Gerjan Navis

University of Groningen, Groningen, Groningen, Netherlands

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Publications (482)3198.12 Total impact

  • Transplantation 01/2015; 99(1):e5-e6. · 3.78 Impact Factor
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    ABSTRACT: -The renin-angiotensin-aldosterone-system (RAAS) is critical for regulation of blood pressure and fluid balance and influences cardiovascular remodeling. Dysregulation of the RAAS contributes to cardiovascular and renal morbidity. The genetic architecture of circulating RAAS components is incompletely understood. -We meta-analyzed genome-wide association data for plasma renin activity (n=5,275), plasma renin concentrations (n=8,014) and circulating aldosterone (n=13,289) from up to four population-based cohorts of European and European-American ancestry, and assessed replication of the top results in an independent sample (n=6,487). Single nucleotide polymorphisms (SNPs) in two independent loci displayed associations with plasma renin activity at genome-wide significance (p<5x10(-8)). A third locus was close to this threshold (rs4253311 in kallikrein B [KLKB1], p=5.5x10(-8)). Two of these loci replicated in an independent sample for both plasma renin and aldosterone concentrations (SNP rs5030062 in kininogen 1 [KNG1]: p=0.001 for plasma renin, p=0.024 for plasma aldosterone concentration; rs4253311 with p<0.001 for both plasma renin and aldosterone concentration). SNPs in the NEBL gene reached genome-wide significance for plasma renin concentration in the discovery sample (top SNP rs3915911, p=8.81x10(-9)), but did not replicate (p=0.81). No locus reached genome-wide significance for aldosterone. SNPs rs5030062 and rs4253311 were not related to blood pressure or renal traits; in a companion study, variants in the kallikrein B locus were associated with B-type natriuretic peptide concentrations in African-Americans. -We identified two genetic loci (kininogen 1 and kallikrein B) influencing key components of the RAAS, consistent with the close interrelation between the kallikrein-kinin system and the RAAS.
    Circulation Cardiovascular Genetics 12/2014; · 6.73 Impact Factor
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    ABSTRACT: The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD.
    Nature Genetics 12/2014; · 35.21 Impact Factor
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    ABSTRACT: Vitamin K modulates calcification by activating calcification inhibitors such as matrix Gla protein (MGP). In kidney transplant recipients, vitamin K insufficiency is common, but implications for long-term outcomes are unclear. Single-center observational study with a longitudinal design. 518 stable kidney transplant recipients; 56% men; mean age, 51±12 (SD) years; and a median of 6 (IQR, 3-12) years after kidney transplantation. Plasma desphosphorylated-uncarboxylated MGP (dp-ucMGP) levels, reflecting vitamin K status. All-cause mortality and transplant failure. At inclusion, median dp-ucMGP level was 1,038 (IQR, 733-1,536) pmol/L, with 473 (91%) patients having vitamin K insufficiency (defined as dp-ucMGP>500pmol/L). During a median follow-up of 9.8 (IQR, 8.5-10.2) years, 152 (29%) patients died and 54 (10%) developed transplant failure. Patients in the highest quartile of dp-ucMGP were at considerably higher mortality risk compared with patients in the lowest quartile (HR, 3.10; 95% CI, 1.87-5.12; P for trend<0.001; P for quartile 1 [Q1] vs Q4<0.001). After adjustment for potential confounders, including kidney function and exclusion of patients treated with a vitamin K antagonist, this association remained significant. Patients in the highest quartile also were at higher risk of developing transplant failure (HR, 2.61; 95% CI, 1.22-5.57; P for trend=0.004; P for Q1 vs Q4=0.01), but this association was lost after adjustment for baseline kidney function (HR, 1.20; 95% CI, 0.52-2.75; P for trend=0.6; P for Q1 vs Q4=0.7). Although MGP exists as various species, only dp-ucMGP was measured. No data were available for vascular calcification as an intermediate end point. Vitamin K insufficiency, that is, a high circulating level of dp-ucMGP, is highly prevalent in stable kidney transplant recipients and is associated independently with increased risk of mortality. Future studies should address whether vitamin K supplementation may lead to improved outcomes after kidney transplantation. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 11/2014; · 5.29 Impact Factor
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    ABSTRACT: Little is known about optimal protein intake after transplantation. The aim of this study was to prospectively investigate associations of urinary urea excretion, a marker for protein intake, with graft failure and mortality in renal transplant recipients (RTR) and potential effect modification by body mass index (BMI) and estimated glomerular filtration rate (eGFR).
    Transplantation 11/2014; · 3.78 Impact Factor
  • Martin H de Borst, Gerjan Navis
    Nature Reviews Nephrology 11/2014; · 7.94 Impact Factor
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    ABSTRACT: Circulating bilirubin, a natural antioxidant, is associated with decreased risk of type 2 diabetes (T2D), but the nature of the relationship remains unknown. We performed Mendelian randomization in a prospective cohort of 3,381 participants free of diabetes at baseline (aged 28-75 years; women, 52.6%). We used rs6742078 located in UDP-glucuronosyltransferase (UGT1A1) locus as instrumental variable (IV) to study a potential causal effect of serum total bilirubin on T2D risk. A total of 210 (6.2%) participants developed T2D during a median follow-up of 7.8 years. In adjusted analyses, rs6742078, which explained 19.5% of bilirubin variation, was strongly associated with total bilirubin (a 0.68-SD increase in bilirubin levels per T allele; P<1×10(-122)) and was also associated with T2D risk (OR 0.69 [95%CI, 0.54-0.90]; P=0.006). Per 1-SD increase in log-transformed bilirubin levels, we observed a 25% (OR 0.75 [95%CI, 0.62-0.92]; P=0.004) lower risk of T2D. In Mendelian randomization analysis, the causal risk reduction for T2D was estimated to be 42% (causal ORIVestimation per 1-SD increase in log-transformed bilirubin 0.58 [95%CI, 0.39-0.84]; P=0.005), which was comparable to the observational estimate (Durbin-Wu-Hausman chi-square test Pfor difference =0.19). These novel results provide evidence that elevated bilirubin is causally associated with risk of T2D and support its role as a protective determinant.
    Diabetes 11/2014; · 7.90 Impact Factor
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    ABSTRACT: Context: Vitamin D deficiency is common in renal transplant recipients (RTR). The long-term implications of vitamin D deficiency in RTR remain unclear. Objective: We investigated whether 25(OH) or 1,25(OH)2 levels are associated with mortality, renal function decline, and graft failure in stable RTR. Design: Observational study with longitudinal design; follow-up of 7.0 [6.2-7.5] years. Setting: Single-center outpatient clinic. Participants: 435 stable RTR, 51% men, mean age 52±12 years, included at a median of 6 [3-12] years after kidney transplantation. Main Outcome Measures: All-cause mortality, annual change of renal function (eGFR), graft failure. Results: Mean 25(OH)D and 1,25(OH)2D were 21.6±9.1 ng/mL and 45.2±19.0 pg/mL, respectively. During follow-up, 99 patients died (22.8%) and 44 patients developed graft failure (10.1%). In univariate analysis, both 25(OH)D and 1,25(OH)2D were significantly associated with mortality (HR 0.64 [95%CI 0.51-0.81], P<0.001 and 0.69 [0.55-0.87], P=0.002 per SD increase, respectively). The inverse association of 25(OH)D with mortality remained significant after adjustment for potential confounders (HR 0.68 [0.52-0.89], P=0.004 per SD increase). The associations of 1,25(OH)2D with mortality and graft failure lost significance after adjustment for renal function. Severe vitamin D deficiency (25[OH]D <12 ng/mL) was independently associated with stronger annual eGFR decline . Conclusions: Low 25(OH)D is independently associated with an increased risk of all-cause mortality and 25(OH)D <12 ng/mL with a rapid eGFR decline in stable RTR. The association of low 1,25(OH)2D with mortality or graft failure depends on renal function. These results should encourage RCTs evaluating the effect of vitamin D supplementation after kidney transplantation..
    The Journal of clinical endocrinology and metabolism. 10/2014;
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    ABSTRACT: Hypertension and proteinuria are important mediators of renal damage. Despite therapeutic interventions, the number of patients with end stage renal disease steadily increases. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilatory, anti-inflammatory and antioxidant properties. These beneficial characteristics make H2S an attractive candidate for pharmacological use in hypertensive renal disease. We investigated the protective properties of H2S in angiotensin II (Ang II)-induced hypertensive renal disease in rats. Treatment with the H2S donor NaHS and major H2S metabolite sodium thiosulfate (STS) during three weeks of Ang II infusion reduced hypertension, proteinuria, oxidative stress and renal functional and structural deterioration. In an ex vivo isolated perfused kidney setup NaHS, but not STS, reduced intrarenal pressure. The effect of NaHS could partially be explained by its activation of the ATP-sensitive potassium channels. In conclusion, treatment with H2S attenuates Ang II-associated functional and structural renal deterioration, suggesting that intervention in H2S production pathways has potential therapeutic benefit and might be a valuable addition to the already existing antihypertensive and renoprotective therapies.
    Nitric Oxide. 10/2014;
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    International Journal of Behavioral Medicine 10/2014; · 2.63 Impact Factor
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    ABSTRACT: -Serelaxin is a promising therapy for acute heart failure. The renal hemodynamic effects of serelaxin in patients with chronic heart failure (CHF) are unknown.
    Circulation Heart Failure 10/2014; · 6.68 Impact Factor
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    ABSTRACT: Background Residual proteinuria during renin-angiotensin-aldosterone system (RAAS) blockade is a major renal and cardiovascular risk factor in chronic kidney disease. Dietary sodium restriction potentiates the antiproteinuric effect of RAAS blockade, but residual proteinuria remains in many patients. Previous studies linked high fibroblast growth factor 23 (FGF-23) levels with volume overload; others linked higher serum phosphate levels with impaired RAAS-blockade efficacy. We hypothesized that FGF-23 reduces the capacity of dietary sodium restriction to potentiate RAAS blockade, impairing the antiproteinuric effect. Study Design Post hoc analysis of cohort data from a randomized crossover trial with two 6-week study periods comparing proteinuria after a regular-sodium diet with proteinuria after a low-sodium diet, both during background angiotensin-converting enzyme inhibition. Setting & Participants 47 nondiabetic patients with CKD with residual proteinuria (median protein excretion, 1.9 [IQR, 0.8-3.1] g/d; mean age, 50 ± 13 [SD] years; creatinine clearance, 69 [IQR, 50-110] mL/min). Predictor Plasma carboxy-terminal FGF-23 levels. Outcomes Difference in residual proteinuria at the end of the regular-sodium versus low-sodium study period. Residual proteinuria during the low-sodium diet period adjusted for proteinuria during the regular-sodium diet period. Results Higher baseline FGF-23 level was associated with reduced antiproteinuric response to dietary sodium restriction (standardized β = −0.46; P = 0.001; model R2 = 0.71). For every 100-RU/mL increase in FGF-23 level, the antiproteinuric response to dietary sodium restriction was reduced by 10.6%. Higher baseline FGF-23 level was a determinant of more residual proteinuria during the low-sodium diet (standardized β = 0.27; P = 0.003) in linear regression analysis adjusted for baseline proteinuria (model R2 = 0.71). There was no interaction with creatinine clearance (P interaction = 0.5). Baseline FGF-23 level did not predict changes in systolic or diastolic blood pressure upon intensified antiproteinuric treatment. Limitations Observational study, limited sample size. Conclusions FGF-23 levels are associated independently with impaired antiproteinuric response to sodium restriction in addition to RAAS blockade. Future studies should address whether FGF-23−lowering strategies may further optimize proteinuria reduction by RAAS blockade combined with dietary sodium restriction.
    American Journal of Kidney Diseases 09/2014; · 5.29 Impact Factor
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    Jelmer K Humalda, Gerjan Navis
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    ABSTRACT: 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.
    Current opinion in nephrology and hypertension. 09/2014;
  • Grigory Sidorenkov, Gerjan Navis
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    ABSTRACT: Introduction: ACE inhibitors are first-line therapy in patients with chronic kidney disease (CKD). The main adverse effects of ACE inhibitors are hypotension, renal function impairment and hyperkalemia. Areas covered: This paper reviews evidence from clinical studies regarding adverse effects of ACE inhibitors in patients with CKD. The safety aspects of ACE inhibitors are discussed in relation to their pharmacological action, drug-drug interactions, drug-diet interaction, precautions needed in certain clinical conditions and other adverse effects. Expert opinion: The main adverse effects of ACE inhibitors follow from their interaction with renin-angiotensin-aldosterone system (RAAS)-activity and volume depletion. This interaction can be turned into clinical benefit and increase efficacy of ACE inhibitors by reduction in dietary sodium or adding diuretics. Dual RAAS-blockade is no longer advocated in patients with CKD because of the safety issues, and combination of ACE inhibitors with moderate reduction in dietary sodium intake is a better alternative. The intensified treatment regimens based on ACE inhibitors can potentially improve renoprotection, but increase the risk of adverse effects. Better strategies to address safety concerns are needed. Introduction of clinical rules and safety indicators may help clinicians to identify hazardous co-prescriptions and adverse dietary habits and can decrease the frequency of adverse effects.
    Expert Opinion on Drug Safety 08/2014; · 2.74 Impact Factor
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    ABSTRACT: Syndecan-1 is a transmembrane heparan sulfate (HS) proteoglycan present on hepatocytes and involved in uptake of triglyceride-rich lipoproteins via its HS polysaccharide side chains. We hypothesized that altered hepatic syndecan-1 metabolism could be involved in dyslipidemia related to renal transplantation. In a rat renal transplantation model elevated plasma triglycerides were associated with fivefold increased expression of hepatic syndecan-1 mRNA (p < 0.01), but not protein. Expression of syndecan-1 sheddases (ADAM17, MMP9) and heparanase was significantly up-regulated after renal transplantation (all p < 0.05). Profiling of HS side chains revealed loss of hepatic HS upon renal transplantation accompanied by significant decreased functional capacity for VLDL binding (p = 0.02). In a human renal transplantation cohort (n = 510), plasma levels of shed syndecan-1 were measured. Multivariate analysis showed plasma syndecan-1 to be independently associated with triglycerides (p < 0.0001) and inversely with HDL cholesterol (p < 0.0001). Last, we show a physical association of syndecan-1 to HDL from renal transplant recipients (RTRs), but not to HDL from healthy controls. Our data suggest that after renal transplantation loss of hepatic HS together with increased syndecan-1 shedding hampers lipoprotein binding and uptake by the liver contributing to dyslipidemia. Our data open perspectives toward improvement of lipid profiles by targeted inhibition of syndecan-1 catabolism in renal transplantation.
    American Journal of Transplantation 08/2014; · 6.19 Impact Factor
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    ABSTRACT: Previous prospective cohort studies on the association between potassium intake and risk of hypertension have almost exclusively relied on self-reported dietary data, whereas repeated 24-hour urine excretions, as estimate of dietary uptake, may provide a more objective and quantitative estimate of this association. Risk of hypertension (defined as blood pressure ≥140/90 mm Hg or initiation of blood pressure-lowering drugs) was prospectively studied in 5511 normotensive subjects aged 28 to 75 years not using blood pressure-lowering drugs at baseline of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study. Potassium excretion was measured in two 24-hour urine specimens at baseline (1997-1998) and midway during follow-up (2001-2003). Baseline median potassium excretion was 70 mmol/24 h (interquartile range, 57-85 mmol/24 h), which corresponds to a dietary potassium intake of ≈91 mmol/24 h. During a median follow-up of 7.6 years (interquartile range, 5.0-9.3 years), 1172 subjects developed hypertension. The lowest sex-specific tertile of potassium excretion (men: <68 mmol/24 h; women: <58 mmol/24 h) had an increased risk of hypertension after multivariable adjustment (hazard ratio, 1.20; 95% confidence interval, 1.05-1.37), compared with the upper 2 tertiles (Pnonlinearity=0.008). The proportion of hypertension attributable to low potassium excretion was 6.2% (95% confidence interval, 1.7%-10.9%). No association was found between the sodium to potassium excretion ratio and risk of hypertension after multivariable adjustment. Low urinary potassium excretion was associated with an increased risk of developing hypertension. Dietary strategies to increase potassium intake to the recommended level of 90 mmol/d may have the potential to reduce the incidence of hypertension.
    Hypertension 07/2014; · 6.87 Impact Factor
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    ABSTRACT: In chronic heart failure (CHF), low body mass as a reflection of low muscle mass has been associated with poor outcome. Urinary creatinine excretion rate (CER) is an established marker of muscle mass, but has not been investigated in CHF. This study aims to evaluate urinary CER as a marker of muscle mass in patients with CHF and establish the relationship with clinical outcome.
    Clinical Research in Cardiology 07/2014; · 3.67 Impact Factor
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    ABSTRACT: Plasma copeptin, a marker of arginine vasopressin, is elevated in patients with autosomal dominant polycystic kidney disease and predicts disease progression. It is unknown whether elevated copeptin levels result from decreased kidney clearance or as compensation for impaired concentrating capacity. Data from patients with autosomal dominant polycystic kidney disease and healthy kidney donors before and after donation were used, because after donation, overall GFR decreases with a functionally normal kidney.DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Data were obtained between October of 2008 and January of 2012 from healthy kidney donors who visited the institution for routine measurements predonation and postdonation and patients with autosomal dominant polycystic kidney disease who visited the institution for kidney function measurement. Plasma copeptin levels were measured using a sandwich immunoassay, GFR was measured as (125)I-iothalamate clearance, and urine concentrating capacity was measured as urine-to-plasma ratio of urea. In patients with autosomal dominant polycystic kidney disease, total kidney volume was measured with magnetic resonance imaging.RESULTS: Patients with autosomal dominant polycystic kidney disease (n=122, age=40 years, men=56%) had significantly higher copeptin levels (median=6.8 pmol/L; interquartile range=3.4-15.7 pmol/L) compared with donors (n=134, age=52 years, men=49%) both predonation and postdonation (median=3.8 pmol/L; interquartile range=2.8-6.3 pmol/L; P<0.001; median=4.4 pmol/L; interquartile range=3.6-6.1 pmol/L; P<0.001). In donors, copeptin levels did not change after donation, despite a significant fall in GFR (from 105±17 to 66±10; P<0.001). Copeptin and GFR were significantly associated in patients with autosomal dominant polycystic kidney disease (β=-0.45, P<0.001) but not in donors. In patients with autosomal dominant polycystic kidney disease, GFR and total kidney volume were both associated significantly with urine-to-plasma ratio of urea (β=0.84, P<0.001; β=-0.51, P<0.001, respectively).CONCLUSIONS: On the basis of the finding in donors that kidney clearance is not a main determinant of plasma copeptin levels, it was hypothesized that, in patients with autosomal dominant polycystic kidney disease, kidney damage and associated impaired urine concentration capacity determine copeptin levels.
    Clinical journal of the American Society of Nephrology : CJASN. 07/2014;
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    ABSTRACT: Background Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. Methods In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that affect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. Findings In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, −0·12 mm Hg, 95% CI −0·20 to −0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97—0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, −0·02 mm Hg, −0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of −0·10 mm Hg in systolic blood pressure (−0·21 to −0·0001; p=0·0498) and a change of −0·08 mm Hg in diastolic blood pressure (−0·15 to −0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96—0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of −0·29 mm Hg in diastolic blood pressure (−0·52 to −0·07; p=0·01), a change of −0·37 mm Hg in systolic blood pressure (−0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87—0·97; p=0·002). Interpretation Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This finding warrants further investigation in an independent, similarly powered study.
    The Lancet Diabetes and Endocrinology. 06/2014;
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    ABSTRACT: Although age-dependent effects on blood pressure (BP) have been reported, they have not been systematically investigated in large-scale genome-wide association studies (GWASs). We leveraged the infrastructure of three well-established consortia (CHARGE, GBPgen, and ICBP) and a nonstandard approach (age stratification and metaregression) to conduct a genome-wide search of common variants with age-dependent effects on systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse (PP) pressure. In a two-staged design using 99,241 individuals of European ancestry, we identified 20 genome-wide significant (p ≤ 5 × 10(-8)) loci by using joint tests of the SNP main effect and SNP-age interaction. Nine of the significant loci demonstrated nominal evidence of age-dependent effects on BP by tests of the interactions alone. Index SNPs in the EHBP1L1 (DBP and MAP), CASZ1 (SBP and MAP), and GOSR2 (PP) loci exhibited the largest age interactions, with opposite directions of effect in the young versus the old. The changes in the genetic effects over time were small but nonnegligible (up to 1.58 mm Hg over 60 years). The EHBP1L1 locus was discovered through gene-age interactions only in whites but had DBP main effects replicated (p = 8.3 × 10(-4)) in 8,682 Asians from Singapore, indicating potential interethnic heterogeneity. A secondary analysis revealed 22 loci with evidence of age-specific effects (e.g., only in 20 to 29-year-olds). Age can be used to select samples with larger genetic effect sizes and more homogenous phenotypes, which may increase statistical power. Age-dependent effects identified through novel statistical approaches can provide insight into the biology and temporal regulation underlying BP associations.
    The American Journal of Human Genetics 06/2014; · 11.20 Impact Factor

Publication Stats

8k Citations
3,198.12 Total Impact Points


  • 1995–2014
    • University of Groningen
      • • Department of Nephrology
      • • Department of Clinical Pharmacology
      • • Department of Cardiology
      • • Faculty of Medical Sciences
      • • Department of Internal Medicine
      Groningen, Groningen, Netherlands
  • 1984–2014
    • Universitair Medisch Centrum Groningen
      • • Department of Internal Medicine
      • • Department of Cardiology
      Groningen, Groningen, Netherlands
  • 2013
    • The Jackson Laboratory
      Bar Harbor, Maine, United States
    • Uppsala University
      Uppsala, Uppsala, Sweden
  • 2012
    • VU University Medical Center
      • Department of Molecular Cell Biology and Immunology
      Amsterdam, North Holland, Netherlands
  • 2011–2012
    • University of Rochester
      • Department of Pathology and Laboratory Medicine
      Rochester, NY, United States
    • Medizinische Universität Innsbruck
      • Sektion für Genetische Epidemiologie
      Innsbruck, Tyrol, Austria
  • 2010
    • University of California, San Diego
      • Department of Medicine
      San Diego, CA, United States
    • University of Amsterdam
      • Faculty of Medicine AMC
      Amsterdam, North Holland, Netherlands
  • 2008
    • Novartis Institutes for BioMedical Research
      Cambridge, Massachusetts, United States
  • 2005
    • Charité Universitätsmedizin Berlin
      • Institute of Clinical Pharmacology and Toxicology
      Berlin, Land Berlin, Germany
  • 1996–2004
    • Mahatma Gandhi Kashi Vidyapith, Varanasi
      Varangaon, Mahārāshtra, India
  • 1996–2002
    • The Ohio State University
      • • Division of Nephrology
      • • Department of Internal Medicine
      • • Division of Hospital Medicine
      Columbus, OH, United States