The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform
Craig B Langman - One of the best experts on this subject based on the ideXlab platform.
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diagnosis assessment and treatment of bone turnover abnormalities in renal Osteodystrophy
American Journal of Kidney Diseases, 2004Co-Authors: Kevin J Martin, Klaus Olgaard, Jared W. Coburn, Giorgio Coen, Craig B Langman, Masafumi FukagawaAbstract:HE ABNORMALITIES of the skeleton in chronic kidney disease (CKD), collectively known as renal Osteodystrophy, are an important cause of morbidity and decreased quality of life. In the management of patients with kidney disease, it is necessary to have a rational approach to the diagnosis and assessment of renal Osteodystrophy in order to devise a treatment plan that hopefully will lead to an improved outcome. In the past, the term renal Osteodystrophy was mainly equated only with abnormalities of bone turnover, but as described in the article by Cunningham and Sprague 1 in this same issue, renal Osteodystrophy is a complex disorder of compromised bone strength in CKD patients. While osteoporosis is a term used to describe fragile bones prone to fracture in the general population and is most often assessed by dual x-ray absorptiometry (DEXA), renal Osteodystrophy should be the principal term to describe fragile bones prone to fracture and other morbidities in CKD. Renal Osteodystrophy is a function of bone turnover (assessed by bone biopsy), bone density (assessed by DEXA or quantitative CT [qCT]), and bone architecture, but the principal determinant of bone fragility in CKD is abnormal bone turnover. However, diagnosing and treating bone turnover abnormalities remains challenging. Our discussion group met to assess the current state of knowledge, understand the basis of our current therapy, and identify the information that needs to be gathered to improve the therapy of bone turnover and thereby improve the disorder of renal Osteodystrophy. A number of important questions, listed in Table 1, were considered.
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Osteoma cutis as a presenting sign of pseudohypoparathyroidism.
Pediatric Dermatology, 1992Co-Authors: Julie S Prendiville, Anne W. Lucky, Zulf Mughal, Susan B Mallory, Francis B Mimouni, Craig B LangmanAbstract:: Four unrelated children with oosteoma cutis and Albright hereditary Osteodystrophy (pseudohypoparathyroidism and pseudopseudohypoparathyroidism) are described. All four patients were normocalcemic when they were first seen with cutaneous ossification. A diagnosis of Albright hereditary Osteodystrophy was established on the basis of associated somatic features, radiographic abnormalities, and family history. Progression to pseudohypoparathyroidism was documented in two children who developed hypocalcemia at 2 and 3 years of age, respectively. Early recognition of the skin manifestations of this syndrome and careful follow-up are important to prevent the deleterious effects of hypocalcemia. Osteoma cutis is a common sign of Albright hereditary Osteodystrophy in infancy and childhood, and its significance should not be overlooked, even in the normocalcemic patient.
Kevin J Martin - One of the best experts on this subject based on the ideXlab platform.
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Pathophysiology of renal Osteodystrophy
Clinical Reviews in Bone and Mineral Metabolism, 2007Co-Authors: Kevin J Martin, Esther A. GonzálezAbstract:Renal Osteodystrophy is a common complication of chronic Kidney disease, and abnormalities of bone metabolism are a reflection of broad-based disturbances in the control mechanisms for mineral metabolism. Secondary hyperparathyroidism is a major contributor to the high turnover form of renal Osteodystrophy. Detailed investigations over the past several decades have uncovered many of the mechanisms involved in the initiation and maintenance of secondary hyperparathyroidism and it is these mechanisms that provide the basis for therapeutic intervention to control this complication of chronic kidney disease. An additional form of renal osteodystropy is characterized by abnormally low bone turnover, which also is multi-factorial in origin. Again, an understanding of the mechanisms involved in abnormal bone and mineral homeostasis provide the basis for therapy. It is only with a through understanding of the mechanisms involved in the initiation and maintenance of these complications that rational approaches to treatment may be instituted.
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diagnosis assessment and treatment of bone turnover abnormalities in renal Osteodystrophy
American Journal of Kidney Diseases, 2004Co-Authors: Kevin J Martin, Klaus Olgaard, Jared W. Coburn, Giorgio Coen, Craig B Langman, Masafumi FukagawaAbstract:HE ABNORMALITIES of the skeleton in chronic kidney disease (CKD), collectively known as renal Osteodystrophy, are an important cause of morbidity and decreased quality of life. In the management of patients with kidney disease, it is necessary to have a rational approach to the diagnosis and assessment of renal Osteodystrophy in order to devise a treatment plan that hopefully will lead to an improved outcome. In the past, the term renal Osteodystrophy was mainly equated only with abnormalities of bone turnover, but as described in the article by Cunningham and Sprague 1 in this same issue, renal Osteodystrophy is a complex disorder of compromised bone strength in CKD patients. While osteoporosis is a term used to describe fragile bones prone to fracture in the general population and is most often assessed by dual x-ray absorptiometry (DEXA), renal Osteodystrophy should be the principal term to describe fragile bones prone to fracture and other morbidities in CKD. Renal Osteodystrophy is a function of bone turnover (assessed by bone biopsy), bone density (assessed by DEXA or quantitative CT [qCT]), and bone architecture, but the principal determinant of bone fragility in CKD is abnormal bone turnover. However, diagnosing and treating bone turnover abnormalities remains challenging. Our discussion group met to assess the current state of knowledge, understand the basis of our current therapy, and identify the information that needs to be gathered to improve the therapy of bone turnover and thereby improve the disorder of renal Osteodystrophy. A number of important questions, listed in Table 1, were considered.
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pathogenesis and treatment of renal Osteodystrophy
Blood Purification, 2003Co-Authors: Eduardo Slatopolsky, Esther Gonzalez, Kevin J MartinAbstract:Renal Osteodystrophy is the term used to describe the many different patterns of the skeletal abnormalities that occur in patients with chronic kidney disease. The main two conditions are osteitis fibrosa, characterized by high bone turnover, increased osteoclastic and osteoblastic activity, and high levels of circulating parathyroid hormone (PTH) and adynamic bone disease characterized by low bone turnover and low levels of circulating PTH. Retention of phosphorus, decreased levels of calcitriol in blood, decreased levels of serum ionized calcium, reduced numbers of vitamin D receptors and calcium sensors in the parathyroid gland, and skeletal resistance to the calcemic action of PTH play a major role in the development of renal Osteodystrophy. This review will describe the current approach for the treatment of renal Osteodystrophy.
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Renal Osteodystrophy: pathogenesis and management.
Nephrology dialysis transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 1995Co-Authors: E A Gonzalez, Kevin J MartinAbstract:Several biochemical and hormonal abnormalities associated with renal insufficiency lead to complex disorders of bone which are described by the term renal Osteodystrophy. Assessment of renal Osteodystrophy in its early stages is primarily biochemical since symptoms generally do not occur until Osteodystrophy is advanced. Therapy should be initiated early in the course of renal insufficiency in order to prevent the development of severe skeletal abnormalities. Foremost among the multiple factors involved in the pathogenesis of hyperparathyroidism are retention of phosphorus and low levels of calcitriol. The principal therapies for the prevention and treatment of hyperparathyroidism include the use of calcium salts taken with meals, as phosphorus binders, to prevent the absorption of phosphorus from the intestine, correction of acidosis and careful use of vitamin D metabolites such as calcitriol or 1-alpha-hydroxycholecalciferol. The prevalence of aluminum induced osteomalacia appears to be declining as aluminum salts have been replaced by calcium containing phosphate binders and there is increased attention to adequate water purification for dialysis. Other disorders such as adynamic bone and the accumulation of beta 2-microglobulin may require bone biopsy for accurate diagnosis and are more difficult to treat effectively.
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renal Osteodystrophy pathogenesis and management
Nephrology Dialysis Transplantation, 1995Co-Authors: Esther Gonzalez, Kevin J MartinAbstract:Several biochemical and hormonal abnormalities associated with renal insufficiency lead to complex disorders of bone which are described by the term renal Osteodystrophy. Assessment of renal Osteodystrophy in its early stages is primarily biochemical since symptoms generally do not occur until Osteodystrophy is advanced. Therapy should be initiated early in the course of renal insufficiency in order to prevent the development of severe skeletal abnormalities. Foremost among the multiple factors involved in the pathogenesis of hyperparathyroidism are retention of phosphorus and low levels of calcitriol. The principal therapies for the prevention and treatment of hyperparathyroidism include the use of calcium salts taken with meals, as phosphorus binders, to prevent the absorption of phosphorus from the intestine, correction of acidosis and careful use of vitamin D metabolites such as calcitriol or 1-α-hydroxycholecalciferol. The prevalence of aluminum induced osteomalacia appears to be declining as aluminum salts have been replaced by calcium containing phosphate binders and there is increased attention to adequate water purification for dialysis. Other disorders such as adynamic bone and the accumulation of β 2 -microglobulin may require bone biopsy for accurate diagnosis and are more difficult to treat effectively.
Gino V Segre - One of the best experts on this subject based on the ideXlab platform.
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Biochemical markers of renal Osteodystrophy in pediatric patients undergoing CAPD/CCPD
Kidney International, 1994Co-Authors: Isidro B Salusky, William Oppenheim, Jorge A Ramirez, Barbara Gales, Gino V Segre, William G GoodmanAbstract:Biochemical markers of renal Osteodystrophy in pediatric patients undergoing CAPD/CCPD. Serum intact PTH [1–84] levels were evaluated as a potential non-invasive method for the diagnosis of renal Osteodystrophy in children treated with CAPD/CCPD. Sixty-eight bone biopsy samples were obtained from 55 patients, aged 13 ± 5 (X ± SD) years, undergoing CAPD/CCPD for 29 ± 13 months; osteitis fibrosa was present in 34 cases, mild lesions of secondary hyperparathyroidism in six, 15 had adynamic lesions, and 13 were classified as normal histology. Serum calcium levels were higher in patients with adynamic bone or normal bone histology than in those with secondary hyperparathyroidism, whereas serum phosphorus, alkaline phosphatase and PTH levels were greater in patients with osteitis fibrosa. The combination of a serum PTH level >200 pg/ml and a serum calcium value 10 mg/dl. Higher serum calcium levels and serum PTH values within or below the normal range characterize patients with the adynamic lesion of renal Osteodystrophy. Serum PTH levels of approximately 200 pg/ml are useful for distinguishing patients with low-turnover lesions of renal Osteodystrophy from those with secondary hyperparathyroidism.
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biochemical markers of renal Osteodystrophy in pediatric patients undergoing capd ccpd
Kidney International, 1994Co-Authors: William Oppenheim, Isidro B Salusky, Jorge A Ramirez, Barbara Gales, Gino V SegreAbstract:Biochemical markers of renal Osteodystrophy in pediatric patients undergoing CAPD/CCPD. Serum intact PTH [1–84] levels were evaluated as a potential non-invasive method for the diagnosis of renal Osteodystrophy in children treated with CAPD/CCPD. Sixty-eight bone biopsy samples were obtained from 55 patients, aged 13 ± 5 (X ± SD) years, undergoing CAPD/CCPD for 29 ± 13 months; osteitis fibrosa was present in 34 cases, mild lesions of secondary hyperparathyroidism in six, 15 had adynamic lesions, and 13 were classified as normal histology. Serum calcium levels were higher in patients with adynamic bone or normal bone histology than in those with secondary hyperparathyroidism, whereas serum phosphorus, alkaline phosphatase and PTH levels were greater in patients with osteitis fibrosa. The combination of a serum PTH level >200 pg/ml and a serum calcium value 10 mg/dl. Higher serum calcium levels and serum PTH values within or below the normal range characterize patients with the adynamic lesion of renal Osteodystrophy. Serum PTH levels of approximately 200 pg/ml are useful for distinguishing patients with low-turnover lesions of renal Osteodystrophy from those with secondary hyperparathyroidism.
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aplastic Osteodystrophy without aluminum the role of suppressed parathyroid function
Kidney International, 1993Co-Authors: Gavril Hercz, William G Goodman, Gino V Segre, Celia M T Greenwood, Arif Manuel, Carl Saiphoo, Stanley S A Fenton, Donald J SherrardAbstract:Aplastic Osteodystrophy without aluminum: The role of "suppressed" parathyroid function. We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pM or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal Osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover Osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 ± 6.1 vs. 36.9 ± 3.2 pM (77 ± 61 vs. 369 ± 32 pg/ml), P 3 intake and diabetes mellitus. These factors may modulate their effect by lowering serum PTH to levels which are inadequate in maintaining normal bone turnover. The long-term sequelae of this non-aluminum related lesion remain to be defined.
Donald J Sherrard - One of the best experts on this subject based on the ideXlab platform.
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aplastic Osteodystrophy without aluminum the role of suppressed parathyroid function
Kidney International, 1993Co-Authors: Gavril Hercz, William G Goodman, Gino V Segre, Celia M T Greenwood, Arif Manuel, Carl Saiphoo, Stanley S A Fenton, Donald J SherrardAbstract:Aplastic Osteodystrophy without aluminum: The role of "suppressed" parathyroid function. We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pM or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal Osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover Osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 ± 6.1 vs. 36.9 ± 3.2 pM (77 ± 61 vs. 369 ± 32 pg/ml), P 3 intake and diabetes mellitus. These factors may modulate their effect by lowering serum PTH to levels which are inadequate in maintaining normal bone turnover. The long-term sequelae of this non-aluminum related lesion remain to be defined.
Giorgio Coen - One of the best experts on this subject based on the ideXlab platform.
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diagnosis assessment and treatment of bone turnover abnormalities in renal Osteodystrophy
American Journal of Kidney Diseases, 2004Co-Authors: Kevin J Martin, Klaus Olgaard, Jared W. Coburn, Giorgio Coen, Craig B Langman, Masafumi FukagawaAbstract:HE ABNORMALITIES of the skeleton in chronic kidney disease (CKD), collectively known as renal Osteodystrophy, are an important cause of morbidity and decreased quality of life. In the management of patients with kidney disease, it is necessary to have a rational approach to the diagnosis and assessment of renal Osteodystrophy in order to devise a treatment plan that hopefully will lead to an improved outcome. In the past, the term renal Osteodystrophy was mainly equated only with abnormalities of bone turnover, but as described in the article by Cunningham and Sprague 1 in this same issue, renal Osteodystrophy is a complex disorder of compromised bone strength in CKD patients. While osteoporosis is a term used to describe fragile bones prone to fracture in the general population and is most often assessed by dual x-ray absorptiometry (DEXA), renal Osteodystrophy should be the principal term to describe fragile bones prone to fracture and other morbidities in CKD. Renal Osteodystrophy is a function of bone turnover (assessed by bone biopsy), bone density (assessed by DEXA or quantitative CT [qCT]), and bone architecture, but the principal determinant of bone fragility in CKD is abnormal bone turnover. However, diagnosing and treating bone turnover abnormalities remains challenging. Our discussion group met to assess the current state of knowledge, understand the basis of our current therapy, and identify the information that needs to be gathered to improve the therapy of bone turnover and thereby improve the disorder of renal Osteodystrophy. A number of important questions, listed in Table 1, were considered.
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renal Osteodystrophy in predialysis and hemodialysis patients comparison of histologic patterns and diagnostic predictivity of intact pth
Nephron, 2002Co-Authors: Giorgio Coen, Paola Ballanti, E Bonucci, Santo Calabria, S Costantini, Michele Ferrannini, Marco Giustini, R Giordano, Giulia Nicolai, Micaela ManniAbstract:Background: Comparison of renal Osteodystrophy in predialysis and hemodialysis has been rarely reported. Distinct patterns of renal Osteodystrophy could be found in these conditions
