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https://www.readbyqxmd.com/read/28437620/american-association-of-clinical-endocrinologists-and-american-college-of-endocrinology-guidelines-for-management-of-dyslipidemia-and-prevention-of-cardiovascular-disease
#1
Paul S Jellinger, Yehuda Handelsman, Paul D Rosenblit, Zachary T Bloomgarden, Vivian A Fonseca, Alan J Garber, George Grunberger, Chris K Guerin, David S H Bell, Jeffrey I Mechanick, Rachel Pessah-Pollack, Kathleen Wyne, Donald Smith, Eliot A Brinton, Sergio Fazio, Michael Davidson
OBJECTIVE: The development of these guidelines is mandated by the American Association of Clinical Endocrinologists (AACE) Board of Directors and American College of Endocrinology (ACE) Board of Trustees and adheres with published AACE protocols for the standardized production of clinical practice guidelines (CPGs). METHODS: Recommendations are based on diligent reviews of the clinical evidence with transparent incorporation of subjective factors, according to established AACE/ACE guidelines for guidelines protocols...
April 2017: Endocrine Practice
https://www.readbyqxmd.com/read/28432640/osteoporosis-bone-mineral-density-and-ckd-mbd-treatment-considerations
#2
REVIEW
Jordi Bover, Lucía Bailone, Víctor López-Báez, Silvia Benito, Paola Ciceri, Andrea Galassi, Mario Cozzolino
Osteoporosis and chronic kidney disease (CKD) have both independently important potential impact on bone health. A significant number of patients with CKD stages 3a-5D have been shown to have low bone mineral density (BMD), leading to a strikingly elevated risk of fractures (mainly hip fractures) and higher associated morbidity and mortality. Mechanical properties of bone beyond age and menopausal status are additionally affected by intrinsic uremic factors. Therefore, we review in this article not only general concepts of osteoporosis and related consequences, but also the diagnostic and therapeutic implications of low BMD and bone fractures in CKD, beyond increased vascular calcification...
April 21, 2017: Journal of Nephrology
https://www.readbyqxmd.com/read/28432595/what-animal-models-have-taught-us-about-the-safety-and-efficacy-of-bisphosphonates-in-chronic-kidney-disease
#3
REVIEW
Matthew R Allen, Mohammad W Aref
PURPOSE OF REVIEW: Bisphosphonates (BPs) have long been the gold-standard anti-remodeling treatment for numerous metabolic bone diseases. Since these drugs are excreted unmetabolized through the kidney, they are not recommended for individuals with compromised kidney function due to concerns of kidney and bone toxicity. The goal of this paper is to summarize the preclinical BP work in models of kidney disease with particular focus on the bone, kidney, and vasculature. RECENT FINDINGS: Summative data exists showing positive effects on bone and vascular calcifications with minimal evidence for bone or kidney toxicity in animal models...
April 21, 2017: Current Osteoporosis Reports
https://www.readbyqxmd.com/read/28429551/the-role-of-calcium-and-non-calcium-based-phosphate-binders-in-chronic-kidney-disease
#4
Grahame J Elder, Jacqueline Center
Rising levels of serum phosphate occur late in the course of chronic kidney disease (CKD) and have been easy targets for nephrologists to treat using phosphate binding drugs, as well as fertile ground for the pharmaceutical industry, for meta-analysis and for the earnest pontifications of guideline writers. Unfortunately, the evidence does little to support this focus, which might be better applied to earlier, adaptive hormonal changes, and to phosphate balance rather than serum phosphate levels. Nevertheless, phosphate binders are ubiquitously prescribed to patients on dialysis, and often prescribed to patients with earlier stages of CKD; for which there is no evidence of benefit and some evidence that calcium-based binders (CBBs) and possibly non-CBBs may cause more harm than placebo...
March 2017: Nephrology
https://www.readbyqxmd.com/read/28429550/parathyroid-hormone-targets-in-chronic-kidney-disease-and-managing-severe-hyperparathyroidism
#5
Carmel M Hawley, Stephen G Holt
Appropriate targets for parathyroid hormone (PTH) in patients with chronic kidney disease (CKD) stages 3-5D are controversial, as are the means by which these targets might be achieved. Secondary hyperparathyroidism is linked to symptoms like bone pain and itch, in addition to less clinically overt issues like bone fragility as well as vascular and soft tissue calcification which may lead to adverse hard endpoints, particularly fracture and death. Recognized therapies for managing a rising PTH include vitamin D analogues, with or without calcimimetic (where available), in addition to management of serum mineral concentrations with diet, binders and dialysis...
March 2017: Nephrology
https://www.readbyqxmd.com/read/28429547/the-use-of-bone-turnover-markers-in-chronic-kidney-disease-mineral-and-bone-disorders
#6
Cherie Chiang
Bone turnover markers assist in fracture risk prediction, management and monitoring of osteoporosis in patients without chronic kidney disease (CKD). The use in CKD-mineral bone disorder (MBD) has been limited as many of these markers and breakdown products are renally excreted, including the most commonly used and well standardized procollagen type I N propeptide and C-terminal cross-linking telopeptide of type I collagen. Of the markers unaffected by renal function, bone specific alkaline phosphatase is associated with mortality and fracture rate in CKD subjects and is now available on several automated analysers...
March 2017: Nephrology
https://www.readbyqxmd.com/read/28429546/should-nephrologists-consider-vascular-calcification-screening
#7
Rathika Krishnasamy, Eugenie Pedagogos
Vascular calcification (VC) has been widely discussed over the last few decades and is associated with significant morbidity and mortality among patients with chronic kidney disease. Importantly, these patients have premature and rapidly progressive calcification when compared with the general population. VC is an active and complex process that is closely regulated by a growing list of inducers and inhibitors. VC can be detected using several non-invasive modalities including plain radiography, echocardiogram and computed tomography scans...
March 2017: Nephrology
https://www.readbyqxmd.com/read/28426428/vascular-calcification-the-role-of-micrornas
#8
Stelina Alkagiet, Konstantinos Tziomalos
Vascular calcification represents the deposition of calcium phosphate salts in the tunica media of the vascular wall. It occurs during aging but is accelerated and pronounced in patients with diabetes mellitus, chronic kidney disease (CKD) and established cardiovascular disease. Due to the loss of elasticity of the vessel wall, vascular calcification might result in left ventricular hypertrophy and compromise coronary perfusion. Accordingly, several studies showed that vascular calcification is associated with increased risk for cardiovascular morbidity and mortality...
April 20, 2017: Biomolecular Concepts
https://www.readbyqxmd.com/read/28411233/vasculopathy-in-the-setting-of-cardiorenal-syndrome-the-roles-of-protein-bound-uremic-toxins
#9
Jingbin Guo, Lu Lu, Yue Hua, Kevin Huang, Ian Wang, Li Huang, Qiang Fu, Aihua Chen, Paul Chan, Huimin Fan, Zhong-Min Liu, Bing Hui Wang
Chronic kidney disease (CKD) often leads to and accelerates the progression of cardiovascular disease (CVD), whilst CVD also causes kidney dysfunction. This bidirectional interaction leads to the development of a complex syndrome known as cardiorenal syndrome (CRS). CRS not only involves both the heart and the kidney, but also the vascular system through a vast array of contributing factors. In addition to hemodynamic, neuro-hormonal, mechanical and biochemical factors, the non-dialyzable protein-bound uremic toxins (PBUTs) are also key contributing factors that have been demonstrated through in vitro, in vivo and clinical observations...
April 14, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28401422/acetate-free-biofiltration-to-remove-fibroblast-growth-factor-23-in-hemodialysis-patients-a-pilot-study
#10
Valeria Cernaro, Silvia Lucisano, Valeria Canale, Annamaria Bruzzese, Daniela Caccamo, Giuseppe Costantino, Michele Buemi, Domenico Santoro
AIM: Serum levels of 32 kDa-phosphaturic hormone fibroblast growth factor 23 (FGF23) rise early in renal failure in order to keep phosphatemia within the normal range; however, this compensatory mechanism itself contributes to chronic kidney disease-mineral bone disorder. High FGF23 is also associated to left ventricular hypertrophy, vascular calcifications and thus increased cardiovascular risk. The aim of this pilot pre-post study was to evaluate the effects of a single hemodiafiltration session with acetate-free biofiltration (AFB) on FGF23 serum levels...
April 11, 2017: Journal of Nephrology
https://www.readbyqxmd.com/read/28392544/impact-of-renal-functional-morphological-dynamics-on-the-calcification-of-coronary-and-abdominal-arteries-in-patients-with-chronic-kidney-disease
#11
Takeo Ichii, Ryota Morimoto, Takahiro Okumura, Hideki Ishii, Yosuke Tatami, Dai Yamamoto, Soichiro Aoki, Hiroaki Hiraiwa, Kenji Furusawa, Toru Kondo, Naoki Watanabe, Naoaki Kano, Kenji Fukaya, Akinori Sawamura, Susumu Suzuki, Yoshinari Yasuda, Toyoaki Murohara
AIM: Fast-progressing vascular calcification (VC) is accompanied by renal atrophy and functional deterioration along with atherosclerosis in patients with chronic kidney disease (CKD). However, the relationship between VC progression and renal functional and/or morphological changes remains unclear. METHODS: We included 70 asymptomatic patients with CKD without hemodialysis in our study. To identify temporal variations, the coronary artery calcification score (CACS), abdominal aortic calcification index (ACI), and renal parenchymal volume index (RPVI) were determined via spiral computed tomography scans taken during the study...
April 8, 2017: Journal of Atherosclerosis and Thrombosis
https://www.readbyqxmd.com/read/28391078/calcifications-de-la-loge-parotidienne-mise-au-point
#12
S Avignon, J M Foletti, C Collet, L Guyot, C Chossegros
INTRODUCTION: . Parotid lithiasis is the main cause of calcifications in the parotid space. However, there are many other less-known causes. The aim of our study was to point out the non lithiasic causes of calcifications in the parotid space. MATERIAL AND METHODS: We conducted an exhaustive review of the literature by mean of PubMed, using the keywords "parotid" and "calcification" and limiting our analysis to the original articles in humans published in English and in French...
April 5, 2017: Journal of Stomatology, Oral and Maxillofacial Surgery
https://www.readbyqxmd.com/read/28386842/vitamin-k2-inhibits-rat-vascular-smooth-muscle-cell-calcification-by-restoring-the-gas6-axl-akt-anti-apoptotic-pathway
#13
Cuiting Qiu, Haijun Zheng, Huiren Tao, Wenjun Yu, Xiaoyu Jiang, Aiqin Li, Hui Jin, Anlin Lv, Huan Li
Vascular calcification is associated with cardiovascular disease as a complication of hypertension, hyperlipidemia, diabetes mellitus, and chronic kidney disease. Vitamin K2 (VK2) delays vascular calcification by an unclear mechanism. Moreover, apoptosis modulates vascular smooth muscle cell (VSMC) calcification. This paper aimed to study VK2-modified VSMC calcification and survival cell signaling mediated by growth arrest-specific gene 6 (Gas6) and its tyrosine kinase receptor Axl. Primary-cultured VSMCs were dose-dependently treated with VK2 in the presence of calcification medium for 8 days, or pre-treated for 1 h with/without the Axl inhibitor R428 (2 μmol/L) or the caspase inhibitor Z-VAD-fmk (20 μmol/L) followed by treatment with VK2 (10 μmol/L) or rmGas6 (200 nmol/L) in calcification medium for 8 days...
April 6, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28379216/nicorandil-attenuates-neuronal-mitochondrial-dysfunction-and-oxidative-stress-associated-with-murine-model-of-vascular-calcification
#14
Sriram Ravindran, Krithika Swaminathan, Abhinaya Ramesh, Gino A Kurian
Evidences suggest that the presence of chronic kidney disease (CKD) is associated with cerebrovascular diseases related cognitive decline in dialysis patients. As mitochondrial dysfunction is implicated in neurodegenerative disorders, we hypothesized that changes in brain mitochondria occur due to vascular calcification induced by renal failure and the opening of the mitochondrial potassium channel using nicorandil may prevent its dysfunction. Brain tissues from rats with vascular calcification were studied...
2017: Acta Neurobiologiae Experimentalis
https://www.readbyqxmd.com/read/28366446/visceral-adipose-tissue-and-leptin-hyperproduction-are-associated-with-hypogonadism-in-men-with-chronic-kidney-disease
#15
Gabriela Cobo, Antonio C Cordeiro, Fernanda Cassulo Amparo, Celso Amodeo, Bengt Lindholm, Juan Jesús Carrero
OBJECTIVE: Hypogonadism is a common endocrine disorder in men with chronic kidney disease (CKD), but its pathophysiology is poorly understood. We here explore the plausible contribution of abdominal adiposity and leptin hyperproduction to testosterone deficiency in this patient population. DESIGN: Cross-sectional analysis with all men included the Malnutrition, Inflammation and Vascular Calcification cohort, which enrolled consecutive nondialyzed patients with CKD stages 3-5...
March 31, 2017: Journal of Renal Nutrition
https://www.readbyqxmd.com/read/28352317/activation-of-peroxisome-proliferator-activated-receptor-%C3%AE-inhibits-vascular-calcification-by-upregulating-klotho
#16
Lijuan Cheng, Lei Zhang, Jun Yang, Lirong Hao
Cardiovascular diseases are common in patients with chronic kidney disease. One of the key symptoms is the calcification of the vascular smooth muscle cells (VSMCs), which is induced by dysregulated mineral metabolism with high circulating levels of inorganic phosphate (Pi) and calcium. Klotho, which was originally identified as an aging suppressor gene, has been shown to be associated with vascular calcification. Since Klotho was recently identified as a target for nuclear receptor peroxisome proliferator-activated receptor (PPAR) γ, the present study aimed to determine whether PPARγ regulates VSMC calcification through modulating the expression levels of Klotho...
February 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28337344/is-fibroblast-growth-factor-23-the-leading-cause-of-increased-mortality-among-chronic-kidney-disease-patients-a-narrative-review
#17
REVIEW
Usama A Sharaf El Din, Mona M Salem, Dina O Abdulazim
The death rate among chronic kidney disease patients is the highest compared to other chronic diseases. 60% of these fatalities are cardiovascular. Cardiovascular calcifications and chronic inflammation affect almost all chronic kidney disease patients and are associated with cardiovascular mortality. Fibroblast growth factor 23 is associated with vascular calcification. Systemic inflammation in chronic kidney disease patients is multifactorial. The role of systemic inflammation in the pathogenesis of vascular calcification was recently reappraised...
May 2017: Journal of Advanced Research
https://www.readbyqxmd.com/read/28332217/imaging-for-vascular-calcification
#18
Paolo Raggi, W Charles O'Neill
Chronic decline in renal function is accompanied by deterioration of bone structure and function and progressive calcification of the vascular system. Both disease states have been linked with increased morbidity and mortality in chronic kidney disease. The severe alterations of mineral metabolism inherent with loss of renal function have an impact on vascular calcification development and progression, and several investigators have focused on ways to reduce their impact on vascular health. Imaging has contributed an important role in the assessment of vascular calcification, and the impact of various interventions aimed at curbing their progression...
March 22, 2017: Seminars in Dialysis
https://www.readbyqxmd.com/read/28294047/klotho-fgf23-cardiovascular-disease-and-vascular-calcification-black-or-white
#19
Giuseppe Cianciolo, Andrea Galassi, Irene Capelli, Roberto Schillaci, Gaetano La Manna, Mario Cozzolino
Patients affected by Chronic Kidney Disease and Mineral Bone Disorder (CKD-MBD) have a high risk of cardiovascular (CV) mortality that is poorly explained by traditional risk factors. The newest medical treatments for CKD-MBD have been associated with encouraging, but still inconsistent, improvement in CV disease complications and patient survival. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy (LVH), atherosclerosis, and vascular calcification (VC) may help with diagnosis and treatment of the organ damage that occurs secondary to CKD-MBD, thus improving survival...
March 9, 2017: Current Vascular Pharmacology
https://www.readbyqxmd.com/read/28291581/a-real-world-cost-effectiveness-analysis-of-sevelamer-versus-calcium-acetate-in-korean-dialysis-patients
#20
Jang-Hee Cho, Hye Min Jang, Hee-Yeon Jung, Ji-Young Choi, Sun-Hee Park, Chan-Duck Kim, Chul Woo Yang, Dong-Chan Jin, Yong-Lim Kim
PURPOSE: Sevelamer, a noncalcium phosphate binder, has been shown to attenuate the progression of vascular calcification and improve survival in patients with chronic kidney disease undergoing dialysis compared with calcium-based binders. Using real-world data from a cohort study and the Health Insurance Review and Assessment Service database, we conducted a cost-effectiveness analysis comparing sevelamer with calcium acetate in dialysis patients from the perspective of the National Health Insurance Service in South Korea...
March 10, 2017: Clinical Therapeutics
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