scholarly journals Polymorphisms within the ARNT2 and CX3CR1 Genes Are Associated with the Risk of Developing Invasive Aspergillosis

2020 ◽  
Vol 88 (4) ◽  
Author(s):  
C. B. Lupiañez ◽  
M. Martínez-Bueno ◽  
J. M. Sánchez-Maldonado ◽  
J. Badiola ◽  
C. Cunha ◽  
...  
Keyword(s):  
Invasive Aspergillosis ◽  
Meta Analysis ◽  
Additive Model ◽  
Population Based ◽  
Nucleotide Polymorphisms ◽  
Hematological Patients ◽  
Number Of Patients ◽  
Increased Risk ◽  
Life Threatening ◽  
Trait Locus

ABSTRACT Invasive aspergillosis (IA) is a life-threatening infection that affects an increasing number of patients undergoing chemotherapy or allo-transplantation, and recent studies have shown that genetic factors contribute to disease susceptibility. In this two-stage, population-based, case-control study, we evaluated whether 7 potentially functional single nucleotide polymorphisms (SNPs) within the ARNT2 and CX3CR1 genes influence the risk of IA in high-risk hematological patients. We genotyped selected SNPs in a cohort of 500 hematological patients (103 of those had been diagnosed with proven or probable IA), and we evaluated their association with the risk of developing IA. The association of the most interesting markers of IA risk was then validated in a replication population, including 474 subjects (94 IA and 380 non-IA patients). Functional experiments were also performed to confirm the biological relevance of the most interesting markers. The meta-analysis of both populations showed that carriers of the ARNT2rs1374213G, CX3CR1rs7631529A, and CX3CR1rs9823718G alleles (where the RefSeq identifier appears as a subscript) had a significantly increased risk of developing IA according to a log-additive model (P value from the meta-analysis [PMeta] = 9.8 · 10−5, PMeta = 1.5 · 10−4, and PMeta =7.9 · 10−5, respectively). Haplotype analysis also confirmed the association of the CX3CR1 haplotype with AGCGG with an increased risk of IA (P = 4.0 · 10−4). Mechanistically, we observed that monocyte-derived macrophages (MDM) from subjects carrying the ARNTR2rs1374213G allele or the GG genotype showed a significantly impaired fungicidal activity but that MDM from carriers of the ARNT2rs1374213G and CX3CR1rs9823718G or CX3CR1rs7631529A alleles had deregulated immune responses to Aspergillus conidia. These results, together with those from expression quantitative trait locus (eQTL) data browsers showing a strong correlation of the CX3CR1rs9823718G allele with lower levels of CX3CR1 mRNA in whole peripheral blood (P = 2.46 · 10−7) and primary monocytes (P = 4.31 · 10−7), highlight the role of the ARNT2 and CX3CR1 loci in modulating and predicting IA risk and provide new insights into the host immune mechanisms involved in IA development.

scholarly journals Polymorphisms within the TNFSF4 and MAPKAPK2 Loci Influence the Risk of Developing Invasive Aspergillosis: A Two-Stage Case Control Study in the Context of the aspBIOmics Consortium

2020 ◽  
Vol 7 (1) ◽  
pp. 4
Author(s):  
Jose Manuel Sánchez-Maldonado ◽  
Ana Moñiz-Díez ◽  
Rob ter Horst ◽  
Daniele Campa ◽  
Antonio José Cabrera-Serrano ◽  
...  
Keyword(s):  
Invasive Aspergillosis ◽  
Case Control Study ◽  
Meta Analysis ◽  
Serum Levels ◽  
Case Control ◽  
Nucleotide Polymorphisms ◽  
Two Stage ◽  
Increased Risk ◽  
Risk Patients ◽  
Control Study

Here, we assessed whether 36 single nucleotide polymorphisms (SNPs) within the TNFSF4 and MAPKAPK2 loci influence the risk of developing invasive aspergillosis (IA). We conducted a two-stage case control study including 911 high-risk patients diagnosed with hematological malignancies that were ascertained through the aspBIOmics consortium. The meta-analysis of the discovery and replication populations revealed that carriers of the TNFSF4rs7526628T/T genotype had a significantly increased risk of developing IA (p = 0.00022). We also found that carriers of the TNFSF4rs7526628T allele showed decreased serum levels of TNFSF14 protein (p = 0.0027), and that their macrophages had a decreased fungicidal activity (p = 0.048). In addition, we observed that each copy of the MAPKAPK2rs12137965G allele increased the risk of IA by 60% (p = 0.0017), whereas each copy of the MAPKAPK2rs17013271T allele was estimated to decrease the risk of developing the disease (p = 0.0029). Mechanistically, we found that carriers of the risk MAPKAPK2rs12137965G allele showed increased numbers of CD38+IgM-IgD- plasmablasts in blood (p = 0.00086), whereas those harboring two copies of the allele had decreased serum concentrations of thymic stromal lymphopoietin (p = 0.00097). Finally, we also found that carriers of the protective MAPKAPK2rs17013271T allele had decreased numbers of CD27-IgM-IgD- B cells (p = 0.00087) and significantly lower numbers of CD14+ and CD14+CD16- cells (p = 0.00018 and 0.00023). Altogether, these results suggest a role of the TNFSF4 and MAPKAPK2 genes in determining IA risk.

Cancer and COVID-19: A proposed mechanism with therapeutic interventions.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 3135-3135
Author(s):  
Yan Leyfman ◽  
Nancy Emmanuel ◽  
Aleksey Tentler ◽  
Jared Cappelli ◽  
Timothy K Erick ◽  
...  
Keyword(s):  
Respiratory Illness ◽  
Organ Damage ◽  
Multiple Organ ◽  
Therapeutic Interventions ◽  
Actual Number ◽  
Data Registry ◽  
Number Of Patients ◽  
Increased Risk ◽  
Life Threatening ◽  
Active Cancer

3135 Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel betacoronavirus that causes the respiratory illness coronavirus disease 2019 (COVID-19). COVID-19 ranges in severity from an asymptomatic viral infection to life-threatening cases of pneumonia, acute respiratory distress syndrome (ARDS), multi-organ damage and sepsis. Cancer patients are at an increased risk of severe SARS-CoV-2 infection due to their immunocompromised status. We propose a mechanism by which SARS-CoV-2 infection causes multiple organ damage through IL-6-mediated inflammation and hypoxia-induced cellular metabolic alterations leading to cell death. Hypoxia is also induced by malignancy due to alterations in metabolism, resulting in greater IL-6 secretion. Methods: To highlight the possible effect of active cancer on the likelihood of hypoxia in COVID-19, we analyzed the correlation between cancer status and the severity of COVID-19 from the COVID-19 and Cancer Consortium data registry. For cancer status, we looked at progressive cancer and remission of cancer only -- those being the two extremes of presence and absence of uncontrolled cancer. Similar to prior studies, the severity of COVID-19 was used as an indication of hypoxia. Results: We observed a 24% positive deviation between expected and actual number of patients with actively progressing cancer who had hypoxic COVID-19 (moderate to severe), and a 26.9% negative deviation between expected and actual number of patients with active cancer who had no hypoxia with COVID-19 (p<0.0001). Conversely, for patients with cancer in remission, there was only a +5.8% and -5.1% deviation between expected and actual number of patients who did not have hypoxia and who had hypoxia, respectively. Conclusions: These results suggest that in the presence of poorly controlled malignancy, there is an increased likelihood of hypoxia in patients with COVID-19, thereby exacerbating downstream cytokine release syndrome and contributing to prolonged systemic inflammatory injury. Appreciating this pathway, future therapies can be developed to target the pathogenesis of both diseases and prevent progression, as seen with mesenchymal stem cells, which demonstrated a 91% overall survival and 100% survival in patients younger than 85 years old at one month after a single treatment.[Table: see text]

scholarly journals Clinical significance of cerebral microbleeds on MRI: A comprehensive meta-analysis of risk of intracerebral hemorrhage, ischemic stroke, mortality, and dementia in cohort studies (v1)

2018 ◽  
Vol 13 (5) ◽  
pp. 454-468 ◽  
Author(s):  
Andreas Charidimou ◽  
Sara Shams ◽  
Jose R Romero ◽  
Jie Ding ◽  
Roland Veltkamp ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
High Risk ◽  
Intracerebral Hemorrhage ◽  
Meta Analysis ◽  
Population Based ◽  
Cerebral Microbleeds ◽  
Clinical Settings ◽  
Memory Clinic ◽  
Increased Risk ◽  
Stroke Death

Background Cerebral microbleeds can confer a high risk of intracerebral hemorrhage, ischemic stroke, death and dementia, but estimated risks remain imprecise and often conflicting. We investigated the association between cerebral microbleeds presence and these outcomes in a large meta-analysis of all published cohorts including: ischemic stroke/TIA, memory clinic, “high risk” elderly populations, and healthy individuals in population-based studies. Methods Cohorts (with > 100 participants) that assessed cerebral microbleeds presence on MRI, with subsequent follow-up (≥3 months) were identified. The association between cerebral microbleeds and each of the outcomes (ischemic stroke, intracerebral hemorrhage, death, and dementia) was quantified using random effects models of (a) unadjusted crude odds ratios and (b) covariate-adjusted hazard rations. Results We identified 31 cohorts ( n = 20,368): 19 ischemic stroke/TIA ( n = 7672), 4 memory clinic ( n = 1957), 3 high risk elderly ( n = 1458) and 5 population-based cohorts ( n = 11,722). Cerebral microbleeds were associated with an increased risk of ischemic stroke (OR: 2.14; 95% CI: 1.58–2.89 and adj-HR: 2.09; 95% CI: 1.71–2.57), but the relative increase in future intracerebral hemorrhage risk was greater (OR: 4.65; 95% CI: 2.68–8.08 and adj-HR: 3.93; 95% CI: 2.71–5.69). Cerebral microbleeds were an independent predictor of all-cause mortality (adj-HR: 1.36; 95% CI: 1.24–1.48). In three population-based studies, cerebral microbleeds were independently associated with incident dementia (adj-HR: 1.35; 95% CI: 1.00–1.82). Results were overall consistent in analyses stratified by different populations, but with different degrees of heterogeneity. Conclusions Our meta-analysis shows that cerebral microbleeds predict an increased risk of stroke, death, and dementia and provides up-to-date effect sizes across different clinical settings. These pooled estimates can inform clinical decisions and trials, further supporting cerebral microbleeds role as biomarkers of underlying subclinical brain pathology in research and clinical settings.

Abstract P027: Fasting Glucose And Risk Of Heart Failure

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Hassan Khan ◽  
Setor Kunutsor ◽  
Jussi Kauhanen ◽  
Sudhir Kurl ◽  
Eiran Gorodeski ◽  
...  
Keyword(s):  
Heart Failure ◽  
Prospective Studies ◽  
Fasting Glucose ◽  
Meta Analysis ◽  
Population Based ◽  
Dose Response Relationship ◽  
Increased Risk ◽  
History Of ◽  
Independent Association

Background: There remains uncertainty regarding the association between fasting glucose (FG) and the risk of heart failure (HF) in individuals without a history of diabetes. Methods and Results: We assessed the association between FG and HF risk in a population-based cohort of 1,740 men aged 42-61 years free from HF or diabetes at baseline. Additionally, we performed a meta-analysis of relevant prospective studies identified from MEDLINE, EMBASE, and Web of Science databases. During a mean follow-up of 20.4 years, 146 participants developed HF (4.1 cases per 1000 person-years). In models adjusted for age, the hazard ratio (HR) for HF per 1 mmol/L increase in FG was 1.34 (95% confidence interval [CI], 1.22, 1.48). This association persisted after adjustment for established HF risk factors (HR 1.27, 95% CI 1.14, 1.42). Compared with FG< 5.6 mmol/L, there was an increased risk amongst those with FG 5.6-6.9 mmol/L (HR 1.24, 95% CI 0.82, 1.88) and ≥ 7.0 mmol/L (HR 3.25, 95% CI 1.50, 7.08). HRs remained consistent across several clinical subgroups. In a meta-analysis of 10 prospective studies (Figure 1) involving a total of 4,213 incident HF cases, the HR for HF per 1 mmol/L increase in FG level was 1.11 (95% CI 1.04, 1.17), consistent with a linear dose-response relationship with evidence of heterogeneity between studies (I2=79%, 63-89%; P<0.001). Conclusions: A positive, continuous, and independent association exists between FG and risk for HF. Further studies are needed to evaluate the causal relevance of these findings.

Abstract P234: Diabetes as Risk Factor for Coronary Heart Disease in Women Compared with Men

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Sanne A Peters ◽  
Rachel R Huxley ◽  
Mark Woodward
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cardiovascular Risk ◽  
Sex Difference ◽  
Prolonged Exposure ◽  
Meta Analysis ◽  
Population Based ◽  
Excess Risk ◽  
Significant Heterogeneity ◽  
Increased Risk

Introduction: A previous pooled analysis suggested that women with diabetes are at substantially increased risk of fatal coronary heart disease (CHD) compared with affected men. Additional findings from larger and more contemporary studies have since published on the sex-specific associations between diabetes and incident CHD. We performed a systematic review with meta-analysis so as to provide the most reliable evidence of any sex difference in the effect of diabetes on subsequent risk of CHD. Methods: PubMed MEDLINE was systematically searched for prospective population-based cohort studies published between on January 1, 1966 and February 13, 2013. Eligible studies had to have reported sex-specific estimates of the relative risk (RR) for incident CHD associated with diabetes, and its associated variability. Random effects meta-analyses with inverse variance weighting were used to obtain sex-specific RRs and their ratio (RRR). Results: Data from 64 cohorts including 858,507 individuals and 28,203 incident CHD events were included. The RR for incident CHD associated with diabetes compared with no diabetes was 2.83 (95% confidence interval [CI]: 2.37, 3.38) in women and 2.11 (95% CI: 1.79, 2.50) in men. The multiple-adjusted RRR for incident CHD was 44% greater in women with diabetes than it was in men with diabetes (95% CI: 27; 63) with no significant heterogeneity between studies (I2=20%). Conclusions: Women with diabetes have more than a 40% greater risk of incident CHD compared with men with diabetes. Sex disparities in pharmacotherapy are unlikely to explain the excess risk in women. Instead, a greater deterioration in cardiovascular risk profile combined with more prolonged exposure to adverse levels of cardiovascular risk factors among pre-diabetic women compared with their male equivalents may be responsible for the excess risk of diabetes-related CHD in women. Future studies are warranted elucidate the mechanisms responsible for the substantial sex-difference in diabetes-related risk of CHD.

scholarly journals Association of VEGF Gene Polymorphisms with Susceptibility to Diabetic Retinopathy: A Systematic Review and Meta-Analysis

2020 ◽  
Vol 52 (05) ◽  
pp. 264-279
Author(s):  
Xiaorong Li ◽  
Juping Liu ◽  
Qianhui Yang ◽  
Yan Zhang ◽  
Xiaomin Zhang
Keyword(s):  
Diabetic Retinopathy ◽  
Gene Polymorphisms ◽  
Meta Analysis ◽  
Vascular Endothelial ◽  
Nucleotide Polymorphisms ◽  
Vegf Gene ◽  
Asian Populations ◽  
Increased Risk ◽  
Endothelial Growth Factor

AbstractThe associations between vascular endothelial growth factor (VEGF) gene polymorphisms and risk of type 2 diabetic retinopathy (DR) – proliferative diabetic retinopathy (PDR), and nonproliferative diabetic retinopathy (NPDR) – remain unclear. A systematic search and meta-analysis using odds ratio (OR) with 95% confidence interval (CI) was performed to evaluate the association. Our study concluded 26 studies containing 10 single nucleotide polymorphisms (SNPs). In Asian populations, rs3025039 polymorphism was associated with DR risk, while in overall populations and Caucasians, the DR risk was increased by association with rs2010963. There was a significant association between rs25648 and rs833061 and DR risk in Caucasians. DR risks were found to be significantly associated between rs3025021, rs13207351, and rs2146323 in either overall populations, Caucasians or Asians. Besides, in overall and Asian populations, rs699947 and rs3025039 were associated with PDR risk. rs1570360, rs3025039, and rs833061 played a key role in PDR etiology in Caucasians. rs2010963 was associated with increased risk of PDR in overall populations. A significant association between rs699947, rs3025039, and rs833061 and NPDR risk in overall populations and Asians was found. A significant association was observed between rs2010963 and increased NPDR risk in overall and Caucasian populations. This study provides a new insight into the parthenogenesis of diabetic retinopathy. Targeting VEGF SNPs may be a potential of therapeutic approach for the treatment of DR, PDR, and NPDR.

scholarly journals The Haplotype of the TGFβ1 Gene Associated with Cerebral Infarction in Chinese

2012 ◽  
Vol 39 (5) ◽  
pp. 626-631 ◽  
Author(s):  
Hong-miao Tao ◽  
Guo-zhong Chen ◽  
Gan-ping Cheng ◽  
Xiao-yun Shan
Keyword(s):  
Cerebral Infarction ◽  
Chinese Population ◽  
Transforming Growth Factor ◽  
Additive Model ◽  
Chinese Patients ◽  
Amplification Refractory Mutation System ◽  
Strong Linkage Disequilibrium ◽  
Nucleotide Polymorphisms ◽  
Individual Snps ◽  
Increased Risk

Background:Transforming growth factor beta1 (TGFβ1) is a multifunctional cytokine involved in inflammation and pathogenesis of atherosclerosis. The aim of the present study was to investigate the relationship between human TGFβ1 gene +869T>C (rs1800470), -509C>T (rs1800469) single nucleotide polymorphisms (SNPs) and haplotypes and cerebral infarction (CI) in a Chinese population.Methods:The genetic association study was performed in 450 Chinese patients (306 male and 144 female) with CI and 450 control subjects (326 male and 124 female). TGFβ1 gene +869T>C and -509C>T polymorphisms were identified with amplification refractory mutation system polymerase chain reaction and DNA sequencing method.Results:The individual SNPs analysis showed the +869T and -509C in an additive model (+869T vs +869C; -509 C vs T), +869TT genotype in a recessive model (TT vs TC+CC) and 509CC genotype in a dominant model (CC+ CT vs TT) were identified to be related to CI (P<0.05). +869T>C and -509C>T SNPs were in strong linkage disequilibrium (d'=0.87, R2=0.75). Haplotype analysis showed that +869C/-509T haplotype was associated with a significant decreased risk of CI (OR= 0.86, 95%CI, 0.70-0.92; P=0.007). Furthermore,+869T/-509C haplotype was associated with a significant increased risk of CI (OR=1.31, 95%CI, 1.10-2.03; P=0.019).Conclusions:The results of this study indicate that polymorphisms and the haplotypes in the TGFβ1 gene might be genetic markers for CI in the Chinese population.

Polymorphisms in the chemokine (C-X-C motif) ligand 10 are associated with invasive aspergillosis after allogeneic stem-cell transplantation and influence CXCL10 epression in monocyte-derived dendritic cells

Blood ◽  
2008 ◽  
Vol 111 (2) ◽  
pp. 534-536 ◽  
Author(s):  
Markus Mezger ◽  
Michael Steffens ◽  
Melanie Beyer ◽  
Carolin Manger ◽  
Johannes Eberle ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Invasive Aspergillosis ◽  
Cell Transplantation ◽  
Allogeneic Stem Cell Transplantation ◽  
Serum Levels ◽  
Risk Haplotype ◽  
Nucleotide Polymorphisms ◽  
Increased Risk

Patients after allogeneic stem-cell transplantation (alloSCT) have an increased risk for invasive aspergillosis (IA). Here, recipients of an allograft with IA (n = 81) or without IA (n = 58) were screened for 84 single nucleotide polymorphisms in 18 immune relevant genes. We found 3 markers in chemokine (C-X-C motif) ligand 10 (CXCL10, 4q21, 11 101 C > T, P = .007; 1642 C < G, P = .003; −1101 A < G, P = .001) significantly associated with an increased risk of developing IA. Furthermore, immature dendritic cells (iDCs) exposed to Aspergillus fumigatus germlings showed markedly higher CXCL10 expression, if carrying the wild type genotype, compared with the “CGAG” high risk haplotype. In addition, serum from patients with proven/probable IA showed increased serum levels of CXCL10, compared with immunocompromised patients without IA. Thus, polymorphisms in CXCL10 determine chemokine secretion by iDCs upon exposure to A fumigatus and most likely thereby genetically determine the risk of IA after alloSCT.

scholarly journals Association of miRNA biosynthesis genes DROSHA and DGCR8 polymorphisms with cancer susceptibility: a systematic review and meta-analysis

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Jing Wen ◽  
Zhi Lv ◽  
Hanxi Ding ◽  
Xinxin Fang ◽  
Mingjun Sun
Keyword(s):  
Cancer Risk ◽  
Genetic Model ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Population Based ◽  
Nucleotide Polymorphisms ◽  
Case Control Studies ◽  
Exclusion Criteria ◽  
Single Nucleotide ◽  
Stratified Analysis

Single nucleotide polymorphisms (SNPs) in miRNA biosynthesis genes DROSHA and DGCR8 were indicated to be correlated with cancer risk. We comprehensively reviewed and analyzed the effect of DROSHA and DGCR8 polymorphisms on cancer risk. Eligible articles were selected according to a series of inclusion and exclusion criteria. Consequently, ten case–control studies (from nine citations) with 4265 cancer cases and 4349 controls were involved in a meta-analysis of seven most prevalent SNPs (rs10719 T/C, rs6877842 G/C, rs2291109 A/T, rs642321 C/T, rs3757 G/A, rs417309 G/A, rs1640299 T/G). Our findings demonstrated that the rs417309 SNP in DGCR8 was significantly associated with an elevated risk of overall cancer in every genetic model. In stratified analysis, correlations of DROSHA rs10719 and rs6877842 SNPs were observed in Asian and laryngeal cancer subgroups, respectively. Moreover, associations of the rs417309 SNP could also be found in numerous subgroups including: Asian and Caucasian population subgroups; laryngeal and breast cancer subgroups; population-based (PB) and hospital-based (HB) subgroups. In conclusion, the DROSHA rs10719, rs6877842 SNPs, and DGCR8 rs417309 SNP play pivotal roles in cancerogenesis and may be potential biomarkers for cancer-forewarning.

scholarly journals GFR in Healthy Aging: an Individual Participant Data Meta-Analysis of Iohexol Clearance in European Population-Based Cohorts

2020 ◽  
Vol 31 (7) ◽  
pp. 1602-1615 ◽  
Author(s):  
Bjørn O. Eriksen ◽  
Runolfur Palsson ◽  
Natalie Ebert ◽  
Toralf Melsom ◽  
Markus van der Giet ◽  
...  
Keyword(s):  
Healthy Aging ◽  
Meta Analysis ◽  
Additive Model ◽  
Healthy Person ◽  
Population Based ◽  
European Population ◽  
Older Age ◽  
Cross Sectional ◽  
Individual Participant ◽  
The Mean

BackgroundPopulation mean GFR is lower in older age, but it is unknown whether healthy aging is associated with preserved rather than lower GFR in some individuals.MethodsWe investigated the cross-sectional association between measured GFR, age, and health in persons aged 50–97 years in the general population through a meta-analysis of iohexol clearance measurements in three large European population-based cohorts. We defined a healthy person as having no major chronic disease or risk factors for CKD and all others as unhealthy. We used a generalized additive model to study GFR distribution by age according to health status.ResultsThere were 935 (22%) GFR measurements in persons who were healthy and 3274 (78%) in persons who were unhealthy. The mean GFR was lower in older age by −0.72 ml/min per 1.73 m2 per year (95% confidence interval [95% CI], −0.96 to −0.48) for men who were healthy versus −1.03 ml/min per 1.73 m2 per year (95% CI, −1.25 to −0.80) for men who were unhealthy, and by −0.92 ml/min per 1.73 m2 per year (95% CI, −1.14 to −0.70) for women who were healthy versus −1.22 ml/min per 1.73 m2 per year (95% CI, −1.43 to −1.02) for women who were unhealthy. For healthy and unhealthy people of both sexes, both the 97.5th and 2.5th GFR percentiles exhibited a negative linear association with age.ConclusionsHealthy aging is associated with a higher mean GFR compared with unhealthy aging. However, both the mean and 97.5 percentiles of the GFR distribution are lower in older persons who are healthy than in middle-aged persons who are healthy. This suggests that healthy aging is not associated with preserved GFR in old age.

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