Posts Tagged ‘2007’

Nephrological Issues in Experimental Research

vrijdag, december 16th, 2011
TitleNephrological Issues in Experimental Research
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Year2007
Estimated date2007-01-12
CategoryScientific presentation
PlatformNone
DescriptionMy presentation for the Nephrology Winterschool in 2007 about the NIER website.
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Nephrological Issues In Experimental Research: Creating a dynamic research field

vrijdag, december 16th, 2011
TitleNephrological Issues In Experimental Research: Creating a dynamic research field
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Year2007
Estimated date2007-03-06
CategoryScientific presentation
PlatformNone
DescriptionOur poster for some symposium about the NIER website initiative. Harm did a graduation project with me.
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Low Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients

woensdag, december 7th, 2011
TitleLow Levels of sRAGE Are Associated With Increased Risk for Mortality in Renal Transplant Recipients
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Year2007
Estimated date2007-05-01
CategoryScientific Publication
PlatformNone
DescriptionObjective. Infusion of the soluble form of the receptor for advanced glycation end-products (sRAGE) was protective against atherosclerosis and nephropathy in animal models. In this study we investigated determinants of endogenous sRAGE in renal transplant recipients and whether sRAGE was associated with mortality and graft loss. Methods and Results. A total of 591 patients participated at a median time of 6 years after transplantation. Independent determinants of sRAGE were mycophenolate mofetil medication (0.21, P0.001), creatinine clearance (0.15, P0.001), BMI (0.12, P0.003) and fasting insulin concentration (0.14, P0.001). Low sRAGE levels were associated with a 2–3 times higher risk for mortality especially after correction for creatinine clearance (P0.006). Conclusion. A lack of sRAGE is a risk factor for mortality in renal transplant recipients. The putatively protective role of sRAGE and in particular its association with mycophenolate mofetil usage needs further investigation. (Transplantation 2007;84: 659–663)
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Renal Function Dependent Association of AGTR1 Polymorphism (A1166C) and Electrocardiographic Left-Ventricular Hypertrophy

woensdag, december 7th, 2011
TitleRenal Function Dependent Association of AGTR1 Polymorphism (A1166C) and Electrocardiographic Left-Ventricular Hypertrophy
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Year2007
Estimated date2007
CategoryScientific Publication
PlatformNone
DescriptionBackground: The association of renin-angiotensin system (RAS) polymorphisms and left-ventricular hypertrophy (LVH) may depend on the presence of risk factors for LVH, such as renal dysfunction. We studied whether renal function modulates the association between RAS polymorphisms and LVH in a cross-sectional study of 8592 inhabitants of Groningen. Methods: Left-ventricular hypertrophy was determined with electrocardiograms, using the Cornell voltage-duration product. The following RAS polymorphisms were determined: angiotensin II type-1 receptor (AGTR1 A1166C), angiotensin-converting enzyme (ACE) insertion/deletion (I/ D), and angiotensinogen (AGT G-6A). The AGTR1 A1166C and ACE I/D polymorphisms were in Hardy-Weinberg equilibrium. Results: Electrocardiographic LVH was present in 417 (5.0%) subjects. Subjects with LVH were older (53 v 49 years) and overall had more cardiovascular risk factors. Using logistic regression, creatinine clearance interacted with the relationship between the AGTR1 A1166C polymorphism and LVH (, 0.19; P  .033). In subjects with the CC genotype, in contrast to carriers of an A allele, the prevalence of LVH increased with more pronounced renal dysfunction. Creatinine clearance also interacted with the relationship between the ACE I/D polymorphism and LVH (, 0.12; P  .037), although less strongly, and the other way around. Creatinine clearance did not influence the association between the AGT G-6A polymorphism and LVH (, 0.006; P  .491). Conclusions: In this population-based study, the AGTR1 A1166C polymorphism was associated with LVH, dependent on concomitant renal dysfunction. A weaker renal function dependent association between the ACE I/D polymorphism and LVH was also observed. Renal function should be taken into account as a relevant environmental factor for the pathogenetic effects of RAS polymorphisms. Am J Hypertens 2007;20:1097–1103 © 2007 American Journal of Hypertension, Ltd.
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