in freezers just before FOG episodes. These abnormalities may play a causal role, as they could hamper stability and fluent weight shifting necessary for continued stepping during turning.

Dual-task-related neural connectivity changes in patients with Parkinson' disease.

BACKGROUND AND OBJECTIVES: Dual-task (DT) gait impairment in people with Parkinson's disease (PD) and specifically in those with freezing of gait (FOG), reflects attentional dependency of movement. This study aimed to elucidate resting-state brain connectivity alterations related to DT gait abnormalities in PD with and without FOG. METHODS: PD patients (n=73) and healthy age-matched controls (n=20) underwent DT gait analysis and resting-state functional Magnetic Resonance Imaging (rs-MRI) while 'off' medication. Patients were classified as freezer (n=13) or non-freezer (n=60). Functional connectivity (FC) alterations between PD and controls and between patient subgroups were assessed in regions of interest (ROIs) within the fronto-parietal and motor network. RESULTS: PD had longer stance times, shorter swing times and more step length asymmetry during DT gait and needed more time and steps during DT turning compared to controls. Additionally, freezers showed similar impairments and longer double support times compared to non-freezers during DT gait. PD demonstrated hyper-connectivity between the inferior parietal lobule and premotor cortex (PMC) and between the cerebellum and the PMC and M1. FOG-specific hypo-connectivity within the striatum and between the caudate and superior temporal lobe and hyper-connectivity between the dorsal putamen and precuneus was correlated with worse DT performance. CONCLUSION: PD showed FC alterations in DT-related networks, which were not correlated to DT performance. However, FOG-specific FC alterations in DT-related regions involving the precuneus and striatum were correlated to worse DT performance, suggesting that the balance between cognitive and motor networks is altered.

Prevalence of "syndrome X" features in parents of type 1 diabetic patients with or without nephropathy.

OBJECTIVE: To compare the prevalence of "syndrome X"-related parameters in parents of type 1 diabetic patients with diabetic nephropathy (DNP) to those in parents of diabetic patients without DNP. RESEARCH DESIGN AND METHODS: In this cross-sectional study, we included 50 parents of type 1 diabetic patients with DNP and 50 parents of diabetic patients without DNP. All parents were investigated in a fasting state for serum lipids including nonesterified fatty acids (NEFAs), glucose, HbA1c, plasma uric acid, fasting insulin levels, and albuminuria. Blood pressure was recorded in the supine position using an automatic device; ankle/brachial index was measured with Doppler ultrasound. Presence of cardiovascular disease was determined by a standardized questionnaire and electrocardiogram registration. Subjects without known diabetes underwent a 2-h oral glucose tolerance test. Anthropometric parameters such as BMI, waist-to-hip ratio, and percentage of body fat were measured. In addition to univariate analysis, a syndrome X score (SXS) was formulated, comprising a number of syndrome X-related biochemical, physiological, and/or anthropometric parameters. RESULTS: Univariate analysis revealed no significant differences in syndrome X parameters between parents of type 1 diabetic patients with or without DNP. Also, the composite SXS was similar in both groups. CONCLUSIONS: In this study, no differences were found in the prevalence of syndrome X features between parents of type 1 diabetic patients with DNP and parents of patients without DNP.

Activation of the sodium-potassium pump contributes to insulin-induced vasodilation in humans.

Systemic hyperinsulinemia induces vasodilation in human skeletal muscle. This vasodilation contributes to insulin-stimulated glucose uptake and has been found to be reduced in various insulin-resistant states. The mechanism of the effect of insulin on vascular tone is not completely understood. We hypothesized that activation of the sodium-potassium pump (Na+, K(+)-ATPase) located in endothelial or smooth muscle cells would be involved in the insulin-mediated vasodilation. Therefore, in 24 healthy, nonsmoking, nonobese, normotensive volunteers, we infused ouabain, a specific inhibitor of Na+, K(+)-ATPase, into the brachial artery before and during euglycemic hyperinsulinemia. As expected, insulin (systemic concentrations, approximately 700 [low] and 1400 [high] pmol.L-1) induced vasodilation in the control arm (forearm blood flow [FBF, plethysmography] from 1.6 +/- 0.2 to 2.1 +/- 0.4 mL.dL-1.min-1 [low insulin] and from 1.6 +/- 0.2 to 2.1 +/- 0.2 [high insulin], P < .05 for both), but the increase in FBF was abolished in the ouabain-infused forearm (from 1.3 +/- 0.1 to 1.4 +/- 0.2 mL.dL-1.min-1 [low] and from 1.3 +/- 0.1 to 1.3 +/- 0.1 [high], P = NS). Ouabain-induced increases in forearm potassium release were partly reversed by insulin. To investigate whether the mechanism of action could be at the endothelial level, we infused NG-monomethyl-I-arginine (L-NMMA), an inhibitor of endothelial nitric oxide synthase (0.05, 0.1, and 0.2 mg.dL-1.min-1) intra-arterially in 12 subjects and induced a clear dose-dependent decrease of FBF from 1.7 +/- 0.2 to 1.2 +/- 0.1 mL.dL-1.min-1 (P < .01). In contrast, after ouabain (and continued insulin) infusion, L-NMMA had no effect on FBF (from 1.6 +/- 0.4 to 1.5 +/- 0.3 mL.dL-1.min-1, n = 6, P = .66). These results demonstrate that insulin induces vasodilation by stimulation of Na+, K(+)-ATPase. This activation of Na+, K(+)-ATPase could occur at the level of the endothelium rather than that of vascular smooth muscle and contributes to the endothelium-dependent vasodilator response to insulin.

Influence of angiotensin converting enzyme inhibition and angiotensin II type 1 receptor antagonism on renal sodium and water handling and albuminuria during infusion of atrial natriuretic factor into healthy volunteers.

BACKGROUND: Atrial natriuretic factor increases urinary sodium and water excretion. It also causes an increase in albuminuria. Angiotensin converting enzyme inhibition attenuates the effects of atrial natriuretic factor on renal sodium and water handling; however, it is not known whether this effect is mediated by the accompanied decrease in blood pressure or by suppression of the renin-angiotensin system. OBJECTIVE: To test the hypothesis that atrial natriuretic factor mediates natriuresis and diuresis by inhibiting angiotensin II, by studying the effects of the angiotensin converting enzyme inhibitor enalapril and the angiotensin II type 1 receptor antagonist losartan. In addition, the effects of these drugs on atrial natriuretic factor-induced albuminuria were examined. DESIGN AND METHODS: We investigated the effects of enalapril and losartan on atrial natriuretic factor-induced changes in urinary excretion of sodium, water and albumin from eight healthy volunteers. Measurements of systemic and renal haemodynamics in these subjects were performed before and during a 2 h infusion of atrial natriuretic factor [0.01 microg/kg per min (low dose) for the first 60 min and 0.02 microg/kg per min (high dose) for the second 60 min]. Measurements were performed after 5 days of pretreatment with placebo, 50 mg losartan or 20 mg enalapril daily. RESULTS: Mean arterial pressures during the clearance study were 84.6 +/- 1.7 mmHg after placebo, 84.0 +/- 2.2 mmHg after losartan treatment and 80.0 +/- 2.5 mmHg after enalapril treatment (P < 0.05). Plasma renin activity was significantly increased both by losartan and by enalapril treatments. Neither enalapril nor losartan treatment attenuated atrial natriuretic factor-induced changes in renal haemodynamics. After placebo pretreatment, fractional urinary excretion of sodium increased significantly during infusion of atrial natriuretic factor. Losartan treatment did not influence the increase in urinary excretion of sodium during infusion of atrial natriuretic factor, whereas enalapril treatment significantly attenuated this increase (P < 0.01). Atrial natriuretic factor significantly increased albuminuria. Neither losartan nor enalapril treatment reduced atrial natriuretic factor-induced albuminuria. CONCLUSIONS: Enalapril treatment lowered blood pressure and attenuated the atrial natriuretic factor-induced increase in urinary excretion of sodium. In contrast, the angiotensin II type 1 receptor antagonist losartan, at a dosage that did not lower blood pressure, did not attenuate the increase in urinary excretion of sodium. These data indicate that atrial natriuretic factor increases natriuresis and diuresis independently of angiotensin II. The increase in albuminuria during infusion of atrial natriuretic factor was not influenced by enalapril and losartan treatments.

Transcapillary escape rate of albumin is increased and related to haemodynamic changes in normo-albuminuric type 1 diabetic patients.

OBJECTIVE: An increase in urinary albumin excretion (UAE) in type 1 diabetic patients might reflect changes in vascular permeability and/or local haemodynamic factors. Indeed, transcapillary escape of albumin (TERalb), a measure of systemic capillary efflux, is increased in diabetic patients, even in those with a modest increase of albuminuria. In normo-albuminuric type 1 diabetic patients, systemic capillary and glomerular flow is increased. We hypothesized that these haemodynamic changes contribute to an elevated TERalb, even in the phase preceding micro-albuminuria. METHODS: We measured TERalb in 39 normo-albuminuric type 1 diabetic patients and 46 healthy controls. TERalb was calculated from the disappearance curve of 125I-albumin. Renal and systemic haemodynamics were measured by standard techniques. Forearm blood flow (FBF) was measured by plethysmography. Endothelial function was assessed by intra-arterial infusion of acetylcholine. The structural integrity of the vessel wall was determined by the post-occlusive reactive hyperaemia test. RESULTS: TERalb was increased in diabetic patients (5.53+/-0.40 versus 4.39+/-0.21 %/h, P = 0.01). Patients were divided into tertiles with respect to their TERalb. There were no differences in UAE, blood pressure, metabolic parameters, endothelial function or maximal vasodilatation after occlusion between the groups. However, filtration fraction and FBF were significantly increased in the group of diabetic patients with the highest levels of TERalb. Overall, in diabetic patients, FBF was significantly correlated with TERalb. CONCLUSIONS: TERalb is increased in normo-albuminuric type 1 diabetic patients. In these patients with an increased capillary permeability, there is no evidence of endothelial dysfunction or vessel wall damage. However, both FBF and filtration fraction are increased. Therefore, the increased vascular permeability in the early phase of type 1 diabetes is associated with general haemodynamic alterations. Notably, such an increase in vascular permeability is not necessarily reflected by abnormal UAE. This could be due to either a lack of change in glomerular permeability or due to the fact that the threshold for tubular reabsorption of albumin has not been exceeded.

The impact of blood pressure measurement methods on the assessment of differences in blood pressure levels between patients with normoalbuminuric type 1 diabetes and healthy controls.

The aim of the study was to investigate the impact of various blood pressure (BP) measurement methods on the assessment of differences in BP levels between patients with normoalbuminuric type 1 diabetes and healthy controls. We measured intra-arterial BP (i.a.), sphygmomanometric BP (sphygmo), 24-h ambulatory blood pressure (ABPM, auscultatory, Profilomat) and oscillometric BP (Dinamap) in 51 patients with normoalbuminuric type 1 diabetes (DP) with a mean diabetes duration of 8.4 years and 42 healthy controls (C). Results are expressed as mean +/- SE. There was no significant difference in i.a. BP between DP and C (systolic/diastolic BP and mean arterial pressure (MAP) 116.2 +/- 1.2/61.7 +/- 0.8 (82.8 +/- 0.9) mm Hg in DP vs 115.6 +/- 1.2/63.2 +/- 0.9 (83.4 +/- 1.1) in C). Sphygmo BP was 117.7 +/- 1.3/69.8 +/- 1.0 mm Hg in DP vs 116.5 +/- 1.5/67.8 +/- 1.3 in C (NS). Also, ABPM was not significantly different between both groups. Daytime BP between 10.00-23.00 h was 120.9 +/- 1.2/84.4 +/- 0.9 mm Hg in DP vs 120.4 +/- 1.5/83.7 +/- 1.0 in C (NS). Night-time BP between 01.00-07.00 h was 102.4 +/- 1.2/69.3 +/- 0.9 mm Hg in DP vs 103.4 +/- 1.5/69.1 +/- 1.3 in C (NS). In contrast, systolic Dinamap BP was higher in DP (118.6 +/- 1.3 in DP vs 113.4 +/- 1.4 mm Hg in C, P = 0.01) as was MAP (85.6 +/- 0.7 in DP vs 83.3 +/- 1.0 mm Hg in C, P = 0.05). Diastolic Dinamap BP was not significantly different (66.6 +/- 0.7 in DP vs 65.0 +/- 1.0 mm Hg in C). We conclude that intra-arterial BP was similar in patients with normoalbuminuric type 1 diabetes and healthy controls. Also, when using auscultatory BP devices there were no apparent differences in blood pressure. In contrast, using the oscillometric method (Dinamap), BP especially systolic, was higher in diabetic patients. Measurements with an oscillometric device (Dinamap) might therefore overestimate BP in patients with normoalbuminuric type 1 diabetes, thus confusing conclusions on the relationship between development of hypertension and microalbuminuria in the early phase of diabetes.

Transient hypoparathyroidism in a patient with fever.

A case history is described of a young man suffering from fever of unknown origin, which was accompanied by transient hypoparathyroidism. There were no indications of a known cause of the hypoparathyroidism. Transient hypoparathyroidism is briefly reviewed and the possibility of parathyroiditis is discussed.

Contribution of change in glycosylated haemoglobin to insulin-associated weight gain: results of a longitudinal study in type 2 diabetic patients.

To investigate the contribution of glycosylated haemoglobin change (HbA1c) on body weight in patients with type 2 diabetes after start of insulin therapy. We analysed 122 individual weight-profiles in relation to the change in HbA1c per se in these patients up to 36 months after the start of insulin therapy. Data were analysed separately for the first 9 months after commencement of insulin therapy and for the period thereafter. Within the first 9 months of insulin therapy mean body weight increased by 0.52 kg per month. HbA1c decreased from 9.9 ± 1.8 to 7.9 ± 1.3%. Only 12% of the initial weight gain could be attributed to the change in HbA1c. Furthermore, the mean monthly increase in body weight gain was reduced by 0.006 kg for every 1 kg higher body weight at baseline. From 9 to 36 months after start of insulin therapy, body weight increased by 0.1 kg/month, which was independent of change in HbA1c. Improvement of glycaemic control per se contributes little to initial weight gain after start of insulin therapy in patients with T2DM. After 9 months of insulin treatment, weight gain is unrelated to change in glycosylated haemoglobin. Other factors have to be responsible for weight gain after start of insulin therapy.

Nurse practitioners improve quality of care in chronic kidney disease: two-year results of a randomised study.

BACKGROUND: Chronic kidney disease (CKD) is associated with increased cardiovascular risk. Here we evaluate whether strict implementation of guidelines aimed at multiple targets with the aid of nurse practitioners (NP) improves management in patients with CKD. METHODS: MASTER PLAN is a randomised controlled clinical trial, performed in nine Dutch hospitals. Patients with CKD (estimated glomerular filtration rate (eGFR) 20-70 ml÷min) were randomised to receive NP support (intervention group (IG)) or physician care (control group (CG)). Patients were followed for a median of five years. Presented data are an interim analysis on risk factor control at two-year follow-up. RESULTS: We included 788 patients (532 M, 256 F), (393 CG, 395 IG), mean (±SD ) age 59 (±13) years, eGFR 38 (±15) ml÷min÷1.73m(2), blood pressure (BP) 138 (±21)÷80 (±11) mmHg. At two years 698 patients (352 IG, 346 CG) could be analysed. IG as compared with CG had lower systolic (133 vs 135 mmHg; p= 0.04) and diastolic BP (77 vs 80 mmHg; p=0.007), LDL cholesterol (2.30 vs 2.45 mmol(-l); p= 0.03), and increased use of ACE inhibitors, statins, aspirin and vitamin D. The intervention had no effect on smoking cessation, body weight, physical activity or sodium excretion. CONCLUSION: In both groups, risk factor management improved. However, changes in BP control, lipid management and medication use were more pronounced in IG than in CG. Lifestyle interventions were not effective. Coaching by NPs thus benefits everyday care of CKD patients. Whether these changes translate into improvement in clinical endpoints remains to be established.

Hospital specific factors affect quality of blood pressure treatment in chronic kidney disease.

BACKGROUND: Blood pressure (BP) is the most important modifiable risk factor for cardiovascular (CV) disease and progression of kidney dysfunction in patients with chronic kidney disease. Despite extensive antihypertensive treatment possibilities, adequate control is notoriously hard to achieve. Several determinants have been identified which affect BP control. In the current analysis we evaluated differences in achieved BP and achievement of the BP goal between hospitals and explored possible explanations. METHODS: At baseline, BP was measured in a supine position with an oscillometric device in 788 patients participating in the MASTER PLAN study. We also retrieved the last measured office BP from the patient records. Additional baseline characteristics were derived from the study database. Univariate and multivariate analyses were performed with general linear modelling using hospital as a random factor. RESULTS: In univariate analysis, hospital was a determinant of the level of systolic and diastolic BP at baseline. Adjustment for patient, kidney disease, treatment or hospital characteristics affected the relation. Yet, in a fully adjusted model, differences between centres persisted with a range of 15 mmHg for systolic BP and 11 mmHg for diastolic BP. CONCLUSION: Despite extensive adjustments, a clinically relevant, statistically significant difference between hospitals was found in standardised BP measurements at baseline of a randomised controlled study. We hypothesise that differences in the approach towards BP control exist at the physician level and that these explain the differences between hospitals.