Journal Article•
K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease
University of Southern California1, United States Department of Veterans Affairs2, University of California, San Francisco3, Washington University in St. Louis4, Children's Memorial Hospital5, University of Kentucky6, Saint Louis University7, Mayo Clinic8, Indiana University – Purdue University Indianapolis9, University of California, Los Angeles10, University of Virginia11
About: This article is published in American Journal of Kidney Diseases.The article was published on 2003-10-01 and is currently open access. It has received 2609 citations till now. The article focuses on the topics: Chronic kidney disease-mineral and bone disorder & Kidney disease.
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TL;DR: The role of vitamin D in skeletal and nonskeletal health is considered and strategies for the prevention and treatment ofitamin D deficiency are suggested.
Abstract: Once foods in the United States were fortified with vitamin D, rickets appeared to have been conquered, and many considered major health problems from vitamin D deficiency resolved. But vitamin D deficiency is common. This review considers the role of vitamin D in skeletal and nonskeletal health and suggests strategies for the prevention and treatment of vitamin D deficiency.
11,849 citations
TL;DR: Hyperphosphatemia and hyperparathyroidism were significantly associated with all-cause, cardiovascular, and fracture-related hospitalization, and the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperph phosphatemia.
Abstract: Mortality rates in ESRD are unacceptably high. Disorders of mineral metabolism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiable. For determining associations among disorders of mineral metabolism, mortality, and morbidity in hemodialysis patients, data on 40,538 hemodialysis patients with at least one determination of serum phosphorus and calcium during the last 3 mo of 1997 were analyzed. Unadjusted, case mix-adjusted, and multivariable-adjusted relative risks of death were calculated for categories of serum phosphorus, calcium, calcium x phosphorus product, and intact parathyroid hormone (PTH) using proportional hazards regression. Also determined was whether disorders of mineral metabolism were associated with all-cause, cardiovascular, infection-related, fracture-related, and vascular access-related hospitalization. After adjustment for case mix and laboratory variables, serum phosphorus concentrations >5.0 mg/dl were associated with an increased relative risk of death (1.07, 1.25, 1.43, 1.67, and 2.02 for serum phosphorus 5.0 to 6.0, 6.0 to 7.0, 7.0 to 8.0, 8.0 to 9.0, and >/=9.0 mg/dl). Higher adjusted serum calcium concentrations were also associated with an increased risk of death, even when examined within narrow ranges of serum phosphorus. Moderate to severe hyperparathyroidism (PTH concentrations >/=600 pg/ml) was associated with an increase in the relative risk of death, whereas more modest increases in PTH were not. When examined collectively, the population attributable risk percentage for disorders of mineral metabolism was 17.5%, owing largely to the high prevalence of hyperphosphatemia. Hyperphosphatemia and hyperparathyroidism were significantly associated with all-cause, cardiovascular, and fracture-related hospitalization. Disorders of mineral metabolism are independently associated with mortality and morbidity associated with cardiovascular disease and fracture in hemodialysis patients.
2,475 citations
Journal Article•
1,723 citations
TL;DR: It is recommended that the term renal osteodystrophy be used exclusively to define alterations in bone morphology associated with CKD, and 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.
1,698 citations
TL;DR: Multivariate analysis revealed that DM, increased urinary albumin/creatinine ratio and lower eGFR predicted lower values of 1,25 OH2 D3, but not 25(OH)D3 levels, were seen across deciles of eG FR (P<0.001).
1,367 citations
Cites result from "K/DOQI clinical practice guidelines..."
...This finding may have therapeutic ramifications as recent Kidney Disease Outcomes Quality Initiative guidelines currently suggest the use of ergocalciferol (vitamin D2) as the initial treatment for HPTH in CKD stage 3 and 4.(16) However, the findings herein of an early low levels of 1,25 OH2 D3 and some preliminary data that show that this treatment regimen may not effectively suppress PTH,(17) may require that those recommendations are revisited....
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Saint Louis University1, Amgen2, University of New South Wales3, University of Toronto4, University College London5, Yale University6, Washington University in St. Louis7, University of Pennsylvania8, Katholieke Universiteit Leuven9, Indiana University – Purdue University Indianapolis10, University of Picardie Jules Verne11, University of Paris12, University of California, Los Angeles13
TL;DR: Cinacalcet lowers parathyroid hormone levels and improves calcium-phosphorus homeostasis in patients receiving hemodialysis who have uncontrolled secondary hyperparathyroidism.
Abstract: BACKGROUND: Treatment of secondary hyperparathyroidism with vitamin D and calcium in patients receiving dialysis is often complicated by hypercalcemia and hyperphosphatemia, which may contribute to cardiovascular disease and adverse clinical outcomes. Calcimimetics target the calcium-sensing receptor and lower parathyroid hormone levels without increasing calcium and phosphorus levels. We report the results of two identical randomized, double-blind, placebo-controlled trials evaluating the safety and effectiveness of the calcimimetic agent cinacalcet hydrochloride. METHODS: Patients who were receiving hemodialysis and who had inadequately controlled secondary hyperparathyroidism despite standard treatment were randomly assigned to receive cinacalcet (371 patients) or placebo (370 patients) for 26 weeks. Once-daily doses were increased from 30 mg to 180 mg to achieve intact parathyroid hormone levels of 250 pg per milliliter or less. The primary end point was the percentage of patients with values in this range during a 14-week efficacy-assessment phase. RESULTS: Forty-three percent of the cinacalcet group reached the primary end point, as compared with 5 percent of the placebo group (P<0.001). Overall, mean parathyroid hormone values decreased 43 percent in those receiving cinacalcet but increased 9 percent in the placebo group (P<0.001). The serum calcium-phosphorus product declined by 15 percent in the cinacalcet group and remained unchanged in the placebo group (P<0.001). Cinacalcet effectively reduced parathyroid hormone levels independently of disease severity or changes in vitamin D sterol dose. CONCLUSIONS: Cinacalcet lowers parathyroid hormone levels and improves calcium-phosphorus homeostasis in patients receiving hemodialysis who have uncontrolled secondary hyperparathyroidism.
1,016 citations