Introduction Although arterial stiffness has been suggested to be associated with poor physical function and mild cognitive impairment (MCI), its association with cognitive frailty (CF), a comorbidity of both, is unclear. This study aims to examine the association between CF and arterial stiffness in community-dwelling older adults.MethodsA cross-sectional analysis of 511 community-dwelling older adults aged 65 years or older (mean age 73.6 ± 6.2 years, 63.6% women), who participated in a community cohort study (Tarumizu Study, 2019), was conducted. Poor physical function was defined as either slowness (walking speed < 1.0 m/sec), or weakness (grip strength < 28 kg for men and < 18 kg for women). MCI was defined by the National Center for Geriatrics and Gerontology Functional Assessment Tool as a decline of at least 1.5 standard deviation from age- and education-adjusted baseline values in any one of the four cognitive domains (memory, attention, executive, and information processing). CF was defined as the combination of poor physical function and MCI. Arterial stiffness was measured using the Cardio-Ankle Vascular Index (CAVI), and the average of the left and right sides (mean CAVI) was used.ResultsMultinomial logistic regression analysis adjusted for covariates was performed with the four groups of robust, poor physical function, MCI, and CF as dependent variables and mean CAVI as an independent variable. Using the robust group as reference, the poor physical function and MCI groups showed no significant relationship with the mean CAVI. The mean CAVI was significantly higher in the CF group (odds ratio 1.62, 95% confidence interval 1.14–2.29).Conclusion A significant association was found between CF and the higher CAVI (progression of arterial stiffness). Careful observation and control of CAVI, which is also an indicator of arterial stiffness, may be a potential target for preventive interventions for CF.

Introduction Although arterial stiffness has been suggested to be associated with poor physical function and mild cognitive impairment (MCI), its association with cognitive frailty (CF), a comorbidity of both, is unclear. This study aims to examine the association between CF and arterial stiffness in community-dwelling older adults.MethodsA cross-sectional analysis of 511 community-dwelling older adults aged 65 years or older (mean age 73.6 ± 6.2 years, 63.6% women), who participated in a community cohort study (Tarumizu Study, 2019), was conducted. Poor physical function was defined as either slowness (walking speed < 1.0 m/sec), or weakness (grip strength < 28 kg for men and < 18 kg for women). MCI was defined by the National Center for Geriatrics and Gerontology Functional Assessment Tool as a decline of at least 1.5 standard deviation from age- and education-adjusted baseline values in any one of the four cognitive domains (memory, attention, executive, and information processing). CF was defined as the combination of poor physical function and MCI. Arterial stiffness was measured using the Cardio-Ankle Vascular Index (CAVI), and the average of the left and right sides (mean CAVI) was used.ResultsMultinomial logistic regression analysis adjusted for covariates was performed with the four groups of robust, poor physical function, MCI, and CF as dependent variables and mean CAVI as an independent variable. Using the robust group as reference, the poor physical function and MCI groups showed no significant relationship with the mean CAVI. The mean CAVI was significantly higher in the CF group (odds ratio 1.62, 95% confidence interval 1.14–2.29).Conclusion A significant association was found between CF and the higher CAVI (progression of arterial stiffness). Careful observation and control of CAVI, which is also an indicator of arterial stiffness, may be a potential target for preventive interventions for CF.

Introduction: While recent investigations show that klotho exerts reno-protective actions, it has not been fully addressed whether klotho protein supplementation reverses renal damage. Methods: The impacts of subcutaneous klotho supplementation on rats with subtotal nephrectomy were examined. Animals were divided into 3 groups: group1 (short remnant, SR): remnant kidney for 4 weeks, group 2 (long remnant, LR): remnant kidney for 12 weeks and group 3 (klotho supplementation: KL): klotho protein (20 μg/kg/day) supplementation on the remnant kidney. Blood pressure, blood and urine compositions with conventional methods such as enzyme-linked immunosorbent assay and radioimmunoassay, kidney histology and renal expressions of various genes were analyzed. In vitro studies were also performed to support in vivo findings. Results: Klotho protein supplementation decreased albuminuria (-43%), systolic blood pressure (-16%), fibroblast growth factor (FGF) 23 (-51%) and serum phosphate levels (-19%), renal angiotensin II concentration (-43%), fibrosis index (-70%), renal expressions of collagen I (-55%) and transforming growth factor β (-59%) (p<0.05 for all). Klotho supplementation enhanced fractional excretion of phosphate (+45%), glomerular filtration rate (+76%), renal expressions of klotho (+148%), superoxide dismutase (+124%) and bone morphogenetic protein (BMP) 7 (+174%) (p<0.05 for all). Conclusion: Our data indicated that klotho protein supplementation inactivated renal renin-angiotensin system, reducing blood pressure and albuminuria in remnant kidney. Furthermore, exogenous klotho protein supplementation elevated endogenous klotho expression to increase phosphate excretion with resultant reductions in FGF23 and serum phosphate. Finally, klotho supplementation reversed renal dysfunction and fibrosis in association with improved BMP7 in remnant kidney.

Introduction: While recent investigations show that klotho exerts reno-protective actions, it has not been fully addressed whether klotho protein supplementation reverses renal damage. Methods: The impacts of subcutaneous klotho supplementation on rats with subtotal nephrectomy were examined. Animals were divided into 3 groups: group1 (short remnant, SR): remnant kidney for 4 weeks, group 2 (long remnant, LR): remnant kidney for 12 weeks and group 3 (klotho supplementation: KL): klotho protein (20 μg/kg/day) supplementation on the remnant kidney. Blood pressure, blood and urine compositions with conventional methods such as enzyme-linked immunosorbent assay and radioimmunoassay, kidney histology and renal expressions of various genes were analyzed. In vitro studies were also performed to support in vivo findings. Results: Klotho protein supplementation decreased albuminuria (-43%), systolic blood pressure (-16%), fibroblast growth factor (FGF) 23 (-51%) and serum phosphate levels (-19%), renal angiotensin II concentration (-43%), fibrosis index (-70%), renal expressions of collagen I (-55%) and transforming growth factor β (-59%) (p<0.05 for all). Klotho supplementation enhanced fractional excretion of phosphate (+45%), glomerular filtration rate (+76%), renal expressions of klotho (+148%), superoxide dismutase (+124%) and bone morphogenetic protein (BMP) 7 (+174%) (p<0.05 for all). Conclusion: Our data indicated that klotho protein supplementation inactivated renal renin-angiotensin system, reducing blood pressure and albuminuria in remnant kidney. Furthermore, exogenous klotho protein supplementation elevated endogenous klotho expression to increase phosphate excretion with resultant reductions in FGF23 and serum phosphate. Finally, klotho supplementation reversed renal dysfunction and fibrosis in association with improved BMP7 in remnant kidney.