Abstract
Secondary hyperparathyroidism is an early complication of chronic kidney disease (CKD). Vitamin D deficiency and reduced synthesis of 1,25-dihydroxyvitamin D (calcitriol) early in the progression of CKD leads to abnormal mineral metabolism. Vitamin D deficiency leads to increased parathyroid hormone and remodeling of bone that releases calcium and phosphorus, resulting in vascular calcification. Vitamin D deficiency is associated with cardiovascular disease and contributes to the high morbidity and mortality in patients with CKD.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Arterial Occlusive Diseases / etiology
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Arterial Occlusive Diseases / pathology
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Calcinosis / etiology
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Calcinosis / pathology
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Calcitriol / physiology
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Calcitriol / therapeutic use
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Cardiovascular Diseases / etiology
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Causality
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Cinacalcet
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Disease Progression
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Drug Monitoring
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Ergocalciferols / therapeutic use
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Glomerular Filtration Rate
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Humans
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Hyperparathyroidism, Secondary* / diagnosis
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Hyperparathyroidism, Secondary* / etiology
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Hyperparathyroidism, Secondary* / therapy
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Hyperphosphatemia / etiology
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Hyperphosphatemia / prevention & control
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Kidney Failure, Chronic / complications*
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Kidney Failure, Chronic / mortality
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Naphthalenes / therapeutic use
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Nurse's Role
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Parathyroid Hormone / physiology
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Phosphorus, Dietary / adverse effects
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Proportional Hazards Models
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Severity of Illness Index
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Treatment Outcome
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Vitamin D / chemistry
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Vitamin D / physiology
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Vitamin D / therapeutic use*
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Vitamin D Deficiency* / diagnosis
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Vitamin D Deficiency* / etiology
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Vitamin D Deficiency* / therapy
Substances
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Ergocalciferols
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Naphthalenes
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Parathyroid Hormone
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Phosphorus, Dietary
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Vitamin D
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1 alpha-hydroxyergocalciferol
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Calcitriol
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Cinacalcet