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"Hyperphosphatemia" "ckd"

Inés Olaizola, Hena Caorsi, Laura Fajardo, Alejandro Ferreiro, Nieves Campistrus, Deyanira Dolinsky, Alicia Petraglia, Pablo Ambrosoni
Introduction: The mineral bone disorder, particularly secondary hyperparathyroidism, in chronic kidney disease (CKD) has a systemic impact affecting not only bone metabolism. Therefore its correction is important to prevent cardiovascular, inflammatory and immune diseases. Objective: To assess the effectiveness and safety of intravenous paricalcitol administered over a 6 month period for the treatment of secondary hyperparathyroidism (SHPT) in patients undergoing conventional hemodialysis, with close follow-up of treatment response...
July 2016: Jornal Brasileiro de Nefrologia: ʹorgão Oficial de Sociedades Brasileira e Latino-Americana de Nefrologia
Giuseppe Cianciolo, Mario Cozzolino
During the last decade, a new view into the molecular mechanisms of chronic kidney disease-mineral bone disorder (CKD-MBD) has been proposed, with fibroblast growth factor 23 (FGF23) as a novel player in the field. Enhanced serum FGF23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism (HPT). In contrast, reduced serum FGF23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, serum FGF23 levels are greatly increased and positively correlated with serum phosphate levels in CKD patients...
October 2016: Clinical Kidney Journal
Toshifumi Sugatani, Olga A Agapova, Yifu Fang, Alycia G Berman, Joseph M Wallace, Hartmut H Malluche, Marie-Claude Faugere, William Smith, Victoria Sung, Keith A Hruska
Dysregulation of skeletal remodeling is a component of renal osteodystrophy. Previously, we showed that activin receptor signaling is differentially affected in various tissues in chronic kidney disease (CKD). We tested whether a ligand trap for the activin receptor type 2A (RAP-011) is an effective treatment of the osteodystrophy of the CKD-mineral bone disorder. With a 70% reduction in the glomerular filtration rate, CKD was induced at 14 weeks of age in the ldlr-/- high fat-fed mouse model of atherosclerotic vascular calcification and diabetes...
September 22, 2016: Kidney International
Steven Habbous, Sebastian Przech, Rey Acedillo, Sisira Sarma, Amit X Garg, Janet Martin
BACKGROUND: It remains unclear which phosphate binders should be preferred for hyperphosphatemia management in chronic kidney disease (CKD). METHODS: We performed a systematic review and meta-analysis of randomized trials comparing sevelamer or lanthanum with other phosphate binders in CKD. RESULTS: Fifty-one trials (8829 patients) were reviewed. Compared with calcium-based binders, all-cause mortality was nonsignificantly lower with sevelamer {risk ratio [RR] 0...
September 20, 2016: Nephrology, Dialysis, Transplantation
Chu Zhou, Fang Wang, Jin-Wei Wang, Lu-Xia Zhang, Ming-Hui Zhao
BACKGROUND: Mineral and bone disorder (MBD), especially hyperphosphatemia, is an independently risk factor for adverse prognosis in patients with chronic kidney disease (CKD). However, CKD-MBD among Chinese population was poorly studied. This study aimed to investigate the status of MBD and its association with cardiovascular parameters in Chinese patients with predialysis CKD. METHODS: Chinese Cohort Study of Chronic Kidney Disease (C-STRIDE) is a prospective multicenter cohort study involving predialysis CKD patients in China...
2016: Chinese Medical Journal
Markus Ketteler, Orfeas Liangos, Patrick H Biggar
INTRODUCTION: Hyperphosphatemia is a hallmark of advanced chronic kidney disease (CKD) and associated with adverse outcomes. Preclinical and epidemiological studies strongly support a causal relationship between hyperphosphatemia and mortality as well as cardiovascular complications, especially including vascular, valvular and soft-tissue calcifications. Thus, appropriate phosphate lowering is considered to play a major role in health and longevity of CKD patients. In this respect, phosphate binders are the most powerful therapeutic option, while dietary phosphate restriction and intensified dialysis are valuable supportive approaches...
October 2016: Expert Opinion on Pharmacotherapy
Wei Ling Lau, Branko N Huisa, Mark Fisher
Chronic kidney disease (CKD) is an independent risk factor for the development of cerebrovascular disease, particularly small vessel disease which can manifest in a variety of phenotypes ranging from lacunes to microbleeds. Small vessel disease likely contributes to cognitive dysfunction in the CKD population. Non-traditional risk factors for vascular injury in uremia include loss of calcification inhibitors, hyperphosphatemia, increased blood pressure variability, elastinolysis, platelet dysfunction, and chronic inflammation...
September 14, 2016: Translational Stroke Research
Ellen Neven, Britt Opdebeeck, Annelies De Maré, Rida Bashir-Dar, Geert Dams, Rita Marynissen, Geert J Behets, Anja Verhulst, Bruce L Riser, Patrick C D'Haese
Vascular calcification significantly contributes to mortality in chronic kidney disease (CKD) patients. Sevelamer and pyrophosphate (PPi) have proven to be effective in preventing vascular calcification, the former by controlling intestinal phosphate absorption, the latter by directly interfering with the hydroxyapatite crystal formation. Since most patients present with established vascular calcification, it is important to evaluate whether these compounds may also halt or reverse the progression of preexisting vascular calcification...
November 2016: Calcified Tissue International
Fumihiko Koiwa, Akira Terao
BACKGROUND: Hyperphosphatemia is common in chronic kidney disease (CKD) and associated with mortality and morbidity. We aimed to evaluate the dose-dependent efficacy and safety of PA21 (sucroferric oxyhydroxide), an iron-based phosphate binder, in Japanese hemodialysis patients with hyperphosphatemia. METHODS: In this double-blind, multicenter, Phase II study, 183 patients were randomized to placebo or PA21 at doses of 250, 500, 750, or 1000 mg (based on iron content) three times/day for 6 weeks...
July 7, 2016: Clinical and Experimental Nephrology
Sanjay Vikrant, Anupam Parashar
BACKGROUND: Disordered mineral metabolism is common complications of chronic kidney disease (CKD). However, there are limited data on the pattern of these disturbances in Indian CKD population. MATERIALS AND METHODS: This was a prospective observational study of CKD-mineral and bone disorder (CKD-MBD) over a period of 3 years. The biochemical markers of CKD-MBD, namely, calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone (iPTH), and 25-hydoxyvitamin Vitamin D3 (25OHD), were measured in newly diagnosed CKD Stage 3-5 and prevalent CKD Stage 5D adult patients...
July 2016: Indian Journal of Endocrinology and Metabolism
Ahmed M Shaman, Stefan R Kowalski
Hyperphosphatemia in chronic kidney disease (CKD) patients is a potentially life altering condition that can lead to cardiovascular calcification, metabolic bone disease (renal osteodystrophy) and the development of secondary hyperparathyroidism (SHPT). It is also associated with increased prevalence of cardiovascular diseases and mortality rates. To effectively manage hyperphosphatemia in CKD patients it is important to not only consider pharmacological and nonpharmacological treatment options but also to understand the underlying physiologic pathways involved in phosphorus homoeostasis...
July 2016: Saudi Pharmaceutical Journal: SPJ: the Official Publication of the Saudi Pharmaceutical Society
Ross Robison, Danielle Cooney, Mary Beth Low, Niraj Desai
BACKGROUND: Hyperphosphatemia is a common problem in patients with chronic kidney disease (CKD). Calcium-containing phosphate binders are typically used as first-line therapy, primarily due to cost considerations. Non-calcium phosphate binders such as sevelamer and lanthanum may be considered in the appropriate setting. It is hypothesized that lanthanum is less costly and has a lower pill burden compared to sevelamer carbonate. OBJECTIVE: Determine the difference in cost (outcome 1) and tablet burden (outcome 2) between sevelamer carbonate and lanthanum within the Veteran population...
April 2016: Hospital Pharmacy
Carla Moschella
Chronic kidney disease affects 23 million Americans and is associated with many complications, one of the most complex of which is mineral and bone disorder. Pathophysiologic mechanisms begin to occur early in CKD but when the glomerular filtration rate declines to <50% of normal, biochemical and bone matrix abnormalities, which vary and are multifactorial, begin to be clinically apparent. Mainstays of treatment remain management of hyperphosphatemia and prevention or treatment of secondary hyperparathyroidism...
July 2016: JAAPA: Official Journal of the American Academy of Physician Assistants
Julie Wuyts, Annemieke Dhondt
Patients with chronic kidney disease (CKD) are prone to vascular calcification. Pathogenetic mechanisms of vascular calcifications have been broadly studied and discussed such as the role of hyperphosphatemia, hypercalcemia, parathormone, and vitamin D. In recent years, new insights have been gained pointing to vitamin K as a main actor. It has been discovered that vitamin K is an essential cofactor for the activation of matrix Gla protein (MGP), a calcification inhibitor in the vessel wall. Patients with CKD often suffer from vitamin K deficiency, resulting in low active MGP and eventually a lack of inhibition of vascular calcification...
May 25, 2016: Acta Clinica Belgica
Motoko Tanaka, Shigeyuki Miyamura, Tadashi Imafuku, Yuna Tominaga, Hitoshi Maeda, Makoto Anraku, Keishi Yamasaki, Daisuke Kadowaki, Yu Ishima, Hiroshi Watanabe, Tomoko Okuda, Kazuko Itoh, Kazutaka Matsushita, Masafumi Fukagawa, Masaki Otagiri, Toru Maruyama
A ferric citrate formulation for treating hyperphosphatemia is a new therapeutic that not only suppresses the accumulation of phosphorus in patients with chronic kidney disease-mineral bone disorders (CKD-MBD), but also ameliorates anemia caused by iron deficiency. In contrast, it has been demonstrated that intravenous iron injection markedly increases oxidative stress. This study was designed to investigate the effect of a ferric citrate formulation on oxidative stress in CKD-MBD patients receiving hemodialysis therapy...
2016: Biological & Pharmaceutical Bulletin
Aiji Yajima, Ken Tsuchiya, Hiroki Yokota, Kosaku Nitta
The pathophysiology and treatment for renal bone disease have made remakable progress. Moreover, osteocyte reseach has made tremendous progress. In the clinical aspect, (1) hyperphosphatemia, (2) hyperparathyroid and hypoparathyroid bone disease in patients with chronic kidney disease, (3) increased serum level of fibroblast growth factor 23 (FGF-23) and(4) reduced level of Klotho should be taken into consideration when analyzing these conditions. On the other hand, hyperphosphatemia must be successfully treated...
June 2016: Clinical Calcium
Charles Ginsberg, Joachim H Ix
PURPOSE OF REVIEW: Higher serum phosphate concentration is a central driver of the chronic kidney disease (CKD) mineral bone disorder (MBD). Although phosphate binders are commonly used to lower phosphate, they are minimally effective in CKD. Nicotinamide (vitamin B3) decreases intestinal phosphate transport in animals. Its efficacy and safety in CKD is uncertain. RECENT FINDINGS: We review data differentiating nicotinamide from nicotinic acid (niacin) and compare the metabolism and side-effect profile of each...
July 2016: Current Opinion in Nephrology and Hypertension
Shahanas Chathoth, Samir Al-Mueilo, Cyril Cyrus, Chittibabu Vatte, Awatif Al-Nafaie, Rudaynah Al-Ali, Brendan J Keating, Fahad Al-Muhanna, Amein Al Ali
BACKGROUND: The osteocyte-derived hormone, fibroblast growth factor 23 (FGF23), regulates the phosphorus metabolism and suppresses 1,25-dihydroxyvitamin D production, thereby mitigating hyperphosphatemia in patients with renal disorders. An elevated FGF23 level is suggested to be an early biomarker of altered phosphorus metabolism in the initial stages of chronic kidney disease (CKD) and acts as a strong predictor of mortality in dialysis patients. In the Saudi population, there is no report on the FGF23 level in CKD patients to date...
December 2015: Cardiorenal Medicine
Jimmy Gentry, Jonathan Webb, Daniel Davenport, Hartmut H Malluche
It is well-established that parathyroid hormone (PTH) correlates with the level of bone turnover in patients with chronic kidney disease stage 5D (CKD-5D). Hyperphosphatemia is a well-established complication of end-stage renal disease and is usually attributed to dietary intake. This study evaluates the relationship between serum phosphorus levels and bone turnover in patients with CKD-5D. 93 patients with CKD-5D from the Kentucky Bone Registry who had sequentially undergone anterior iliac bone biopsies were reviewed...
July 2016: Clinical Nephrology
Wen Xiu Chang, Ning Xu, Takanori Kumagai, Takeshi Shiraishi, Takahiro Kikuyama, Hiroki Omizo, Kazuhiro Sakai, Shigeyuki Arai, Yoshifuru Tamura, Tatsuru Ota, Shigeru Shibata, Yoshihide Fujigaki, Zhong Yang Shen, Shunya Uchida
BACKGROUND: Although hyperphosphatemia is deemed a risk factor of the progression of chronic kidney disease (CKD), it remains unclear whether the normal range of serum phosphorus likewise deteriorates CKD. A propensity score analysis was applied to examine the causal effect of the normal range of serum phosphorus on the incidence of end-stage renal disease (ESRD). METHODS: A retrospective CKD cohort of 803 participants in a single institution was analyzed. Propensity score was estimated using 22 baseline covariates by multivariate binary logistic regression for the different thresholds of time-averaged phosphorus (TA-P) in the normal range of serum phosphorus incremented by 0...
2016: PloS One
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