Urinary Potassium Excretion, Fibroblast Growth Factor 23, and Incident Hypertension in the General Population-Based PREVEND Cohort.
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ABSTRACT:
SUBMITTER: Yeung SMH
PROVIDER: S-EPMC8707837 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundType 2 diabetes is associated with both impaired insulin action at target tissues and impaired insulin secretion in pancreatic beta cells. Mitochondrial dysfunction may play a role in both insulin resistance and impaired insulin secretion. Plasma creatine has been proposed as a potential marker for mitochondrial dysfunction. We aimed to investigate the association between plasma creatine and incident type 2 diabetes.MethodsWe measured fasting plasma creatine concentrations by nuclear magnetic resonance spectroscopy in participants of the general population-based PREVEND study. The study outcome was incident type 2 diabetes, defined as a fasting plasma glucose ≥7.0 mmol/L (126 mg/dl); a random sample plasma glucose ≥11.1 mmol/L (200 mg/dl); self-report of a physician diagnosis or the use of glucose-lowering medications based on a central pharmacy registration. Associations of plasma creatine with type 2 diabetes were quantified using Cox proportional hazards models and were adjusted for potential confounders.ResultsWe included 4735 participants aged 52 ± 11 years, of whom 49% were male. Mean plasma creatine concentrations were 36.7 ± 17.6 µmol/L, with lower concentrations in males than in females (30.4 ± 15.1 µmol/L vs. 42.7 ± 17.7 µmol/L; p for difference <.001). During 7.3 [6.2-7.7] years of follow-up, 235 (5.4%) participants developed type 2 diabetes. Higher plasma creatine concentrations were associated with an increased risk of incident type 2 diabetes (HR per SD change: 1.27 [95% CI: 1.11-1.44]; p < .001), independent of potential confounders. This association was strongly modified by sex (p interaction <.001). Higher plasma creatine was associated with an increased risk of incident type 2 diabetes in males (HR: 1.40 [1.17-1.67]; p < .001), but not in females (HR: 1.10 [0.90-1.34]; p = .37).ConclusionFasting plasma creatine concentrations are lower in males than in females. Higher plasma creatine is associated with an increased risk of type 2 diabetes in males.
| S-EPMC8048485 | biostudies-literature
Project description:OBJECTIVE:Research into dietary factors associated with hypertension has focused on the sodium component of salt. However, chloride has distinct physiological effects that may surpass the effect of sodium on blood pressure. This study aims to separate the specific effects of chloride and sodium intake on blood pressure. METHODS:We studied 5673 participants from the Prevention of Renal and Vascular End-Stage Disease(PREVEND) study. Urinary chloride(uCl) and sodium(uNa) were measured in two 24-hour collections. We used generalized-linear-regression to evaluate the relation of uCl and uNa with baseline blood pressure and Cox-proportional-hazards-analysis to assess the association with hypertension. Multicollinearity was assessed with Ridge regression. RESULTS:Baseline 24-hour uCl was 135±39mmol and uNa was 144±54mmol. The correlation between uCl and uNa was high (Pearson's r = 0.96). UCl and uNa had similar non-significant positive and linear associations with blood pressure. In 3515 normotensive patients, 1021 patients developed hypertension during a median follow-up of 7.4 years. UCl and uNa had a comparable but non-significant J-shaped effect on the risk of hypertension. Adding both uCl and uNa to the same model produced instability, demonstrated by Ridge coefficients that converged or changed sign. The single index of uNa minus uCl showed a non-significant higher risk of hypertension of 2% per 10mmol/24-hour difference (HR1.02, 95%CI 0.98-1.06). CONCLUSION:UCl and uNa had similar positive but non-significant associations with blood pressure and risk of hypertension and their effects could not be disentangled. Hence, the alleged adverse effects of high salt intake could be due to sodium, chloride or both. This encourages further study into the effect of chloride in order to complement dietary recommendations currently focused on sodium alone.
| S-EPMC7001936 | biostudies-literature
Project description:Background and objectivesData on whether low or high urinary potassium excretion is associated with poor kidney outcome have been conflicting. The aim of this study was to clarify the association between urinary potassium excretion and CKD progression.Design, setting, participants, & measurementsWe investigated the relationship between lower urinary potassium excretion and CKD progression and compared three urinary potassium indices among 1821 patients from the Korean Cohort Study for Outcome in Patients with CKD. Urinary potassium excretion was determined using spot urinary potassium-to-creatinine ratio, spot urinary potassium concentration, and 24-hour urinary potassium excretion. Patients were categorized into four groups according to quartiles of each urinary potassium excretion metric. The study end point was a composite of a ≥50% decrease in eGFR from baseline values and ESKD.ResultsDuring 5326 person-years of follow-up, the primary outcome occurred in 392 (22%) patients. In a multivariable cause-specific hazard model, lower urinary potassium-to-creatinine ratio was associated with higher risk of CKD progression (adjusted hazard ratio, 1.47; 95% confidence interval, 1.01 to 2.12) comparing the lowest quartile with the highest quartile. Sensitivity analyses with other potassium metrics also showed consistent results in 855 patients who completed 24-hour urinary collections: adjusted hazard ratios comparing the lowest quartile with the highest quartile were 3.05 (95% confidence interval, 1.54 to 6.04) for 24-hour urinary potassium excretion, 1.95 (95% confidence interval, 1.05 to 3.62) for spot urinary potassium-to-creatinine ratio, and 3.79 (95% confidence interval, 1.51 to 9.51) for spot urinary potassium concentration.ConclusionsLow urinary potassium excretion is associated with progression of CKD.
| S-EPMC6419276 | biostudies-literature
Project description:Inactivating mutations of the SOST (sclerostin) gene are associated with overgrowth and sclerosis of the skeleton. To determine mechanisms by which increased amounts of calcium and phosphorus are accreted to enable enhanced bone mineralization in the absence of sclerostin, we measured concentrations of calciotropic and phosphaturic hormones, and urine and serum calcium and inorganic phosphorus in mice in which the sclerostin (sost) gene was replaced by the ?-D-galactosidase (lacZ) gene in the germ line. Knockout (KO) (sost(-/-)) mice had increased bone mineral density and content, increased cortical and trabecular bone thickness, and greater net bone formation as a result of increased osteoblast and decreased osteoclast surfaces compared with wild-type (WT) mice. ?-Galactosidase activity was detected in osteocytes of sost KO mice but was undetectable in WT mice. Eight-week-old, male sost KO mice had increased serum 1?,25-dihydroxyvitamin D, decreased 24,25-dihydroxyvitamin D, decreased intact fibroblast growth factor 23, and elevated inorganic phosphorus concentrations compared with age-matched WT mice. 25-Hydroxyvitamin D 1?-hydroxylase cytochrome P450 (cyp27B1) mRNA was increased in kidneys of sost KO mice compared with WT mice. Treatment of cultured proximal tubule cells with mouse recombinant sclerostin decreased cyp27B1 mRNA transcripts. Urinary calcium and renal fractional excretion of calcium were decreased in sost KO mice compared with WT mice. Sost KO and WT mice had similar serum calcium and parathyroid hormone concentrations. The data show that sclerostin not only alters bone mineralization, but also influences mineral metabolism by altering concentrations of hormones that regulate mineral accretion.
| S-EPMC3625358 | biostudies-literature
Project description:It has been reported that an increase in urinary albumin excretion (UAE) within the normal range could be a risk factor for incident hypertension. However, it remains unclear how the subtle increases in UAE and renal function interact in the development of hypertension. We examined the modification of UAE as a risk factor for incident hypertension by glomerular filtration rate (GFR) in the Japanese population. We prospectively followed 1281 normotensive individuals from Watari town (34.3% men; mean age, 58.0±12.3 years old) whose UAE was <30 mg g-1· Cr. Hypertension was diagnosed as a systolic blood pressure (BP)⩾140 mm Hg and/or a diastolic BP⩾90 mm Hg, or antihypertensive medication use. The relationship between sex-specific quartiles of UAE and incident hypertension was examined with Cox proportional hazard analysis. During a mean follow-up of 3.7 years, 315 individuals developed hypertension. Multivariate Cox proportional hazard analysis revealed that a subtle increase in UAE was a risk factor for incident hypertension, but there was a significant interaction between UAE and estimated GFR (eGFR) (P=0.018). The risk of incident hypertension dose dependently increased in the highest eGFR quartile (⩾90 ml min-1 per 1.73 m2). Decline in renal function alone increased the risk of incident hypertension but the increased risk with a subtle increase in UAE became smaller and less clear in the lower eGFR quartiles. The present data suggest that UAE as a risk factor for incident hypertension is largely dependent on eGFR levels.
| S-EPMC5746590 | biostudies-literature
Project description:CKD is a major risk factor for ESRD, cardiovascular disease, and premature death. Whether dietary sodium and potassium intake affect CKD progression remains unclear. We prospectively studied the association of urinary sodium and potassium excretion with CKD progression and all-cause mortality among 3939 patients with CKD in the Chronic Renal Insufficiency Cohort Study. Urinary sodium and potassium excretion were measured using three 24-hour urine specimens, and CKD progression was defined as incident ESRD or halving of eGFR. During follow-up, 939 CKD progression events and 540 deaths occurred. Compared with the lowest quartile of urinary sodium excretion (<116.8 mmol/24 h), hazard ratios (95% confidence intervals) for the highest quartile of urinary sodium excretion (≥194.6 mmol/24 h) were 1.54 (1.23 to 1.92) for CKD progression, 1.45 (1.08 to 1.95) for all-cause mortality, and 1.43 (1.18 to 1.73) for the composite outcome of CKD progression and all-cause mortality after adjusting for multiple covariates, including baseline eGFR. Additionally, compared with the lowest quartile of urinary potassium excretion (<39.4 mmol/24 h), hazard ratios for the highest quartile of urinary potassium excretion (≥67.1 mmol/24 h) were 1.59 (1.25 to 2.03) for CKD progression, 0.98 (0.71 to 1.35) for all-cause mortality, and 1.42 (1.15 to 1.74) for the composite outcome. These data indicate that high urinary sodium and potassium excretion are associated with increased risk of CKD progression. Clinical trials are warranted to test the effect of sodium and potassium reduction on CKD progression.
| S-EPMC4814179 | biostudies-literature
Project description:A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Dietary sodium intake was measured by sodium excretion in two complete consecutive 24 h urine collections in 6132 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Fatty Liver Index (FLI) ≥60 and Hepatic Steatosis Index (HSI) >36 were used as proxies of suspected NAFLD. 1936 (31.6%) participants had an FLI ≥60, coinciding with the increased prevalence of type 2 diabetes (T2D), metabolic syndrome, hypertension and history of cardiovascular disease. Sodium intake was higher in participants with an FLI ≥60 (163.63 ± 61.81 mmol/24 h vs. 136.76 ± 50.90 mmol/24 h, p < 0.001), with increasing incidence in ascending quartile categories of sodium intake (p < 0.001). Multivariably, an FLI ≥60 was positively associated with a higher sodium intake when taking account for T2D, a positive cardiovascular history, hypertension, alcohol intake, smoking and medication use (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.44-1.64, p < 0.001). Additional adjustment for the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) diminished this association (OR 1.30, 95% CI 1.21-1.41, p < 0.001). HSI >36 showed similar results. Associations remained essentially unaltered after adjustment for body surface area or waist/hip ratio. In conclusion, suspected NAFLD is a feature of higher sodium intake. Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake.
| S-EPMC6947413 | biostudies-literature
Project description:BackgroundThe incidence of atrial fibrillation (AF) increases with age. Telomere length is considered a marker of biological ageing. We investigated the association between leukocyte telomere length and incident AF in the Dutch Prevention of Renal and Vascular End-stage Disease (PREVEND) study.MethodsWe included 7775 individuals without prevalent AF, and with leukocyte telomere length measured. Mean telomere length was determined by a monochrome multiplex quantitative polymerase chain reaction-based assay.ResultsMean age of our cohort was 49±13 years, and 50% were men. During a mean follow-up of 11.4±2.9 years incident AF was detected in 367 (4.7%) individuals. Telomere length was shorter in individuals developing incident AF compared to those without AF (p = 0.013). Incident AF was inversely related to the telomere length. In the quartile with the longest telomere length 68 (3.5%) individuals developed AF, in the shortest telomere length quartile 100 (5.1%) individuals (p = 0.032). Telomere length was associated with incident AF in the second shortest telomere length quartile using the longest telomere length quartile as reference (hazard ratio 1.64; 95% CI 1.02-2.66; p = 0.043). After including age or AF risk factors, the relation between telomere length and incident AF was no longer significant. We found a significant interaction of age, male sex, systolic blood pressure, BMI, heart failure, and myocardial infarction with telomere length for the association with incident AF.ConclusionsWe found that shorter leukocyte telomere length is not independently associated with incident AF in a community-based cohort.
| S-EPMC5291433 | biostudies-literature
Project description:Blacks have the highest prevalence of hypertension in the United States. Higher levels of FGF23 (fibroblast growth factor-23) have been associated with worse cardiovascular outcomes. Whether FGF23 is associated with rising blood pressure (BP) and racial differences in incident hypertension is unclear. We studied 1758 adults (45.0±3.7 years; 57.8% female; 36.9% black) without hypertension or cardiovascular disease who participated in the year 20 (2005-2006) follow-up examination of the CARDIA study (Coronary Artery Risk Development in Young Adults). We investigated the associations of baseline (year 20) cFGF23 (C-terminal FGF23) levels with longitudinal BP patterns and incident hypertension (defined as being on antihypertensive medication, systolic BP ?130 or diastolic BP ?80 mm?Hg) during 2 follow-up visits (years 25 and 30). During follow-up, 35.2% of participants developed hypertension. In multivariable linear mixed models, there were greater increases in systolic BP from year 20 to 25 and year 25 to 30 in the highest FGF23 quartile relative to the lowest quartile (+2.1 mm?Hg, P=0.0057 and +2.2 mm?Hg, P=0.0108, respectively for each time period), whereas there were greater increases in diastolic BP from year 20 to 25 in the highest quartile relative to the lowest (+1.6 mm?Hg; P=0.0024). In multivariable modified Poisson regression analyses, the highest FGF23 quartile was associated with a 45% greater risk of developing hypertension during follow-up compared with the lowest quartile (relative risk, 1.45 [1.18-1.77]). Results did not vary by race (Pinteraction=0.1523). Higher FGF23 levels are independently associated with rising BP over time and an increased risk of incident hypertension but not racial differences in hypertension.
| S-EPMC6002950 | biostudies-literature
Project description:ObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.
| S-EPMC6415648 | biostudies-literature