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author:("iversen, Per")
1.  Hemodynamics and Function of Resistance Arteries in Healthy Persons and End Stage Renal Disease Patients 
PLoS ONE  2014;9(4):e94638.
Introduction
Cardiovascular disease is the leading cause of death in patients with end stage renal disease (ESRD). The vasodilator mechanisms in small resistance arteries are in earlier studies shown to be reduced in patients with end stage renal disease. We studied whether endothelium dependent vasodilatation were diminished in ESRD patients and the interaction between the macro- and microcirculation.
Methods
Eleven patients with ESRD had prior to renal transplant or insertion of peritoneal dialysis catheter measured pulse wave velocity. During surgery, a subcutaneous fat biopsy was extracted. Resistance arteries were then dissected and mounted on a wire myograph for measurements of dilator response to increasing concentrations of acetylcholine after preconstriction with noradrenaline. Twelve healthy kidney donors served as controls.
Results
Systolic blood pressure was elevated in patients compared to the healthy controls; no difference in the concentration of asymmetric dimethyl arginine was seen. No significant difference in the endothelium dependent vasodilatation between patients and controls was found. Correlation of small artery properties showed an inverse relationship between diastolic blood pressure and nitric oxide dependent vasodilatation in controls. Pulse pressure was positively correlated to the total endothelial vasodilatation in patients. A negative association between S-phosphate and endothelial derived hyperpolarisation-like vasodilatation was seen in resistance arteries from controls.
Conclusion
This study finds similar vasodilator properties in kidney patients and controls. However, correlations of pulse pressure and diastolic blood pressure with resistance artery function indicate compensating measures in the microcirculation during end stage renal disease.
doi:10.1371/journal.pone.0094638
PMCID: PMC3983241  PMID: 24722412
2.  Effect of hyperinsulinemia during hemodialysis on the insulin-like growth factor system and inflammatory biomarkers: a randomized open-label crossover study 
BMC Nephrology  2013;14:80.
Background
A marked reduction in serum levels of bioactive insulin-like growth factor-I (IGF-I) has been observed in fasting hemodialysis (HD) patients during a 4-h HD session. The aim of the present study was to investigate the beneficial effect of hyperinsulinemia during HD on bioactive IGF-I and inflammatory biomarkers.
Methods
In a randomized cross-over study, 11 non-diabetic HD patients received a standardised HD session with either: 1) no treatment, 2) glucose infusion (10% glucose, 2.5 mL/kg/h), or 3) glucose-insulin infusion (10% glucose added 30 IU NovoRapid® per litre, 2.5 mL/kg/h). Each experiment consisted of three periods: pre-HD (−120 to 0 min), HD (0 to 240 min), and post-HD (240 to 360 min). A meal was served at baseline (−120 min); infusions were administered from baseline to 240 min. The primary outcome was change in bioactive IGF-I during the experiment. Secondary outcomes were changes in high-sensitivity C-reactive protein, interleukin-1β, interleukin-6, and tumor necrosis factor α. Comparisons were performed using mixed-model analysis of variance for repeated measures.
Results
From baseline to the end of study, no significant differences were observed in the changes in either serum bioactive IGF-I or total IGF-I between study days. Overall, serum bioactive IGF-I levels rose above baseline at 120 to 300 min with a maximum increase of 20% at 120 min (95% confidence interval (CI), 9 to 31%; p < 0.001), whereas total IGF-I levels rose above baseline at 180 to 300 min with a maximum increase of 5% at 240 min (95% CI, 2 to 9%; p = 0.004). A significant difference was observed in the changes in serum IGF-binding protein-1 (IGFBP-1) between study days (p = 0.008), but differences were only significant in the post-HD period. From baseline to the end of HD, no significant difference was observed in the changes in serum IGFBP-1 levels between study days, and in this time period overall serum IGFBP-1 levels were below baseline at all time points with a maximum decrease of 51% at 180 min (95% CI, 45 to 57%; p < 0.001). None of the investigated inflammatory biomarkers showed any differences in the changes over time between study days.
Conclusions
Postprandial insulin secretion stimulated the IGF-system during HD with no further effect of adding glucose or glucose-insulin infusion. Hyperinsulinemia during HD had no effect on biomarkers of inflammation.
Trial registration
ClinicalTrials.gov registry: NCT01209403
doi:10.1186/1471-2369-14-80
PMCID: PMC3637492  PMID: 23557110
Bioactive IGF-I; Hemodialysis; IGFBP-1; Inflammation; Insulin; Nutrition
3.  Effect of vitamin-D analogue on albuminuria in patients with non-dialysed chronic kidney disease stage 4–5: a retrospective single center study 
BMC Nephrology  2012;13:102.
Background
The vitamin D receptor activator paricalcitol has been shown to reduce albuminuria. Whether this is a unique property of paricalcitol, or common to all vitamin D analogues, is unknown. The primary aim of this study was to evaluate the effect of alfacalcidol on proteinuria, measured as 24 hour (24 h) albuminuria, in patients with chronic kidney disease (CKD) stage 4–5 being treated for secondary hyperparathyroidism (sHPT).
Methods
A retrospective single-center study including adult patients with CKD 4–5, undergoing treatment for sHPT with alfacalcidol, with macroalbuminuria in minimum one 24 h urine collection. Patients were identified in a prospectively collected database of all patients with S-creatinine > 300 μM or creatinine clearance < 30 ml/min. The observation period was from 1st of January 2005 to 31st of December 2009. Phosphate binders and alfacalcidol were provided to patients free of charge.
Results
A total of 146 macroalbuminuric patients were identified, and of these, 59 started alfacalcidol treatment during the observation period. A 12% reduction in 24 h albuminuria was seen after starting treatment. In 19 patients with no change in renin-angiotensin-aldosteron-system (RAAS) inhibition, the reduction in albuminuria was 16%. The reduction remained stable over time (9%) in a subgroup of patients (n = 20) with several urine collections before and after the start of alfacalcidol-treatment.
Conclusion
The present study supports experimental and clinical data on antiproteinuric actions of activated vitamin D analogues, and suggests that this may be a class-effect.
doi:10.1186/1471-2369-13-102
PMCID: PMC3475058  PMID: 22958603
Chronic kidney disease; Hyperparathyroidism; Vitamin D; Albuminuria; Alfacalcidol

Results 1-3 (3)