Chronic Kidney Disease: A Clinical Model of Premature Aging

2013 ◽  
Vol 62 (2) ◽  
pp. 339-351 ◽  
Author(s):  
Peter Stenvinkel ◽  
Tobias E. Larsson
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Premature Aging ◽  
Clinical Model

Continuous medication monitoring: A clinical model to predict adherence to medications among chronic kidney disease patients

2021 ◽  
Author(s):  
Farida Islahudin ◽  
Fei Yee Lee ◽  
Tengku Nur Izzati Tengku Abd Kadir ◽  
Muhammad Zulhilmi Abdullah ◽  
Mohd Makmor-Bakry
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Model ◽  
Medication Monitoring

scholarly journals Early vascular ageing in chronic kidney disease: impact of inflammation, vitamin K, senescence and genomic damage

2020 ◽  
Vol 35 (Supplement_2) ◽  
pp. ii31-ii37 ◽  
Author(s):  
Lu Dai ◽  
Leon J Schurgers ◽  
Paul G Shiels ◽  
Peter Stenvinkel
Keyword(s):  
Chronic Kidney Disease ◽  
Dna Damage ◽  
Kidney Disease ◽  
Vitamin K ◽  
Strong Predictor ◽  
Related Factor ◽  
Clinical Model ◽  
Novel Treatments ◽  
Vascular Ageing ◽  
Cardiovascular Morbidity And Mortality

Abstract Chronic kidney disease (CKD) is a clinical model of premature ageing characterized by cardiovascular disease, persistent uraemic inflammation, osteoporosis muscle wasting and frailty. The accelerated early vascular ageing (EVA) process mediated by medial vascular calcification (VC) is a hallmark of senescence as well as a strong predictor of cardiovascular morbidity and mortality in the CKD population. Current clinical therapeutic strategies and novel treatments for VC have not yet been proven to prevent or reverse VC progression in patients with CKD. Knowledge of the fundamental mechanism underlying EVA is urgently needed to identify and develop novel and efficient therapeutic targets for VC and EVA. An accumulating body of evidence indicates that deoxyribonucleic acid (DNA) damage–induced cellular senescence and ‘inflammaging’ may largely contribute to such pathological conditions characterized by accelerated EVA. Growing evidence shows that nuclear factor erythroid 2–related factor 2 (NRF2) signalling and vitamin K play a crucial role in counteracting oxidative stress, DNA damage, senescence and inflammaging, whereby NRF2 activation and vitamin K supplementation may provide a novel treatment target for EVA. In this review we discuss the link between senescence and EVA in the context of CKD, with a focus on the role of NRF2 and vitamin K in DNA damage signalling, senescence and inflammaging.

scholarly journals The decreased SIRT1 level may account for the lipid profile in chronic kidney disease

2019 ◽  
Vol 26 (1) ◽  
Author(s):  
Gang Chen ◽  
Xuemei Li
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Lipid Profile ◽  
Regulatory Element ◽  
Low Density Lipoprotein ◽  
Lipid Synthesis ◽  
Density Lipoprotein ◽  
Premature Aging ◽  
Silent Information Regulator 1 ◽  
Sterol Regulatory Element

Abstract Dysregulated lipid profile with hypertriglyceridemia and increased low-density lipoprotein (LDL) is common in chronic kidney disease (CKD) whereas the reason is unclear. A similar phenomenon is found in the elder population. Silent information regulator-1 (SIRT1) associates with many modulators regulating lipid metabolism and results in increased expression of sterol regulatory element-binding proteins (SREBPs), which functions as a key modulator in lipid synthesis. Since CKD is being viewed as a premature aging model and SIRT1 is known to decrease during the process of aging, we hypothesize that SIRT1 level is reduced in the liver when CKD develops and eventually result in dysregulated lipid profile.

scholarly journals Premature Aging of the Microcirculation in Patients with Advanced Chronic Kidney Disease

Nephron Extra ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. 283-292 ◽  
Author(s):  
Oanh H.D. Thang ◽  
Erik H. Serné ◽  
Muriel P.C. Grooteman ◽  
Yvo M. Smulders ◽  
Piet M. ter Wee ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Premature Aging ◽  
Advanced Chronic Kidney Disease

scholarly journals Pre-Operative Kidney Biomarkers and Risks for Death, Cardiovascular and Chronic Kidney Disease Events: The TRIBE-AKI Study

2021 ◽  
Author(s):  
George Vasquez-Rios ◽  
Dennis G. Moledina ◽  
Yaqi Jia ◽  
Eric McArthur ◽  
Sherry G. Mansour ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiac Surgery ◽  
Cohort Study ◽  
High Risk ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Kidney Injury ◽  
Multicenter Cohort Study ◽  
Clinical Model

Background: Soluble tumor necrosis factor receptor (sTNFR)1, sTNFR2, and plasma kidney injury molecule 1 (KIM1) are associated with kidney events in patients with and without diabetes. However, their associations with clinical outcomes when obtained pre operatively have not been explored. Methods: The TRIBE AKI cohort study is a prospective, multicenter, cohort study of high risk adults undergoing cardiac surgery. We assessed the associations between pre operative concentrations of plasma sTNFR1, sTNFR2, and KIM1 and post operative long term outcomes including mortality, cardiovascular events, and chronic kidney disease (CKD) incidence or progression, ascertained after discharge. Results: Among 1378 participants included in the analysis with a median follow up period was 6.7 (IQR 4.0,7.9), 434 (31%) patients died, 256 (19%) experienced cardiovascular events and out of 837 with available long term kidney function data, 30% developed CKD. After adjustment for clinical covariates, each log increase in biomarker concentration was independently associated with mortality with 95% CI adjusted hazard ratios (aHRs) of 3.0 (2.3,4.0), 2.3 (1.8,2.9) and 2.0 (CI 1.6,2.4) for sTNFR1, sTNFR2 and KIM1, respectively. For cardiovascular events, the 95%CI aHRs were 2.1 (1.5,3.1), 1.9 (1.4,2.6) and 1.6 (1.2,2.1) for sTNFR1, sTNFR2 and KIM1, respectively. For CKD events, the aHRs were 2.2 (1.5,3.1) for sTNFR1, 1.9 (1.3,2.7) for sTNFR2, and 1.7 (1.3,2.3) for KIM1. Despite the associations, each of the biomarkers alone or in combination failed to result in robust discrimination on an absolute basis or compared to a clinical model. Conclusion: sTNFR1, sTNFR2, and KIM1 were independently associated with longitudinal outcomes after discharge from a cardiac surgery hospitalization including death, cardiovascular and CKD events when obtained pre operatively in high risk individuals. Pre operative plasma biomarkers could serve to assist during the evaluation of patients in whom cardiac surgery is planned.

scholarly journals Reduced skeletal muscle expression of mitochondrial-derived peptides humanin and MOTS-C and Nrf2 in chronic kidney disease

2019 ◽  
Vol 317 (5) ◽  
pp. F1122-F1131 ◽  
Author(s):  
Chang Liu ◽  
Eva-Karin Gidlund ◽  
Anna Witasp ◽  
Abdul Rashid Qureshi ◽  
Magnus Söderberg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Levels ◽  
Premature Aging ◽  
12S Rrna ◽  
C Protein ◽  
Mitochondrial Density ◽  
Reading Frame

Advanced chronic kidney disease (CKD) is characterized by a premature aging phenotype of multifactorial origin. Mitochondrial dysfunction is prevalent in CKD and has been proposed as a major contributor to poor muscle function. Although the mitochondria-derived peptides (MDPs) humanin and mitochondrial open reading frame of 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and glucose control, the implications of MDP in CKD are unknown. We investigated humanin and MOTS-c protein expression in skeletal muscle and serum levels in CKD at stage 5 (glomerular filtration rate: <15 ml/min) patients and age-matched controls with normal renal function. Whereas circulating levels of humanin were increased in CKD, local muscle expression was reduced. In contrast, MOTS-c levels were reduced in both skeletal muscle and serum in CKD. Humanin in serum correlated positively to circulating TNF levels. Reduced MDP levels in skeletal muscle were associated with lower mitochondrial density and evidence of oxidative stress. These results indicate a differential regulation of MDPs in CKD and suggest an alternative site for humanin production than skeletal muscle in the uremic milieu. MDP levels were linked to systemic inflammation and evidence of oxidative stress in the muscle, two hallmark features of premature aging and uremia.

scholarly journals Premature Aging in Chronic Kidney Disease: The Outcome of Persistent Inflammation beyond the Bounds

2021 ◽  
Vol 18 (15) ◽  
pp. 8044
Author(s):  
Andrea Figuer ◽  
Guillermo Bodega ◽  
Patricia Tato ◽  
Gemma Valera ◽  
Nadia Serroukh ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Aging Process ◽  
Developed Countries ◽  
Premature Aging ◽  
Geriatric Syndrome ◽  
Physiological Changes ◽  
Multiple Factors ◽  
Persistent Inflammation ◽  
Healthier Living

Over the last hundred years, life expectancy in developed countries has increased because of healthier living habits and the treatment of chronic pathologies causing premature aging. Aging is an inexorable, time-dependent, multifactorial process characterized by a series of progressive and irreversible physiological changes associated with loss of functional, psychological, and social capabilities. Numerous factors, such as oxidative stress, inflammation, and cellular senescence, and an irreversible geriatric syndrome known as frailty, contribute to human body deterioration in aging. The speed of aging may differ between individuals depending on the presence or absence of multiple factors (genetic and/or environment) and the subsequent misbalance of homeostasis, together with the increase of frailty, which also plays a key role in developing chronic diseases. In addition, pathological circumstances have been reported to precipitate or accelerate the aging process. This review investigated the mechanisms involved in the developing pathologies, particularly chronic kidney disease, associated with aging.

scholarly journals Gut Microbial Product Predicts Cardiovascular Risk in Chronic Kidney Disease Patients

2018 ◽  
Vol 48 (4) ◽  
pp. 269-277 ◽  
Author(s):  
Adil Jadoon ◽  
Anna V. Mathew ◽  
Jaeman Byun ◽  
Crystal A. Gadegbeku ◽  
Debbie S. Gipson ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Secondary Outcome ◽  
Training Set ◽  
Clinical Model ◽  
History Of ◽  
Validation Set

Background: The gut microbiota is altered in patients with chronic kidney disease (CKD), and cardiovascular risk increases with progressive CKD. This study examined the potential link between short chain fatty acids (SCFAs), which are produced by the gut microbiota, and cardiovascular outcomes in patients with CKD. Methods: SCFAs were measured using a targeted liquid chromatography-mass spectrometry platform in baseline plasma samples from 214 patients with CKD enrolled in the Clinical Phenotyping Resource and Biobank Core; 81 patients with coronary artery disease (CAD) and 133 without CAD were randomly assigned to training and validation subsets. The primary outcome was a history of CAD and the secondary outcome was a composite history of cardiovascular disease (CVD) at enrollment. Results: We found significantly higher levels of the SCFA valerate among patients with CAD as compared with patients without CAD in the training set (p < 0.001). The valerate concentrations were also significantly higher among subjects with composite outcomes of CVD compared to those without CVD (p = 0.006). These results were subsequently replicated in the validation set. Logistic regression analysis revealed a strong independent association between plasma valerate levels and CVD in both training and validation sets. When valerate was added to the base clinical model comprising of diabetes, hypertension, urinary protein-creatinine ratio, and estimated glomerular filtration rate, it increased the c-statistics for predicting CVD from 0.68 to 0.79 (p = 0.02) in the training set, an observation which was confirmed in the validation set. ­Conclusion: This study provides evidence for alterations in gut-microbiota-derived SCFAs with advancing CKD, demonstrates the association of higher plasma valerate levels with pre-existing CVD, and reveals areas for future exploration of cardiovascular risk in patients with CKD.

Sign in / Sign up

Export Citation Format

Share Document