Medical emergencies encountered in dental clinics: A study from the Eastern Province of Saudi Arabia.

Objectives: To report the prevalence of medical emergencies in dental clinics and self-perceived competence of dentists in the Eastern Province of Kingdom of Saudi Arabia (KSA).

Materials And Methods: In this cross-sectional study, a self administered questionnaire was distributed to a random sample of 198 dentists working in private and government dental clinics in the Eastern Province of KSA. The respondents were approached twice to ensure good participation in the study.

Activation of FGF-23 mediated vitamin D degradative pathways by cholecalciferol.

Context: The optimal circulating concentration of 25(OH) vitamin D is controversial.

Objective: The aim was to investigate if FGF-23 and 24,25(OH)2D can guide cholecalciferol replacement.

Design: Oral cholecalciferol (10,000 IU weekly) administered to subjects with 25(OH)D levels < 20 ηg/mL and eGFR > 60 mL/min/1.

Chronic kidney disease and diabetes mellitus predict resistance to vitamin D replacement therapy.

Background: 25-Hydroxyvitamin D [25(OH)D] is a marker of nutritional status; however, chronic kidney disease (CKD) results in alterations in vitamin D metabolism, including the loss of vitamin D-binding proteins and alterations in CYP27B1 and CYP24 enzymes that metabolize 25(OH)D. This study was designed to determine the predictors of responsiveness to correction of vitamin D deficiency with oral vitamin D2 (ergocalciferol) in adults.

Methods: A retrospective study of 183 veterans with 25(OH)D level <30 ng/mL, who were treated with 50,000 IU per week of vitamin D2, was performed.

CKD-mineral and bone disorder management in kidney transplant recipients.

Kidney transplantation, the most effective treatment for the metabolic abnormalities of chronic kidney disease (CKD), only partially corrects CKD-mineral and bone disorders. Posttransplantation bone disease, one of the major complications of kidney transplantation, is characterized by accelerated loss of bone mineral density and increased risk of fractures and osteonecrosis. The pathogenesis of posttransplantation bone disease is multifactorial and includes the persistent manifestations of pretransplantation CKD-mineral and bone disorder, peritransplantation changes in the fibroblast growth factor 23-parathyroid hormone-vitamin D axis, metabolic perturbations such as persistent hypophosphatemia and hypercalcemia, and the effects of immunosuppressive therapies.

Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites.

Progressive elevations of fibroblastic growth factor 23 (FGF23) in chronic kidney disease may reduce serum 25-hydroxyvitamin D (25(OH)) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels, via stimulation of 24-hydroxylase (Cyp24a1)-mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)(2)D), a product of Cyp24a1 hydroxylation of 25(OH)D, in the Col4a3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)(2)D in the mouse model, but no significant relationship was observed in the cross-sectional patient cohort.