scholarly journals Vitamin K, Vascular Calcification, and Chronic Kidney Disease: Current Evidence and Unanswered Questions

2019 ◽  
Vol 3 (9) ◽  
Author(s):  
M Kyla Shea ◽  
Sarah L Booth
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vitamin K ◽  
Animal Studies ◽  
Arterial Calcification ◽  
Current Evidence ◽  
Age Related ◽  
Increased Risk ◽  
The Us

ABSTRACTMore than 15% of the US population is currently >65 y old. As populations age there is a concomitant increase in age-related chronic diseases. One such disease is chronic kidney disease (CKD), which becomes more prevalent with age, especially over age 70 y. Individuals with CKD are at increased risk of cardiovascular disease, in part because arterial calcification increases as kidney function declines. Vitamin K is a shortfall nutrient among older adults that has been implicated in arterial calcification. Evidence suggests CKD patients have low vitamin K status, but data are equivocal because the biomarkers of vitamin K status can be influenced by CKD. Animal studies provide more compelling data on the underlying role of vitamin K in arterial calcification associated with CKD. The purpose of this review is to evaluate the strengths and limitations of the available evidence regarding the role of vitamin K in CKD.

P0895THE RELATIONSHIP OF ARTERIAL CALCIFICATIONS IN CHRONIC KIDNEY DISEASE PATIENTS WITH INDIRECT ANTICOAGULANT INTAKE AND HEART MORBIDITY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Asen Kamenov ◽  
Stoyanka Georgieva ◽  
Dobrina Mlachkova ◽  
Daniela Valentinova Monova
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vertebral Body ◽  
Vitamin K ◽  
Abdominal Aorta ◽  
Lumbar Vertebrae ◽  
Calcium Score ◽  
Arterial Calcification ◽  
Vitamin K Deficiency ◽  
K Deficiency

Abstract Background and Aims In patients with chronic kidney disease (CKD), arterial calcification (AC) is a potential mechanism for the progression of cardiovascular disease. AC is common in CKD patients and is a consequence of mineral-bone disorders. Indirect anticoagulants or vitamin K deficiency lead to matrix γ-carboxyglutamate decarboxylation, which may potentiate vascular calcification formation. The impaired renal function and indirect anticoagulants intake may lead to vitamin K deficiency and increased AC. The aim of this study is to determine if oral intake of Acenocoumarol has influence on abdominal aorta calcium score (AACS) and the AC relation with atrial fibrillation (AF) and / or ischemic heart disease (IHD) morbidity. Method We observe 129 patients with CKD (glomerular filtration rate below 44 ml/min/1,73 m2, MDRD formula calculated). X - ray of the lateral abdominal aorta is performed for the AACS assessment according to L. I. Kauppila et al. method. The assessment of calcium score is formed by the involvement grade of each segment on the anterior and posterior wall of the vessel along the first four lumbar vertebrae. Calcification affecting less than 1/3 of the anterior wall of the aorta along the lumbar vertebral body receives 1 score and calcification extending over ½ of the vertebral body length receives 3 scores (total score - 24). The patients are distributed into three groups: I group with calcium score from 0 to 7, II - from 8 to 15 and III group - from 16 to 24. The data from assessed AACS are compared with Acenocoumarol intake and the presence/absence of AF and/or IHD. The results are processed with χ2 statistical analysis. Results One hundred twenty nine patients with CKD (95 males and 34 females) are included in the study. The patients data (mean, percentages, degrees, etc.) are summarized in tabl.1 and tabl. 2. Clinically significant is the correlation between the grades of AACS and Acenocoumarol intake (p < 0,05). With the calcium score increasing, the patients percentage treated with Acenocoumarol also increases (fig. 1). There is a moderate correlation (Cramer’s coefficient is 0,39) between the AACS grades and heart morbidity from AF and / or IHD (p < 0,05). The data shows that the higher calcium score is related with increased patients percentage with AF and / or IHD morbidity (fig. 2). In our study, vascular calcifications are found in the abdominal aorta walls in all of the observed patients. We found that a higher AACS is associated with an Acenocoumarol intake in CKD patients and corresponds to an increased morbidity of AF and / or IHD. Acenocoumarol intake may lead to increased AACS. The higher calcium score is associated with a higher incidence of AF and / or IHD morbidity. Conclusion The study outcome supported the hypothesis that the increased AC formation and cardiovascular morbidity high risk could be a reason for the limited vitamin K antagonists (acenocoumarol) use in CKD patients. Furthermore, vitamin K2 supplementation is reasonable and may reduce the progression of AC.

scholarly journals Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Reciprocal Relationship ◽  
Current Evidence ◽  
Renal Disease Progression ◽  
Lowering Therapy ◽  
The Relationship

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

scholarly journals Pelacarsen for lowering lipoprotein(a): implications for patients with chronic kidney disease

2020 ◽  
Vol 13 (5) ◽  
pp. 753-757
Author(s):  
Raul Fernandez-Prado ◽  
Maria Vanessa Perez-Gomez ◽  
Alberto Ortiz
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Messenger Rna ◽  
Controlled Trial ◽  
Good News ◽  
Phase 2 ◽  
Phase 3 ◽  
Lipoprotein A ◽  
Increased Risk

Abstract Chronic kidney disease (CKD) patients are at an increased risk of cardiovascular disease (CVD) and statins may not be protective in advanced CKD. The reasons for the limited efficacy of statins in advanced CKD are unclear, but statins may increase plasma levels of the highly atherogenic molecule lipoprotein(a), also termed Lp(a), as well as PCSK9 (protein convertase subtilisin/kexin type 9) levels. Lp(a) has also been linked to calcific aortic stenosis, which is common in CKD. Moreover, circulating Lp(a) levels increase in nephrotic syndrome with declining renal function and are highest in patients on peritoneal dialysis. Thus, the recent publication of the Phase 2 randomized controlled trial of pelacarsen [also termed AKCEA-APO(a)-LRx and TQJ230], a hepatocyte-directed antisense oligonucleotide targeting the LPA gene messenger RNA, in persons with CVD should be good news for nephrologists. Pelacarsen safely and dose-dependently decreased Lp(a) levels by 35–80% and a Phase 3 trial [Lp(a)HORIZON, NCT04023552] is planned to run from 2020 to 2024. Unfortunately, patients with estimated glomerular filtration rate <60 mL/min or urinary albumin:creatinine ratio >100 mg/g were excluded from Phase 2 trials and those with ‘significant kidney disease’ will be excluded from the Phase 3 trial. Optimized exclusion criteria for Lp(a)HORIZON would provide insights into the role of Lp(a) in CVD in CKD patients.

scholarly journals The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease

Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 285 ◽  
Author(s):  
Pieter Evenepoel ◽  
Sander Dejongh ◽  
Kristin Verbeke ◽  
Bjorn Meijers
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Mineral Density ◽  
Bone Mineral Density Loss ◽  
Gut Dysbiosis ◽  
Increased Risk ◽  
Fermentation Pattern

Patients with chronic kidney disease (CKD) are at increased risk of bone mineral density loss and vascular calcification. Bone demineralization and vascular mineralization often concur in CKD, similar to what observed in the general population. This contradictory association is commonly referred to as the ‘calcification paradox’ or the bone–vascular axis. Mounting evidence indicates that CKD-associated gut dysbiosis may be involved in the pathogenesis of the bone–vascular axis. A disrupted intestinal barrier function, a metabolic shift from a predominant saccharolytic to a proteolytic fermentation pattern, and a decreased generation of vitamin K may, alone or in concert, drive a vascular and skeletal pathobiology in CKD patients. A better understanding of the role of gut dysbiosis in the bone–vascular axis may open avenues for novel therapeutics, including nutriceuticals.

scholarly journals Magnesium: A Magic Bullet for Cardiovascular Disease in Chronic Kidney Disease?

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 455 ◽  
Author(s):  
Nicoline Leenders ◽  
Marc Vervloet
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Excretion ◽  
Arterial Calcification ◽  
Magic Bullet ◽  
Reference Ranges ◽  
Magnesium Intake ◽  
Clinical Endpoints

Magnesium is essential for many physiological functions in the human body. Its homeostasis involves dietary intake, absorption, uptake and release from bone, swifts between the intra- and extracellular compartment, and renal excretion. Renal excretion is mainly responsible for regulation of magnesium balance. In chronic kidney disease (CKD), for a long time the general policy has been limiting magnesium intake. However, this may not be appropriate for many patients. The reference ranges for magnesium are not necessarily optimal concentrations, and risks for insufficient magnesium intake exist in patients with CKD. In recent years, many observational studies have shown that higher (in the high range of “normal” or slightly above) magnesium concentrations are associated with better survival in CKD cohorts. This review gives an overview of epidemiological associations between magnesium and overall and cardiovascular survival in patients with CKD. In addition, potential mechanisms explaining the protective role of magnesium in clinical cardiovascular outcomes are described by reviewing evidence from in vitro studies, animal studies, and human intervention studies with non-clinical endpoints. This includes the role of magnesium in cardiac arrhythmia, heart failure, arterial calcification, and endothelial dysfunction. Possible future implications will be addressed, which will need prospective clinical trials with relevant clinical endpoints before these can be adopted in clinical practice.

scholarly journals Cognitive Impairment in Chronic Kidney Disease: Vascular Milieu and the Potential Therapeutic Role of Exercise

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ulf G. Bronas ◽  
Houry Puzantian ◽  
Mary Hannan
Keyword(s):  
Quality Of Life ◽  
Chronic Kidney Disease ◽  
Cognitive Impairment ◽  
Kidney Disease ◽  
Physical Function ◽  
Vascular Dysfunction ◽  
Therapeutic Modality ◽  
Increased Risk

Chronic kidney disease (CKD) is considered a model of accelerated aging. More specifically, CKD leads to reduced physical functioning and increased frailty, increased vascular dysfunction, vascular calcification and arterial stiffness, high levels of systemic inflammation, and oxidative stress, as well as increased cognitive impairment. Increasing evidence suggests that the cognitive impairment associated with CKD may be related to cerebral small vessel disease and overall impairment in white matter integrity. The triad of poor physical function, vascular dysfunction, and cognitive impairment places patients living with CKD at an increased risk for loss of independence, poor health-related quality of life, morbidity, and mortality. The purpose of this review is to discuss the available evidence of cerebrovascular-renal axis and its interconnection with early and accelerated cognitive impairment in patients with CKD and the plausible role of exercise as a therapeutic modality. Understanding the cerebrovascular-renal axis pathophysiological link and its interconnection with physical function is important for clinicians in order to minimize the risk of loss of independence and improve quality of life in patients with CKD.

scholarly journals Toll-Like Receptors in Acute Kidney Injury

2021 ◽  
Vol 22 (2) ◽  
pp. 816
Author(s):  
Cristina Vázquez-Carballo ◽  
Melania Guerrero-Hue ◽  
Cristina García-Caballero ◽  
Sandra Rayego-Mateos ◽  
Lucas Opazo-Ríos ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Pathological Condition ◽  
Kidney Injury ◽  
Preclinical Studies ◽  
Toll Like Receptors ◽  
Middle Income ◽  
Increased Risk

Acute kidney injury (AKI) is an important health problem, affecting 13.3 million individuals/year. It is associated with increased mortality, mainly in low- and middle-income countries, where renal replacement therapy is limited. Moreover, survivors show adverse long-term outcomes, including increased risk of developing recurrent AKI bouts, cardiovascular events, and chronic kidney disease. However, there are no specific treatments to decrease the adverse consequences of AKI. Epidemiological and preclinical studies show the pathological role of inflammation in AKI, not only at the acute phase but also in the progression to chronic kidney disease. Toll-like receptors (TLRs) are key regulators of the inflammatory response and have been associated to many cellular processes activated during AKI. For that reason, a number of anti-inflammatory agents targeting TLRs have been analyzed in preclinical studies to decrease renal damage during AKI. In this review, we updated recent knowledge about the role of TLRs, mainly TLR4, in the initiation and development of AKI as well as novel compounds targeting these molecules to diminish kidney injury associated to this pathological condition.

scholarly journals Prognostic Value of Soluble Suppression of Tumorigenicity 2 in Chronic Kidney Disease Patients: A Meta-Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Guangying Guo ◽  
Aoran Huang ◽  
Xin Huang ◽  
Tianhua Xu ◽  
Li Yao
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sample Size ◽  
Subgroup Analysis ◽  
Meta Analysis ◽  
Prognostic Role ◽  
Increased Risk ◽  
All Cause Mortality ◽  
Cvd Mortality

Objective. Previous studies have controversial results about the prognostic role of soluble suppression of tumorigenicity 2 (sST2) in chronic kidney disease (CKD). Therefore, we conduct this meta-analysis to access the association between sST2 and all-cause mortality, cardiovascular disease (CVD) mortality, and CVD events in patients with CKD. Methods. The publication studies on the association of sST2 with all-cause mortality, CVD mortality, and CVD events from PubMed and Embase were searched through August 2020. We pooled the hazard ratio (HR) comparing high versus low levels of sST2 and subgroup analysis based on treatment, continent, and diabetes mellitus (DM) proportion, and sample size was also performed. Results. There were 15 eligible studies with 11,063 CKD patients that were included in our meta-analysis. Elevated level of sST2 was associated with increased risk of all-cause mortality (HR 2.05; 95% confidence interval (CI), 1.51–2.78), CVD mortality (HR 1.68; 95% CI, 1.35–2.09), total CVD events (HR 1.88; 95% CI, 1.26–2.80), and HF (HR 1.35; 95% CI, 1.11–1.64). Subgroup analysis based on continent, DM percentage, and sample size showed that these factors did not influence the prognostic role of sST2 levels to all-cause mortality. Conclusions. Our results show that high levels of sST2 could predict the all-cause mortality, CVD mortality, and CVD events in CKD patients.

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