Serum phosphate and chronic kidney and cardiovascular disease: Phosphorus potential implications in general population.
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ABSTRACT:
SUBMITTER: Raikou VD
PROVIDER: S-EPMC8477270 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:We hypothesized that phosphorus has an effect on anemia in both normal kidney function and early chronic kidney disease (CKD). We sought to determine whether higher phosphorus levels are associated with anemia in a large diverse population without CKD and early CKD.This study is a historical population-based study within the Kaiser Permanente Southern California health system (1 January 1998 to 31 December 2013) among individuals aged 18 years and older with estimated glomerular filtration rate >30 mL/min/1.73 m(2) and measurements of serum phosphorus, creatinine and hemoglobin. Individuals were excluded if they had secondary causes of anemia. Odds ratio (OR) estimated for moderate anemia defined as hemoglobin <11 g/dL for both sexes. Mild anemia was defined as <12 g/dL (females) and <13 g/dL (males).Among 155 974 individuals, 4.1% had moderate anemia and 12.9% had mild anemia. Serum phosphorus levels ?3.5 mg/dL were associated with both mild and moderate anemia. Moderate anemia OR (95% confidence interval) was 1.16 (1.04-1.29) for every 0.5 mg/dL phosphorus increase and 1.26 (1.07-1.48) in the highest versus middle phosphorus tertile. Additional independent anemia risk factors, including female sex, Asian race, diabetes, low albumin and low iron saturation, were observed, but did not alter the anemia-phosphorus association.Higher phosphorus levels were associated with a greater likelihood for anemia in a population with early CKD and normal kidney function. Phosphorus may be a biomarker for anemia and may affect aspects of hematopoiesis.
| S-EPMC4805130 | biostudies-literature
Project description:BackgroundSerum sulfhydryl groups (R-SH, free thiols) reliably reflect the systemic redox status in health and disease. As oxidation of R-SH occurs rapidly by reactive oxygen species (ROS), oxidative stress is accompanied by reduced levels of free thiols. Oxidative stress has been implicated in the pathophysiology of chronic kidney disease (CKD), in which redox imbalance may precede the onset of CKD. Therefore, we aimed to investigate associations between serum free thiols and the risk of incident CKD as defined by renal function decline and albuminuria in a population-based cohort study.MethodsSubjects without CKD (n = 4,745) who participated in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, a prospective, population-based cohort study in the Netherlands, were included. Baseline protein-adjusted serum free thiols were studied for their associations with the development of CKD, defined as a composite outcome of an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2, urinary 24-h albumin excretion (UAE) > 30 mg/24-h, or both.ResultsMedian level of protein-adjusted serum free thiols at baseline was 5.14 μmol/g of protein (interquartile range [IQR]: 4.50-5.75 μmol/g) and median eGFR was 96 mL/min/1.73 m2 [IQR: 85-106]. Protein-adjusted serum free thiols were significantly associated with incident CKD (hazard ratio [HR] per doubling 0.42 [95% confidence interval [CI]: 0.36-0.52, P < 0.001), even after adjustment for traditional risk factors (HR 0.67 [95% CI: 0.47-0.94], P=0.022). In secondary analyses, the highest tertile of protein-adjusted serum free thiols was inversely associated with incident UAE >30 mg/24-h after full adjustment for confounding factors (HR per doubling 0.70 [95% CI: 0.51-0.96], P=0.028).ConclusionHigher levels of serum R-SH, reflecting less oxidative stress, are associated with a decreased risk of developing CKD in subjects from the general population. This association is primarily driven by incident CKD as defined by UAE.
| S-EPMC8671125 | biostudies-literature
Project description:Lower phosphorus intake to prevent hyperphosphatemia for those with chronic kidney disease (CKD) is often recommended. Plant proteins are frequently restricted for their high phosphorus content despite having lower bioavailability. To summarize the evidence on protein type and dietary phosphorus intake, serum phosphate concentrations, and nutritional adequacy in adults with CKD, a search in MEDLINE via Ovid was conducted. Citation lists were reviewed to identify any additional articles. Sixteen articles were included-7 intervention (n = 290) and 9 observational (n = 4933). All intervention trials reported high-plant-protein diets provided adequate protein and adhered to low phosphorus diet guidelines. All intervention trials reported higher plant-protein intake was associated with lower serum phosphate; however, only 2 achieved statistical significance. For observational studies, 2 reported that higher proportions of plant to animal protein resulted in lower phosphorus intake but equivalent serum phosphate concentrations. Two reported that plant protein and animal protein had equivalent correlation values to phosphorus intake and no correlation to serum phosphate concentrations. One trial reported lower total phosphorus and protein intake among those who consumed more plant proteins but did not examine serum concentrations. Four reported lower serum phosphate concentrations among those who consumed more plant proteins but did not report dietary phosphorus intake. Of the observational studies that reported on protein intake, all reported lower protein intake among those with higher versus lower plant-protein intake. BMI tended to be lower among those consuming more plant protein. There was not a consistent relation between protein type and albumin concentrations. Routine restriction of plant-protein foods to prevent hyperphosphatemia in CKD would likely benefit from re-evaluation, as evidence does not suggest that higher plant-protein intake leads to higher serum phosphate concentrations or worse nutritional status, although longer-duration intervention trials with larger sample sizes appear to be warranted.
| S-EPMC8634523 | biostudies-literature
Project description:Risk factors for disease states are rigorously defined. This analysis considers the definition of a risk factor as applied to the question of whether the serum phosphorus level is a risk factor for cardiovascular disease. Observational studies strongly suggest that phosphorus is associated with cardiovascular risk, and definitive prospective animal studies are supportive. A plausible mechanism of action has been discovered demonstrating that phosphorus stimulates osteoblastic transition of cells in the neointima of atherosclerotic plaques, which, if prevented, blocks vascular calcification. However, prospective studies demonstrating that modulation of the putative risk factor affects clinical outcomes are lacking, and phosphorus, as yet, does not qualify as a cardiovascular risk factor. This is a clarion call for additional research.
| S-EPMC3260961 | biostudies-other
Project description:BackgroundSerum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.MethodsWe performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.ResultsWe identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10-101), rs2077119 (p = 3.34 × 10-18), and rs9870756 (p = 3.10 × 10-8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01-1.28)] and all-cause mortality alone [1.14 (1.00-1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06-1.84), relative excess risk due to interaction 0.54 (0.01-1.08)].ConclusionsWe identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease.
| S-EPMC8795369 | biostudies-literature
Project description:BackgroundConflicting results have been reported from studies evaluating serum uric acid (SUA) levels as an independent risk factor for cardiovascular mortality in patients with chronic kidney disease (CKD).MethodsWe systematically searched MEDLINE, Web of Science, and bibliographies of retrieved articles to identify studies reporting on the association between SUA levels and cardiovascular mortality in patients with CKD. Random-effects models were used to calculate the pooled hazard ratios (HR) and corresponding 95% confidence intervals (CI).ResultsWe included 11 studies with an overall sample of 27,081 patients with CKD in this meta-analysis. By meta-analysis, restricted to 7 studies (n?=?11,050), patients with the highest SUA were associated with an increased risk of cardiovascular mortality (HR 1.47, 95% CI 1.11-1.96) compared with patients with the lowest SUA. There was no indication of publication bias or significant heterogeneity (I2 =?40.4%; P?=?0.109). Meta-analysis of 10 studies (n?=?26,660) indicated that every 1?mg/dl increase in SUA levels increased a 12% risk in cardiovascular mortality (HR 1.12, 95% CI 1.02-1.24), with significant heterogeneity (I2 =?79.2%, P?<?0.001).ConclusionsHigher SUA levels are associated with significantly increased risk of cardiovascular mortality in patients with CKD. More designed studies, especially randomized controlled trials, should be conducted to determine whether high SUA levels is a potentially modifiable risk factor for cardiovascular mortality in patients with CKD.
| S-EPMC6330757 | biostudies-literature
Project description:Introduction:High urinary calcium excretion (UCaE) has been shown to lead to accelerated renal function decline in individuals with renal tubular diseases. It is not known whether this association also exists in the general population. Therefore, we investigated whether high UCaE is associated with risk of developing chronic kidney disease (CKD) in community-dwelling subjects. Methods:Urine samples of 5491 subjects who were free of CKD at baseline and participated in the Prevention of Renal and Vascular End-Stage Disease study (a prospective, observational, general population-based cohort of Dutch men and women aged 28-75 years) were examined for UCaE. UCa concentration was measured in two 24-hour urine samples at baseline (1997-1998) by indirect potentiometry. UCaE was treated as a continuous variable and a categorical variable grouped according to sex-specific quintiles for UCaE. UCaE was compared with de novo development of estimated glomerular filtration rate <60 ml/min per 1.73 m2 and/or albuminuria >30 mg/24 h. Results:Baseline median UCaE was 4.13 mmol/24 h for men and 3.52 mmol/24 h for women. During a median follow-up of 10.3 years, 899 subjects developed CKD. After multivariable adjustment, every 1 mmol/24 h higher baseline UCaE was associated with a 6% lower risk for incident CKD during follow-up (hazard ratio: 0.94 [0.88-0.99], P = 0.02). The association was shown to be significantly nonlinear, with highest risk of CKD in the lowest quintile for UCaE (hazard ratio: 1.28 [0.97-1.68], P = 0.09). There was no association between UCaE and mortality or cardiovascular health during follow-up, suggesting that this association was not a reflection of poor nutritional intake due to bad health. Discussion:These findings indicate that high UCaE does not increase risk of CKD, but rather that low UCaE may be harmful.
| S-EPMC5720525 | biostudies-literature
Project description:BackgroundChronic kidney disease (CKD) patients show an increased burden of atherosclerosis and high risk of cardiovascular events (CVEs). There are several biomarkers described as being associated with CVEs, but their combined effectiveness in cardiovascular risk stratification in CKD has not been tested. The objective of this work is to analyse the combined ability of 19 biomarkers associated with atheromatous disease in predicting CVEs after 4 years of follow-up in a subcohort of the NEFRONA study in individuals with different stages of CKD without previous CVEs.MethodsNineteen putative biomarkers were quantified in 1366 patients (73 CVEs) and their ability to predict CVEs was ranked by random survival forest (RSF) analysis. The factors associated with CVEs were tested in Fine and Gray (FG) regression models, with non-cardiovascular death and kidney transplant as competing events.ResultsRSF analysis detected several biomarkers as relevant for predicting CVEs. Inclusion of those biomarkers in an FG model showed that high levels of osteopontin, osteoprotegerin, matrix metalloproteinase-9 and vascular endothelial growth factor increased the risk for CVEs, but only marginally improved the discrimination obtained with classical clinical parameters: concordance index 0.744 (95% confidence interval 0.609-0.878) versus 0.723 (0.592-0.854), respectively. However, in individuals with diabetes treated with antihypertensives and lipid-lowering drugs, the determination of these biomarkers could help to improve cardiovascular risk estimates.ConclusionsWe conclude that the determination of four biomarkers in the serum of CKD patients could improve cardiovascular risk prediction in high-risk individuals.
| S-EPMC7467598 | biostudies-literature
Project description:Background and objectivesMolecular evidence suggests that levels of vitamin D are associated with kidney function loss. Still, population-based studies are limited and few have considered the potential confounding effect of baseline kidney function. This study evaluated the association of serum 25-hydroxyvitamin D with change in eGFR, rapid eGFR decline, and incidence of CKD and albuminuria.Design, setting, participants, & measurementsBaseline (2003-2006) and 5.5-year follow-up data from a Swiss adult general population were used to evaluate the association of serum 25-hydroxyvitamin D with change in eGFR, rapid eGFR decline (annual loss >3 ml/min per 1.73 m(2)), and incidence of CKD and albuminuria. Serum 25-hydroxyvitamin D was measured at baseline using liquid chromatography-tandem mass spectrometry. eGFR and albuminuria were collected at baseline and follow-up. Multivariate linear and logistic regression models were used considering potential confounding factors.ResultsAmong the 4280 people included in the analysis, the mean±SD annual eGFR change was -0.57±1.78 ml/min per 1.73 m(2), and 287 (6.7%) participants presented rapid eGFR decline. Before adjustment for baseline eGFR, baseline 25-hydroxyvitamin D level was associated with both mean annual eGFR change and risk of rapid eGFR decline, independently of baseline albuminuria. Once adjusted for baseline eGFR, associations were no longer significant. For every 10 ng/ml higher baseline 25-hydroxyvitamin D, the adjusted mean annual eGFR change was -0.005 ml/min per 1.73 m(2) (95% confidence interval, -0.063 to 0.053; P=0.87) and the risk of rapid eGFR decline was null (odds ratio, 0.93; 95% confidence interval, 0.79 to 1.08; P=0.33). Baseline 25-hydroxyvitamin D level was not associated with incidence of CKD or albuminuria.ConclusionsThe association of 25-hydroxyvitamin D with eGFR decline is confounded by baseline eGFR. Sufficient 25-hydroxyvitamin D levels do not seem to protect from eGFR decline independently from baseline eGFR.
| S-EPMC4491284 | biostudies-literature
Project description:Our aim was to determine the serum uric acid (SUA) levels associated with an increased risk of cardiovascular (CV) and all-cause death in the general adult population. We analyzed data obtained in two independent cross-sectional surveys performed in the Czech Republic in 2006-09 and 2015-18, involving 1% population random samples in nine districts, aged 25-64 years, stratified by age and gender. Ten-year mortality data were obtained in a cohort with examination in 2006-09. Final analyses included 3542 individuals (48.2% men) examined in 2006-09, and 2304 (47.4% men) examined in 2015-18. From a cohort examined in 2006-09, 122 men and 60 women were reported dead (33% and 27% from CV disease). In men, there was no association of baseline SUA levels with baseline SCORE category or 10-year mortality rates. In women, each 10 µmol/L increase in baseline SUA levels was associated with an increase in baseline SCORE category (P < .001). Receiver operating characteristic curve analyses in women identified the baseline SUA cutoff values discriminating: 1. between low/intermediate and high/very high SCORE categories (309 µmol/L), 2. CV mortality (325 µmol/L), and 3. all-cause mortality (298 µmol/L). After adjusting for confounders including SCORE, Cox regression analysis confirmed that the baseline SUA cutoffs of 309 µmol/L and 325 µmol/L were associated with 4-times (P = .010) and 6-times (P = .036) greater risk of CV mortality, whereas the cutoff of 298 µmol/L was associated with 87% greater risk of all-cause mortality (P = .025). In conclusion, the SUA cutoff value of 309 µmol/L identified women at high/very high SCORE category and was associated with 4-times greater risk of observed CV mortality over 10 years.
| S-EPMC8029678 | biostudies-literature