{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T02:57:40Z","timestamp":1780541860976,"version":"3.54.1"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"S2","license":[{"start":{"date-parts":[[2007,12,1]],"date-time":"2007-12-01T00:00:00Z","timestamp":1196467200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Chronic kidney disease (CKD) has been recognized as a significant public health problem, with \u223c20 million Americans, or \u223c11% of the adult population, currently living with CKD. A significant source of morbidity associated with CKD is the development of disturbances of mineral metabolism, which occurs in virtually all patients during the progression of their disease, and is associated with bone loss and fractures, cardiovascular disease, immune suppression, and increased mortality. As kidney disease develops, there is decreased functional renal mass and a tendency to retain phosphorus. The reduction in functional renal mass and the retained phosphorus act to reduce renal 1\u03b1-hydroxylase activity and thus the renal production of calcitriol. Further compensation to maintain normal serum calcium and phosphorus homeostasis includes increased production and release of PTH and potentially other phosphaturic factors, such as fibroblast growth factor-23 (FGF23). This increase in FGF23 contributes to maintain normal serum phosphate independent of PTH but may worsen calcitriol deficiency by also inhibiting renal 1\u03b1-hydroxylase activity. The decrease in calcitriol also results in promoting further hyperparathyroidism and parathyroid gland hyperplasia, because calcitriol normally inhibits the production of prepro-PTH and parathyroid cell proliferation.<\/jats:p>","DOI":"10.1359\/jbmr.07s203","type":"journal-article","created":{"date-parts":[[2008,2,21]],"date-time":"2008-02-21T15:02:25Z","timestamp":1203606145000},"page":"V91-V94","source":"Crossref","is-referenced-by-count":25,"title":["Role of Vitamin D Deficiency in Chronic Kidney Disease"],"prefix":"10.1093","volume":"22","author":[{"given":"Anca","family":"Gal-Moscovici","sequence":"first","affiliation":[{"name":"Hadassah Hospital Medical Center, Hebrew University, Ein Keren, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart M","family":"Sprague","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Evanston Northwestern Healthcare, Northwestern University Feinberg School of Medicine, Evanston, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,12,4]]},"reference":[{"key":"2024020319230925300_bib1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1053\/ajkd.2003.50007","article-title":"Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey","volume":"41","author":"Coresh","year":"2003","journal-title":"Am J Kidney Dis"},{"key":"2024020319230925300_bib2","author":"U.S. Renal Data System","year":"2003"},{"key":"2024020319230925300_bib3","author":"U.S. Renal Data System","year":"2005"},{"key":"2024020319230925300_bib4","doi-asserted-by":"crossref","first-page":"876","DOI":"10.1210\/jcem-67-5-876","article-title":"Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure","volume":"67","author":"Pitts","year":"1988","journal-title":"J Clin Endocrinol Metab"},{"key":"2024020319230925300_bib5","doi-asserted-by":"crossref","first-page":"162","DOI":"10.1093\/ndt\/6.3.162","article-title":"Calcium metabolism in early chronic renal failure: Implications for the pathogenesis of hyperparathyroidism","volume":"6","author":"Reichel","year":"1991","journal-title":"Nephrol Dial Transplant"},{"key":"2024020319230925300_bib6","doi-asserted-by":"crossref","first-page":"2205","DOI":"10.1681\/ASN.2005010052","article-title":"Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease","volume":"16","author":"Gutierrez","year":"2005","journal-title":"J Am Soc Nephrol"},{"key":"2024020319230925300_bib7","doi-asserted-by":"crossref","first-page":"1580","DOI":"10.1172\/JCI111365","article-title":"Effect of dietary phosphorus on circulating concentrations of 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone in children with moderate renal insufficiency","volume":"73","author":"Portale","year":"1984","journal-title":"J Clin Invest"},{"key":"2024020319230925300_bib8","doi-asserted-by":"crossref","first-page":"135","DOI":"10.1172\/JCI110586","article-title":"Metabolic acidosis suppresses 25-hydroxyvitamin in D3-1alpha-hydroxylase in the rat kidney. 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