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Garabed Eknoyan - One of the best experts on this subject based on the ideXlab platform.
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Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006; 69
2015Co-Authors: S Moe, Garabed EknoyanAbstract:Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and are an important cause of morbidity, decreased quality of life, and Extraskeletal Calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified based on bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) sponsored a Controversies Conference on Renal Osteodystrophy to (1) develop a clear, clinically relevant, and internationally acceptable definition and classification system, (2) develop a consensus for bone biopsy evaluation and classification, and (3) evaluate laboratory and imaging markers for the clinical assessment of patients with CKD. It is recommended that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD, which ca
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chronic kidney disease mineral bone disorder a new paradigm
Advances in Chronic Kidney Disease, 2007Co-Authors: Sharon M Moe, Tilman B Drueke, Norbert Lameire, Garabed EknoyanAbstract:Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and an important cause of morbidity, decreased quality of life, and Extraskeletal Calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified on the basis of bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) recently sponsored a Controversies Conference to evaluate this definition. The recommendations were that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD and (2) the term CKD-mineral and bone disorder (CKD-MBD) be used to describe the broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is manifested by an abnormality of any one or a combination of the following: laboratory-abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; bone-changes in bone turnover, mineralization, volume, linear growth, or strength; and Calcification-vascular or other soft-tissue Calcification. The pathogenesis and clinical manifestations of these components of CKD-MBD are described in detail in this issue of Advances in Chronic Kidney Disease.
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Definition, evaluation, and classification of renal osteodystrophy: A position statement from kidney disease: Improving global outcomes (KDIGO)
KIDNEY INT, 2006Co-Authors: Garabed EknoyanAbstract:Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and are an important cause of morbidity, decreased quality of life, and Extraskeletal Calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified based on bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) sponsored a Controversies Conference on Renal Osteodystrophy to (1) develop a clear, clinically relevant, and internationally acceptable definition and classification system, (2) develop a consensus for bone biopsy evaluation and classification, and (3) evaluate laboratory and imaging markers for the clinical assessment of patients with CKD. It is recommended that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD, which can be further assessed by histomorphometry, and the results reported based on a unified classification system that includes parameters of turnover, mineralization, and volume, and (2) the term CKD-Mineral and Bone Disorder (CKD-MBD) be used to describe a broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism due to CKD, which is manifested by abnormalities in bone and mineral metabolism and/or extra-skeletal Calcification. The international adoption of these recommendations will greatly enhance communication, facilitate clinical decision-making, and promote the evolution of evidence-based clinical practice guidelines worldwide.
Sharon M Moe - One of the best experts on this subject based on the ideXlab platform.
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ckd mineral and bone disorder core curriculum 2011
American Journal of Kidney Diseases, 2011Co-Authors: Ranjani N Moorthi, Sharon M MoeAbstract:Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) is a term that encompasses a constellation of abnormalities seen in progressive kidney disease that include altered levels of calcium, phosphorus, parathyroid hormone (PTH), and vitamin D; disturbances in bone modeling and remodeling, with the associated development of fractures or impaired linear bone growth (in children); and Extraskeletal Calcification in soft tissues and arteries. The kidney is responsible for maintenance of serum calcium and phosphorus within the normal range in people without kidney disease. In CKD stages 2 and 3, compensatory mechanisms in the form of elevated PTH, elevated fibroblast growth factor 23 (FGF-23), and decreased calcitriol result in normal to near-normal blood calcium and phosphorus levels. These compensatory mechanisms become overwhelmed in later stages of CKD, eventually failing and resulting in the group of abnormalities encompassed by CKD-MBD (Box 1). Box 1 Definition of CKD-MBD A systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism abnormalities in bone turnover, mineralization, volume, linear growth, or strength vascular or other soft tissue Calcification View it in a separate window Abbreviations: CKD, chronic kidney disease; CKD-MBD, chronic kidney disease-mineral and bone disorder; PTH, parathyroid hormone.
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chronic kidney disease mineral bone disorder a new paradigm
Advances in Chronic Kidney Disease, 2007Co-Authors: Sharon M Moe, Tilman B Drueke, Norbert Lameire, Garabed EknoyanAbstract:Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease (CKD) and an important cause of morbidity, decreased quality of life, and Extraskeletal Calcification that have been associated with increased cardiovascular mortality. These disturbances have traditionally been termed renal osteodystrophy and classified on the basis of bone biopsy. Kidney Disease: Improving Global Outcomes (KDIGO) recently sponsored a Controversies Conference to evaluate this definition. The recommendations were that (1) the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD and (2) the term CKD-mineral and bone disorder (CKD-MBD) be used to describe the broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is manifested by an abnormality of any one or a combination of the following: laboratory-abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; bone-changes in bone turnover, mineralization, volume, linear growth, or strength; and Calcification-vascular or other soft-tissue Calcification. The pathogenesis and clinical manifestations of these components of CKD-MBD are described in detail in this issue of Advances in Chronic Kidney Disease.
Moe, Sharon M. - One of the best experts on this subject based on the ideXlab platform.
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Effect of Etelcalcetide vs Cinacalcet on Serum Parathyroid Hormone in Patients Receiving Hemodialysis With Secondary Hyperparathyroidism A Randomized Clinical Trial
'American Medical Association (AMA)', 2017Co-Authors: Block, Geoffrey A., Bushinsky, David A., Cheng Sunfa, Cunningham John, Dehmel Bastian, Drueke, Tilman B., Ketteler Markus, Kewalramani Reshma, Martin, Kevin J., Moe, Sharon M.Abstract:Importance Secondary hyperparathyroidism contributes to Extraskeletal Calcification and is associated with all-cause and cardiovascular mortality. Control is suboptimal in the majority of patients receiving hemodialysis. An intravenously (IV) administered calcimimetic could improve adherence and reduce adverse gastrointestinal effects. Objective To evaluate the relative efficacy and safety of the IV calcimimetic etelcalcetide and the oral calcimimetic cinacalcet. Design, Setting, and Participants A randomized, double-blind, double-dummy active clinical trial was conducted comparing IV etelcalcetide vs oral placebo and oral cinacalcet vs IV placebo in 683 patients receiving hemodialysis with serum parathyroid hormone (PTH) concentrations higher than 500 pg/mL on active therapy at 164 sites in the United States, Canada, Europe, Russia, and New Zealand. Patients were enrolled from August 2013 to May 2014, with end of follow-up in January 2015. Interventions Etelcalcetide intravenously and oral placebo (n = 340) or oral cinacalcet and IV placebo (n = 343) for 26 weeks. The IV study drug was administered 3 times weekly with hemodialysis; the oral study drug was administered daily. Main Outcomes and Measures The primary efficacy end point was noninferiority of etelcalcetide at achieving more than a 30% reduction from baseline in mean predialysis PTH concentrations during weeks 20-27 (noninferiority margin, 12.0%). Secondary end points included superiority in achieving biochemical end points (>50% and >30% reduction in PTH) and self-reported nausea or vomiting. Results The mean (SD) age of the trial participants was 54.7 (14.1) years and 56.2% were men. Etelcalcetide was noninferior to cinacalcet on the primary end point. The estimated difference in proportions of patients achieving reduction in PTH concentrations of more than 30% between the 198 of 343 patients (57.7%) randomized to receive cinacalcet and the 232 of 340 patients (68.2%) randomized to receive etelcalcetide was −10.5% (95% CI, −17.5% to −3.5%, P for noninferiority,
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A comparison of calcium to zoledronic acid for improvement of cortical bone in an animal model of CKD
'Wiley', 2014Co-Authors: Moe, Sharon M., Chen, Neal X., Newman, Christopher L., Gattone Ii, Vincent H., Organ, Jason M., Chen Xianming, Allen, Matthew R.Abstract:Patients with chronic kidney disease (CKD) have increased risk of fractures, yet the optimal treatment is unknown. In secondary analyses of large randomized trials, bisphosphonates have been shown to improve bone mineral density and reduce fractures. However, bisphosphonates are currently not recommended in patients with advanced kidney disease due to concern about oversuppressing bone remodeling, which may increase the risk of developing arterial Calcification. In the present study we used a naturally occurring rat model of CKD with secondary hyperparathyroidism, the Cy/+ rat, and compared the efficacy of treatment with zoledronic acid, calcium given in water to simulate a phosphate binder, and the combination of calcium and zoledronic acid. Animals were treated beginning at 25 weeks of age (approximately 30% of normal renal function) and followed for 10 weeks. The results demonstrate that both zoledronic acid and calcium improved bone volume by micro-computed tomography (µCT) and both equally suppressed the mineral apposition rate, bone formation rate, and mineralizing surface of trabecular bone. In contrast, only calcium treatment with or without zoledronic acid improved cortical porosity and cortical biomechanical properties (ultimate load and stiffness) and lowered parathyroid hormone (PTH). However, only calcium treatment led to the adverse effects of increased arterial Calcification and fibroblast growth factor 23 (FGF23). These results suggest zoledronic acid may improve trabecular bone volume in CKD in the presence of secondary hyperparathyroidism, but does not benefit Extraskeletal Calcification or cortical biomechanical properties. Calcium effectively reduces PTH and benefits both cortical and trabecular bone yet increases the degree of extra skeletal Calcification
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A comparison of calcium to zoledronic acid for improvement of cortical bone in an animal model of CKD
'Wiley', 2013Co-Authors: Moe, Sharon M., Chen, Neal X., Newman, Christopher L., Gattone Ii, Vincent H., Organ, Jason M., Chen Xianming, Allen, Matthew R.Abstract:Bone Biology Laboratory http://www.iupui.edu/~bonelab/ Department of Anatomy and Cell Biology Indiana University School of MedicinePatients with chronic kidney disease (CKD) have increased risk of fractures, yet the optimal treatment is unknown. In secondary analyses of large randomized trials, bisphosphonates have been shown to improve bone mineral density and reduce fractures. However, bisphosphonates are currently not recommended in patients with advanced kidney disease due to concern about over-suppressing bone remodeling, which may increase the risk of developing arterial Calcification. In the present study we used a naturally occurring rat model of CKD with secondary hyperparathyroidism, the Cy/+ rat, and compared the efficacy of treatment with zoledronic acid, calcium given in water to simulate a phosphate binder, and the combination of calcium and zoledronic acid. Animals were treated beginning at 25 weeks of age (approximately 30% of normal renal function) and followed for ten weeks. The results demonstrate that both zoledronic acid and calcium improved bone volume by microCT and both equally suppressed mineral apposition rate, bone formation rate, and mineralizing surface of trabecular bone. In contrast, only calcium treatment with or without zoledronic acid improved cortical porosity and cortical biomechanical properties (ultimate load and stiffness) and lowered parathyroid hormone (PTH). However, only calcium treatment led to the adverse effects of increased arterial Calcification and fibroblast growth factor 23 (FGF23). These results suggest zoledronic acid may improve trabecular bone volume in CKD in the presence of secondary hyperparathyroidism, but does not benefit Extraskeletal Calcification or cortical biomechanical properties. Calcium effectively reduces PTH and benefits both cortical and trabecular bone yet increases the degree of extra skeletal Calcification.This work was supported by the NIH NIAMS R01 5R01AR058005 (SMM) and S10-RR023710 (microCT equipment grant). We thank Drew Brown for tissue dissections, CT scanning and analysis
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Improving Global Outcomes in Mineral and Bone Disorders
American Society of Nephrology, 2024Co-Authors: Moe, Sharon M., Drüeke TilmanAbstract:Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease and an important cause of morbidity, decreased quality of life, and Extraskeletal Calcification that have been associated with increased cardiovascular mortality. Kidney Disease: Improving Global Outcomes (KDIGO)'s Global Mineral and Bone Initiative has sought to update the definition, evaluation, and classification of this mineral and bone disorder; improve standardization of assessment tools; enhance education about these complications; and stimulate research. In addition, this international organization sponsored a Controversies Conference in 2005 to define these complications better. The recommendations from that conference were that (1) the term “renal osteodystrophy” be used exclusively to define alterations in bone morphology that are associated with chronic kidney disease and (2) the term “chronic kidney disease–mineral and bone disorder” (CKD-MBD) can be used to describe the broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism as a result of chronic kidney disease. Chronic kidney disease–related mineral and bone disorders is manifested by an abnormality of any one or a combination of the following: Laboratory (abnormalities of calcium, phosphorus, parathyroid hormone, or vitamin D metabolism), bone (changes in bone turnover, mineralization, volume, linear growth, or strength), and Calcification (vascular or other soft tissue Calcification). The use of a common, internationally accepted terminology should ease the comparison of studies in this field and eventually improve patient care worldwide
Escolastico Aguileratejero - One of the best experts on this subject based on the ideXlab platform.
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metabolic acidosis inhibits soft tissue Calcification in uremic rats
Kidney International, 2008Co-Authors: F J Mendoza, Ignacio Gonzalez Lopez, Mariano Rodriguez, J. Pérez, Escolastico AguileratejeroAbstract:Metabolic acidosis is common in patients with chronic kidney disease, which is known to affect bone metabolism. We examined the effect of metabolic acidosis on the development of vascular and other soft-tissue Calcifications in uremic rats treated with calcitriol. Extraskeletal Calcification was measured in vivo, in control rats and rats with a remnant kidney model of uremia with or without ammonium chloride-induced acidosis. Soft-tissue Calcification was assessed histologically, by measurement of the expression of the sodium-dependent phosphate cotransporter Pit-1 and by quantification of tissue calcium and phosphorus. Calcitriol administration to uremic rats resulted in significant deposition of material positive for von Kossa stain in the aorta, stomach, and kidney, elevated aortic calcium and phosphorus, increased aortic Pit-1 expression, and high mortality. Calcitriol-treated uremic rats with acidosis did not develop aortic or soft-tissue Calcification, did not increase aortic Pit-1 expression, and had significantly lower mortality. Additionally, an acidotic environment prevented Calcification of vascular smooth muscle cells in vitro. Our study shows that metabolic acidosis inhibits Extraskeletal Calcification.
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the effect of calcitriol paricalcitol and a calcimimetic on extraosseous Calcifications in uremic rats
Kidney International, 2008Co-Authors: Ignacio Gonzalez Lopez, F J Mendoza, Escolastico Aguileratejero, Fatima Guerrero, J. Pérez, David Martin, Mariano RodriguezAbstract:Vitamin D derivatives and calcimimetics are used to treat secondary hyperparathyroidism in patients with chronic renal failure. We investigated the effect of calcitriol, paricalcitol, and the calcimimetic AMG 641 on soft-tissue Calcification in uremic rats with secondary hyperparathyroidism. Control and uremic rats were treated with vehicle, calcitriol, paricalcitol, AMG 641, or a combination of AMG 641 plus calcitriol or paricalcitol. Parathyroid hormone levels were reduced by all treatments but were better controlled by the combination of paricalcitol and AMG 641. The calcimimetic alone did not induce extraosseous Calcification but co-administration of AMG 641 reduced soft-tissue Calcification and aortic mineralization in both calcitriol- and paricalcitol-treated rats. Survival was significantly reduced in rats treated with calcitriol and this mortality was attenuated by co-treatment with AMG 641. Our study shows that Extraskeletal Calcification was present in animals treated with calcitriol and paricalcitol but not with AMG 641. When used in combination with paricalcitol, AMG 641 provided excellent control of secondary hyperparathyroidism and prevented mortality associated with the use of vitamin D derivatives without causing tissue Calcification.
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metabolic acidosis inhibits soft tissue Calcification in uremic rats commentary
Kidney International, 2008Co-Authors: Z Alaly, F J Mendoza, Ignacio Gonzalez Lopez, Mariano Rodriguez, J. Pérez, Escolastico AguileratejeroAbstract:Metabolic acidosis is common in patients with chronic kidney disease, which is known to affect bone metabolism. We examined the effect of metabolic acidosis on the development of vascular and other soft-tissue Calcifications in uremic rats treated with calcitriol. Extraskeletal Calcification was measured in vivo, in control rats and rats with a remnant kidney model of uremia with or without ammonium chloride-induced acidosis. Soft-tissue Calcification was assessed histologically, by measurement of the expression of the sodium-dependent phosphate cotransporter Pit-1 and by quantification of tissue calcium and phosphorus. Calcitriol administration to uremic rats resulted in significant deposition of material positive for von Kossa stain in the aorta, stomach, and kidney, elevated aortic calcium and phosphorus, increased aortic Pit-1 expression, and high mortality. Calcitriol-treated uremic rats with acidosis did not develop aortic or soft-tissue Calcification, did not increase aortic Pit-1 expression, and had significantly lower mortality. Additionally, an acidotic environment prevented Calcification of vascular smooth muscle cells in vitro. Our study shows that metabolic acidosis inhibits Extraskeletal Calcification.
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metabolic acidosis inhibits soft tissue Calcification in uremic rats commentary
Kidney International, 2008Co-Authors: Z Alaly, F J Mendoza, Ignacio Gonzalez Lopez, Mariano Rodriguez, J. Pérez, Escolastico AguileratejeroAbstract:Metabolic acidosis is common in patients with chronic kidney disease, which is known to affect bone metabolism. We examined the effect of metabolic acidosis on the development of vascular and other soft-tissue Calcifications in uremic rats treated with calcitriol. Extraskeletal Calcification was measured in vivo, in control rats and rats with a remnant kidney model of uremia with or without ammonium chloride-induced acidosis. Soft-tissue Calcification was assessed histologically, by measurement of the expression of the sodium-dependent phosphate cotransporter Pit-1 and by quantification of tissue calcium and phosphorus. Calcitriol administration to uremic rats resulted in significant deposition of material positive for von Kossa stain in the aorta, stomach, and kidney, elevated aortic calcium and phosphorus, increased aortic Pit-1 expression, and high mortality. Calcitriol-treated uremic rats with acidosis did not develop aortic or soft-tissue Calcification, did not increase aortic Pit-1 expression, and had significantly lower mortality. Additionally, an acidotic environment prevented Calcification of vascular smooth muscle cells in vitro. Our study shows that metabolic acidosis inhibits Extraskeletal Calcification.
Ranjani N Moorthi - One of the best experts on this subject based on the ideXlab platform.
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recent advances in the noninvasive diagnosis of renal osteodystrophy
Kidney International, 2013Co-Authors: Ranjani N MoorthiAbstract:Chronic kidney disease–mineral and bone disorder (CKD-MBD) is the term used to describe a constellation of biochemical abnormalities, bone disturbances that may lead to fractures, and Extraskeletal Calcification in soft tissues and arteries seen in CKD. This review focuses on the noninvasive diagnosis of renal osteodystrophy, the term used exclusively to define the bone pathology associated with CKD. Transiliac bone biopsy and histomorphometry with double-labeled tetracycline or its derivatives remains the gold standard for diagnosis of renal osteodystrophy. However, histomorphometry provides a ‘window’ into bone only at a single point in time, and is not clinically practical for studying continuous changes in bone morphology. Furthermore, the etiology of fractures in CKD is multifactorial and not fully explained by histomorphometry findings alone. The propensity of a bone to fracture is determined by bone strength, which is affected by bone mass and bone quality; the latter is a term used to describe the structure and composition of bone. Bone quantity is traditionally assessed by dual X-ray absorptiometry (DXA) and CT-based methods. Bone quality is more difficult to assess noninvasively, but newer techniques are emerging and are described in this review. Ultimately, the optimal diagnostic strategy for renal osteodystrophy may be a combination of multiple imaging techniques and biomarkers that are specific to each gender and race in CKD, with a goal of predicting fracture risk and optimizing therapy.
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ckd mineral and bone disorder core curriculum 2011
American Journal of Kidney Diseases, 2011Co-Authors: Ranjani N Moorthi, Sharon M MoeAbstract:Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) is a term that encompasses a constellation of abnormalities seen in progressive kidney disease that include altered levels of calcium, phosphorus, parathyroid hormone (PTH), and vitamin D; disturbances in bone modeling and remodeling, with the associated development of fractures or impaired linear bone growth (in children); and Extraskeletal Calcification in soft tissues and arteries. The kidney is responsible for maintenance of serum calcium and phosphorus within the normal range in people without kidney disease. In CKD stages 2 and 3, compensatory mechanisms in the form of elevated PTH, elevated fibroblast growth factor 23 (FGF-23), and decreased calcitriol result in normal to near-normal blood calcium and phosphorus levels. These compensatory mechanisms become overwhelmed in later stages of CKD, eventually failing and resulting in the group of abnormalities encompassed by CKD-MBD (Box 1). Box 1 Definition of CKD-MBD A systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism abnormalities in bone turnover, mineralization, volume, linear growth, or strength vascular or other soft tissue Calcification View it in a separate window Abbreviations: CKD, chronic kidney disease; CKD-MBD, chronic kidney disease-mineral and bone disorder; PTH, parathyroid hormone.
