Background:Cystatin C (CysC), a low-molecular-weight protein, is widely used as a biomarker of renal function. The relationship between CysC and cognitive impairment remains controversial. This study aimed to investigate the association between CysC and cognitive impairment in the Hanzhong Adolescent Hypertension Study. Methods:A total of 2,347 participants completed the Mini-Mental State Examination (MMSE) in 2023, after excluding the participants missing data, 1929 participants were included. Multivariable logistic regression was used to assess the cross-sectional association between serum CysC levels and cognitive impairment. Subgroup and interaction analyses were performed to examine effect modification by albuminuria status. The nonlinear relationship was explored using restricted cubic splines (RCS). Results:Cognitive impairment was identified in 149 participants (7.72%). Each 1-SD increase in CysC levels was significantly associated with 49% higher odds of cognitive impairment after full adjustment [odds ratio (OR) = 1.49, 95% confidence interval (CI): 1.24-1.79, p < 0.001]. Compared with participants in the lowest CysC quartile, those in the highest quartile had significantly higher odds of cognitive impairment (OR = 1.79, 95% CI = 1.09-2.98, p = 0.022). The association was stronger in participants without albuminuria (OR per SD = 1.48, 95% CI: 1.22-1.80, p < 0.001) but absent in those with albuminuria (OR per SD = 1.00, 95% CI: 0.73-1.25, p = 0.981), with a significant interaction when CysC was modeled continuously (p for interaction = 0.028). A linear and positive association was observed between cystatin C levels and the prevalence of cognitive impairment (p for linearity < 0.001). This association remained significant in the non-albuminuria subgroup. Conclusion:Elevated CysC is associated with cognitive impairment assessed by MMSE in this midlife natural population cohort. This association is stronger in participants without albuminuria.

ABSTRACT Background Interleukin‐17A (IL‐17A) is a key pro‐inflammatory cytokine implicated in acute myocardial infarction, but its upstream regulatory mechanisms remain unclear. Emerging evidence reveals the role of the gut–heart axis in cardiovascular diseases, suggesting that the gut microbiota influences inflammatory responses following myocardial ischemia. Methods and Results By performing Mendelian randomization analysis on human genomic data, we identified four gut bacterial genera with a potential causal relationship to elevated IL‐17A levels, including Barnesiella . Integrated multi‐omics network analysis reveals that Barnesiella regulates IL‐17A‐related inflammatory gene expression through its metabolite succinate. In a myocardial infarction (MI) mouse model, inoculating Barnesiella intestinihominis significantly elevated succinate concentrations in both serum and myocardial tissue, exacerbated cardiac injury, and amplified inflammatory responses in Pseudo‐Germ‐free (pGF) mice. Flow cytometry analysis demonstrated that within the CD3 + T cell population of the ischemic myocardium, IL‐17A + γδ T cells consistently outnumbered IL‐17A + CD4 + T cells across all experimental groups. Co‐immunoprecipitation (Co‐IP) assays further demonstrated that Barnesiella ‐derived succinate promotes MAPK3 lysine succinylation in the ischemic myocardium. In vitro Transwell co‐culture of HL‐1 cardiomyocytes and γδ T cells confirmed that succinate directly promotes IL‐17A expression in γδ T cells and upregulates MAPK3 and NLRP3/caspase‐1 pathways, effects that were abrogated by MAPK3 inhibition. Conclusion Barnesiella intestinihominis exacerbates myocardial injury and inflammatory responses following MI by promoting IL‐17A expression in γδ T cells through succinate‐mediated MAPK3 lysine succinylation and downstream NLRP3 inflammasome activation. This study reveals a novel “gut–metabolite–immune–heart” regulatory pathway linking a specific gut bacterium to localized myocardial immune pathology.

The sensitive period during which the adult cardiovascular system is particularly vulnerable to body mass index (BMI) changes remains unclear. This study aimed to examine how rates of BMI change from childhood to adulthood influence the risk of subclinical cardiovascular outcomes in mid-adulthood. This cohort study included 2446 participants from the Hanzhong Adolescent Hypertension Study who had at least two BMI measurements in childhood/adolescence (6–18 years) and at least two in adulthood (≥ 19 years). The BMI growth curve from ages 6 to 52 years was modeled using random-effects mixed models with restricted cubic splines. These models yielded age-specific estimates of BMI levels and rates of change, the latter of which were subsequently residual-adjusted for concurrent BMI levels. Multivariable logistic regression models were used to examine the associations of BMI levels and level-adjusted rates of change from 6 to 52 years with left ventricular hypertrophy (LVH) and arterial stiffness in mid-adulthood. BMI at each age from 10 to 52 years was associated with mid-adult LVH and arterial stiffness, and these associations became stronger with increasing age at BMI measurement. Additionally, age-level–adjusted rates of BMI change at most ages from childhood to adulthood were positively associated with a higher risk of both subclinical cardiovascular outcomes. However, the odds ratios (ORs) for both LVH and arterial stiffness per 1-SD increase in BMI change rate declined with increasing age. For LVH, the ORs decreased from 2.49 (95

Insulin resistance promotes both arterial stiffening and carotid atherosclerosis, but the comparative value of TyG-related indices for these phenotypes is unclear. Using a cohort with childhood anthropometry measured in 1987, we compared two vascular phenotypes, functional arterial stiffness (AS) and structural carotid intima–media thickening (cIMT), in relation to a common metabolic exposure, tested independence from early-life adiposity, and examined how the choice of exposure design (baseline, cumulative, or change) shaped these associations. Within the Hanzhong Adolescent Hypertension Cohort (established 1987), we analysed 1,294 (incident AS) and 1,408 (incident cIMT) adults free of the respective outcome in 2017 and re-examined in 2023. Eight indices (TyG, TyG-BMI, TyG-WC, TyG-WHtR, TyG-WWI, TyG-BRI, TyG-CVAI, METS-IR) were modelled as baseline, cumulative, and 6-year change exposures. Incident AS was defined as brachial–ankle pulse wave velocity ≥ 1,400 cm/s, and incident cIMT thickening as mean cIMT ≥ 0.9 mm. Logistic regression, restricted cubic splines, and discrimination/reclassification metrics were applied, with additional adjustment for childhood (1987) BMI Z-score. Over 6 years, 296 (22.9

Objective To examine the associations between cumulative body mass index (BMI) burden from childhood to adulthood and the risk of adult metabolic multimorbidity. Research Design and Methods This prospective cohort study used data from the Hanzhong Adolescent Hypertension Study (1987-2023). A total of 2,446 participants with at least two BMI measurements in both childhood (6-18 years) and adulthood (19-52 years) were included. Cumulative BMI exposure was quantified using total and incremental area under the curve (AUC). Outcomes included metabolic multimorbidity, defined as the presence of ≥2 or ≥3 metabolic diseases, specifically hypertension, diabetes, dyslipidemia, elevated liver enzymes/bilirubin, and kidney damage. Results Higher total and incremental BMI AUC during childhood, adulthood, and over the life course were consistently associated with an increased risk of adult metabolic multimorbidity (≥2 diseases). For total AUC, odds ratios (ORs) ranged from 1.51 to 2.59 (all P<0.05); for incremental AUC, ORs ranged from 1.94 to 4.33 (all P<0.05). Compared with total AUC, incremental AUC showed a stronger association with metabolic multimorbidity in childhood (OR: 4.33, 95%CI: 2.93-6.40 vs. 1.51, 1.17-1.95, respectively). Conversely, total AUC exhibited a stronger association in adulthood than in childhood (OR: 2.51, 95%CI: 2.08-3.04 vs. 1.94, 1.62-2.31). Furthermore, the associations for adulthood and life-course BMI AUC were significantly stronger in males than in females (P for interaction <0.05). Conclusions These findings highlight the importance of life stage-specific strategies: curbing rapid BMI gain in childhood and maintaining long-term weight control throughout adulthood.

BACKGROUND:Blood pressure (BP) is a dynamic trait associated with cardiovascular disease. We aimed to estimate age-specific BP levels and rates of change from childhood to mid-adulthood and to examine their associations with subsequent subclinical target organ damage. METHODS:We included 2508 participants from the Hanzhong Adolescent Hypertension Study with BP measured ≥4× from 1987 to 2023. Surrogate markers of target organ damage were assessed, including arterial stiffness, left ventricular hypertrophy, and albuminuria. Growth models were used to construct BP trajectories and estimate age-specific BP levels and rates of change (slopes). RESULTS:Rates of change in BP at each age point from childhood to mid-adulthood were positively associated with arterial stiffness and albuminuria in mid-adulthood, independent of corresponding BP levels. The magnitude of the associations rose from childhood, peaked in adolescence, and declined thereafter. For example, odds ratios (95% CIs) per 1 SD increase in systolic BP change rates for arterial stiffness increased from 1.94 (1.69-2.24) at age 6 to 2.11 (1.82-2.44) at age 13, then declined to 1.13 (1.01-1.28) by age 52. Faster BP increases were more strongly associated with arterial stiffness and albuminuria than concurrent BP levels during childhood and adolescence, whereas the opposite trend was observed in young and mid-adulthood. Similar age-dependent trends were identified for left ventricular hypertrophy, with minor variations in the ages at which associations reached statistical significance. CONCLUSIONS:Accelerated BP increases during childhood and adolescence show a stronger association with mid-adult subclinical target organ damage than increases occurring in adulthood.

The associations of long-term body mass index (BMI) exposure, including both cumulative burden and increasing trends from childhood to adulthood, with subclinical cardiovascular outcomes remain incompletely understood, especially across distinct life stages. This study aimed to examine these associations and evaluate the potential mediating roles of established cardiovascular risk factors. We analyzed data from 2,446 participants in the Hanzhong Adolescent Hypertension Study, all of whom had at least four BMI measurements over a 36-year follow-up period. Cumulative burden and increasing trends of BMI were quantified using total and incremental areas under the curve (AUCs). Multivariable logistic regression and exploratory multiple-mediator analyses were used to examine associations and potential indirect-effect patterns, respectively. Higher total and incremental BMI AUCs during childhood, adulthood, and across the life course were significantly associated with an increased risk of arterial stiffness in mid-adulthood. For childhood, the odds ratios (ORs) with 95

OBJECTIVE:We investigated the associations between BMI transitions from childhood to adulthood and cardiovascular-kidney-metabolic (CKM) syndrome and its components in midlife. RESEARCH DESIGN AND METHODS:Using data from the Hanzhong Adolescent Hypertension Study, 1,997 participants aged 6-18 years were followed for 36 years into midlife (mean age 48.12 years). Participants were categorized into four groups based on BMI transitions from childhood to midlife: control, incident, persistent, and resolution. CKM stages ranged from early (stages 0-1), to intermediate (stage 2), to advanced (stages 3-4), defined by cardiovascular disease, chronic kidney disease, and metabolic disorders. Multivariable regression models were used to assess associations between BMI transitions and CKM outcomes. RESULTS:Individuals transitioning from normal childhood BMI to overweight in adulthood had higher risks of intermediate (odds ratio [OR] 5.19 [95% CI 3.15-8.53]) and advanced CKM stages (OR 6.70 [95% CI 3.96-11.33]) compared with those with persistently normal BMI. These risks were attenuated if elevated childhood BMI resolved by adulthood. For specific CKM components, individuals with normal childhood BMI but overweight in adulthood showed higher risks of left ventricular diastolic dysfunction, subclinical kidney damage, albuminuria, and metabolic abnormalities compared with those with persistently normal BMI. These risks were reduced if high childhood BMI normalized by adulthood. CONCLUSIONS:Transitioning from normal childhood BMI to overweight in adulthood is associated with increased risks of higher CKM stages in midlife. However, individuals whose high childhood BMI resolved by adulthood exhibit similar risk to those with persistently normal BMI.

MicroRNAs (miRNAs) are small endogenous RNA molecules that play an essential role in various disease processes including elevated blood pressure (BP). Although the effects of dietary salt and potassium intake on BP regulation have been established, their co-interaction with miRNAs are still unclear. The purpose of the current study was to explore the connection between miRNA gene polymorphisms and BP response to salt and potassium intake, and the relationship between miRNA gene polymorphisms and long-term BP changes and hypertension development. A total of 333 participants underwent a chronic sodium-potassium dietary intervention trial, which included a 3-day normal diet, followed by a 7-day low-salt diet, then a 7-day high-salt diet, and finally a 7-day high-salt with potassium-supplemented diet. This cohort was subsequently followed for up to 14 years. Single-nucleotide polymorphisms (SNPs) rs115254818 in miR-26b-3p, rs11191676 and rs2292807 in miR-1307-5p, and rs4143957 in miR-382-5p were significantly correlated with systolic BP (SBP) and mean arterial pressure (MAP) responses to high-salt intake, whereas rs11191676 and rs2292807 in miR-1307-5p exhibited significant associations with SBP response to potassium-supplemented diet. Furthermore, SNPs rs2070960 in miR-3620-5p and rs12364149 in miR-210-3p demonstrated significant correlations with diastolic BP and MAP alterations at 14 years of follow-up. Generalized linear mixed model analysis revealed a significant association between rs2070960 in miR-3620-5p and hypertension development over a 14-year period. Our study indicates that miRNA gene polymorphisms are pivotal in the salt and potassium sensitivity of BP, as well as in the longitudinal BP progression and hypertension incidence. Trial Registration: ClinicalTrials.gov identifier: NCT02734472.

Background Elevated blood pressure (BP) in childhood is associated with adult hypertension and arterial stiffness. However, the effect of long-term time in target range (TTR) for BP since childhood on the risk of arterial stiffness in midlife remains unclear. Objectives The purpose of this study was to determine the independent association of TTR for systolic blood pressure (SBP) from childhood to midlife with arterial stiffness in adulthood. Methods This study used data from the ongoing cohort of the Hanzhong Adolescent Hypertension Study. SBP-TTR was assessed over 36 years, with the target ranges of SBP defined as the 90th to 95th percentile of SBP for age, sex, and height in childhood, and 110 to 130 mm Hg in adulthood. Arterial stiffness was defined as brachial-ankle pulse wave velocity >1,400 cm/s. Results Of the total 1,959 participants, 55.5% (1,088 of 1,959) were men, and the mean age was 49 years. The risk of arterial stiffness exhibited a gradual decrease with increasing SBP-TTR over the 36-year follow-up. Compared with the participants in the lowest quartile of SBP-TTR from childhood to midlife, those in the highest quartile showed significantly reduced arterial stiffness risk in midlife. This association persisted even after adjusting for mean SBP and SBP variability. Furthermore, men in the highest quartile of SBP-TTR demonstrated a markedly lower arterial stiffness risk than those in the lowest quartile, whereas this effect was not observed in women. Conclusions Higher long-term SBP-TTR from childhood to midlife is associated with a reduced risk of arterial stiffness in midlife, regardless of the mean SBP or SBP variability.

To investigate the association of frailty status and its changes with new-onset diabetes. A total of 4638 participants from the China Health and Retirement Longitudinal Study (CHARLS) were included. Frailty status was assessed by the frailty index (FI) and categorized as robust, pre-frail, and frail. Changes in frailty were assessed based on frailty status at wave1 and wave3 of CHARLS. New-onset diabetes was identified by self-reported physician-diagnosed or diagnosed by glucose or glycosylated haemoglobin during follow-up period. Logistic regression was used to examine the association of frailty and outcomes. 51.6

Body mass index (BMI) is strongly associated with the development of type 2 diabetes. However, the association between long-term time in target range (TTR) for BMI and the incidence of new-onset diabetes remains unclear. This study utilized a non-diabetic population aged 45 years or older from the China Health and Retirement Longitudinal Study (CHARLS). BMI-TTR was assessed in Waves 1, 2, and 3 over a 5-year period, with the target range defined as 18.5 kg/m² ≤ BMI < 23 kg/m². New-onset diabetes in Waves 2, 3, and 4 over a 6-year follow-up served as the study endpoint. After applying exclusion criteria, 6662 participants (3143 men and 3519 women; mean age 58.93 ± 8.85 years) were enrolled. Participants were categorized into four groups (TTR1–TTR4) based on the number of times BMI was within the target range (0–3 times). The risk of new-onset diabetes decreased progressively with increasing BMI-TTR during follow-up. Compared with the TTR1 group, participants in the TTR4 group exhibited a significantly lower risk of diabetes (adjusted HR: 0.577, 95

Objective: Elevated blood pressure (BP) in childhood is associated with adult hypertension and arterial stiffness. We aimed to determine the independent association of time in target range (TTR) for systolic blood pressure (SBP) from childhood to midlife with arterial stiffness in midlife. Design and method: Using data from the ongoing cohort of Hanzhong Adolescent Hypertension study, 1959 children and adolescents aged 6 to 18 years were enrolled at baseline. We assessed SBP-TTR from childhood to adulthood for 36 years, with the target range of SBP defined as 90th – 95th percentile for age, sex, and height in childhood, and 110 to 130 mmHg in adulthood. Results: During the 36 years of follow-up, the risk of arterial stiffness gradually decreased with increasing TTR for SBP. After fully adjustment for traditional cardiovascular risk factors, comparing the highest vs. lowest quartiles of TTR for SBP, the odds ratios (ORs) [95% confidence intervals (CIs)] were 0.642 (0.452-0.911) for the risk of arterial stiffness in adulthood. TTR remained significantly associated with arterial stiffness despite adjustment for mean SBP or SBP variability. In addition, males with highest quartile of SBP-TTR was significantly associated with a decreased risk of arterial stiffness [OR 95% CI, 0.432 (0.262-0.710)], while no significant difference was found in females compared with the lowest TTR group. Conclusions: Higher long-term TTR for SBP from childhood to adulthood was associated with a decreased risk of arterial stiffness in adulthood independent of mean BP or BP variability. Therefore, SBP-TTR from an early age might serve as a modifiable risk factor for future cardiovascular diseases in later life.

Childhood blood pressure (BP) is associated with increased arterial stiffness later in life. This study aimed to investigate the contributions of BP across different life stages to midlife arterial stiffness and the mediating role of metabolic factors. Using data from the Hanzhong Adolescent Hypertension Study, 1448 participants aged 6-18 years at baseline were prospectively followed for 30 years into adulthood. We used linear regression models to examine the associations between BP at different life stages and brachial-ankle pulse wave velocity (baPWV). In addition, parallel multiple mediation analyses were conducted to evaluate the mediating roles of blood glucose and lipid metabolism in these associations. Significant associations between BP and adult baPWV were observed across childhood, adulthood, and cumulative long-term BP burden, with BP in adulthood showing the strongest association. Additionally, the triglyceride-glucose index was identified as a mediator in the relationship between adult BP and midlife baPWV, with the mediation effects more pronounced among males. Our findings suggest that the detrimental impact of elevated BP on arterial stiffness begins early in life and intensifies over the lifespan, particularly during adulthood. Furthermore, the association between adult BP and arterial stiffness appears to be partially mediated by insulin resistance.

Abstract The E‐proteinoid 3 receptor (PTGER3), a member of the prostaglandin E2 (PGE2) subtype receptor, belongs to the G‐protein‐coupled superfamily of receptors. Animal studies have demonstrated its involvement in salt sensitivity by regulating sodium reabsorption. This study aimed to investigate the association between genetic variants of PTGER3 and salt sensitivity, longitudinal blood pressure (BP) changes, and the incidence of hypertension in Chinese adults. A chronic salt intake intervention was conducted involving 514 adults from 124 families in the 2004 Baoji Salt‐Sensitivity Study Cohort in northern China. These participants followed a 3‐day regular baseline diet, followed by a 7‐day low‐salt diet (3.0 g/d) and a 7‐day high‐salt diet (18 g/d), and were subsequently followed for 14 years. The findings revealed a significant relationship between the single nucleotide polymorphism (SNP) rs17482751 of PTGER3 and diastolic blood pressure (DBP) response to high salt intervention. Additionally, SNPs rs11209733, rs3765894, and rs2268062 were significantly associated with longitudinal changes in systolic blood pressure (SBP), DBP, and mean arterial pressure (MAP) during the 14‐year follow‐up period. SNP rs6424414 was significantly associated with longitudinal changes in DBP over 14 years. Finally, SNP rs17482751 showed a significant correlation with the incidence of hypertension over 14 years. These results emphasize the significant role of PTGER3 gene polymorphism in salt sensitivity, longitudinal BP changes, and the development of hypertension in the Chinese population.

Recent evidence suggests that necroptosis may contribute to the development of kidney injury. Renalase is a novel secretory protein that exerts potent prosurvival and anti-inflammatory effects. We hypothesized that renalase could protect the kidney from salt-induced injury by modulating necroptosis. High salt and renalase treatments were administered to Dahl salt-sensitive (SS) rats, renalase knockout (KO) mice, and HK-2 cells. Furthermore, a cohort of 514 eligible participants was utilized to investigate the association between single nucleotide polymorphisms (SNPs) in the genes RIPK1, RIPK3, and MLKL, and the risk of subclinical renal damage (SRD) over 14 years. A high-salt diet significantly increased the expression of key components of necroptosis, namely RIPK1, RIPK3, and MLKL, as well as the release of inflammatory factors in SS rats. Treatment with recombinant renalase reduced both necroptosis and inflammation. In renalase KO mice, salt-induced kidney injury was more severe than in wild-type mice, but supplementation with renalase attenuated the kidney injury. In vitro experiments with HK-2 cells revealed high salt increased necroptosis and inflammation. Renalase exhibited a dose-dependent decrease in salt-induced necroptosis, and this cytoprotective effect was negated by the knockdown of PMCA4b, which is the receptor of renalase. Furthermore, the cohort study showed that SNP rs3736724 in RIPK1 and rs11640974 in MLKL were significantly associated with the risk of SRD over 14 years. Our analysis shows that necroptosis plays a significant role in the development of salt-induced kidney injury and that renalase confers its cytoprotective effects by inhibiting necroptosis and inflammation.

BackgroundLimited data exists on how early-life weight changes relate to metabolic syndrome (MetS) risk in midlife. This study examines the association between long-term trajectories of body mass index (BMI), its variability, and MetS risk in Chinese individuals.MethodsIn the Hanzhong Adolescent Hypertension study (March 10, 1987–June 3, 2017), 1824 participants with at least five BMI measurements from 1987 to 2017 were included. Using group-based trajectory modeling, different BMI trajectories were identified. BMI variability was assessed through standard deviation (SD), variability independent of the mean (VIM), and average real variability (ARV). Logistic regression analyzed the relationship between BMI trajectory, BMI variability, and MetS occurrence in midlife (URL: https://www.clinicaltrials.gov; Unique identifier: NCT02734472).FindingsBMI trajectories were categorized as low-increasing (34.4%), moderate-increasing (51.8%), and high-increasing (13.8%). Compared to the low-increasing group, the odds ratios (ORs) [95% CIs] for MetS were significantly higher in moderate (4.27 [2.63–6.91]) and high-increasing groups (13.11 [6.30–27.31]) in fully adjusted models. Additionally, higher BMI variabilities were associated with increased MetS odds (ORs for SDBMI, VIMBMI, and ARVBMI: 2.30 [2.02–2.62], 1.22 [1.19–1.26], and 4.29 [3.38–5.45]). Furthermore, BMI trajectories from childhood to adolescence were predictive of midlife MetS, with ORs in moderate (1.49 [1.00–2.23]) and high-increasing groups (2.45 [1.22–4.91]). Lastly, elevated BMI variability in this period was also linked to higher MetS odds (ORs for SDBMI, VIMBMI, and ARVBMI: 1.24 [1.08–1.42], 1.00 [1.00–1.01], and 1.21 [1.05–1.38]).InterpretationOur study suggests that both early-life BMI trajectories and BMI variability could be predictive of incident MetS in midlife.FundingThis work was supported by the National Natural Science Foundation of China No. 82070437 (J.-J.M.), the Clinical Research Award of the First Affiliated Hospital of Xi'an Jiaotong University of China (No. XJTU1AF-CRF-2022-002, XJTU1AF2021CRF-021, and XJTU1AF-CRF-2023-004), the Key R&D Projects in Shaanxi Province (Grant No. 2023-ZDLSF-50), the Chinese Academy of Medical Sciences & Peking Union Medical College (2017-CXGC03-2), and the International Joint Research Centre for Cardiovascular Precision Medicine of Shaanxi Province (2020GHJD-14).

Objective: Elevated blood pressure (BP) is associated with increased risk of chronic kidney disease. However, it is uncertain whether this risk is attenuated in individuals who acquire normal BP by adulthood. The present study examined the effect of child and adult BP levels on subclinical kidney damage (SKD) and albuminuria in adulthood. Design and method: Using data from the longitudinal cohort of Hanzhong Adolescent Hypertension Study, 1897 participants aged 6 to 18 years were enrolled and followed up for 36 years. Childhood elevated BP was defined according to the tables from the National Health Commission of the People's Republic of China. In adulthood, BP was classified as elevated if systolic BP greater than or equal to 140 mmHg, diastolic BP greater than or equal to 90 mmHg, or self-reported use of antihypertensive medications. Presence of SKD was defined as estimated glomerular filtration rate between 30 and 60 mL/min per 1.73 m2 or elevated urinary albumin-to creatinine ratio at least 30 mg/g. Albuminuria was defined as urinary albumin-to creatinine ratio greater than or equal to 30 mg/g. Results: Individuals with persistently elevated BP and individuals with normal childhood BP, but elevated adult BP had increased risk of SKD [odds ratios (ORs) 95% confidence interval (CI) were 2.46(1.68-3.60) and 3.28(1.85-5.82), respectively] in comparison with individuals with normal child and adult BP. In contrast, individuals with elevated BP as children but not as adults did not have significantly increased risk [OR 95% CI, 0.93(0.58-1.50)]. In addition, these individuals had a lower risk of increased SKD [OR 95% CI, 0.28(0.14-0.57)] in compared with those with persistently elevated BP. Consistent findings were observed in the risk of albuminuria. Conclusions: Individuals with persistently elevated BP from childhood to adulthood had increased risks of SKD and albuminuria. These risks were reduced if elevated BP during childhood resolved by adulthood.