Abstract
Deficiency of 25-hydroxyvitamin D (25[OH]D) is common in patients with chronic kidney disease stages 3 and 4 and is associated with poor outcomes. However, the evaluation and management of vitamin D deficiency in nephrology remains controversial. This article reports on the proceedings from a "controversies conference" on vitamin D in chronic kidney disease that was sponsored by the National Kidney Foundation. The report outlines the deliberations of the 3 work groups that participated in the conference. Until newer measurement methods are widely used, the panel agreed that clinicians should classify 25(OH)D "adequacy" as concentrations > 20ng/mL without evidence of counter-regulatory hormone activity (ie, elevated parathyroid hormone). The panel also agreed that 25(OH)D concentrations< 15ng/mL should be treated irrespective of parathyroid hormone level. Patients with 25(OH)D concentrations between 15 and 20ng/mL may not require treatment if there is no evidence of counter-regulatory hormone activity. The panel agreed that nutritional vitamin D (cholecalciferol, ergocalciferol, or calcifediol) should be supplemented before giving activated vitamin D compounds. The compounds need further study evaluating important outcomes that observational studies have linked to low 25(OH)D levels, such as progression to end-stage kidney disease, infections, fracture rates, hospitalizations, and all-cause mortality. We urge further research funding in this field.
Highlights
Studies confirm that the prevalence of 25(OH)D deficiency (Table 1) is greater in individuals with chronic kidney disease (CKD) than in the general population.[5,6] Levin et al[7] reported that in CKD stage 3, w20% of patients are found to have low 25(OH) D concentrations, whereas in CKD stages 4 and 5, >30% of patients are deficient
In an analysis of the National Health and Nutrition Examination Survey (NHANES), participants with estimated glomerular filtration rates of 15 to 29 mL/min/1.73 m2 had 25(OH) D concentrations that were 4.7 ng/mL lower than for participants with estimated glomerular filtration rates > 90 mL/min/1.73 m2.8 25(OH)D is hydroxylated to 1,25dihydroxyvitamin D (1,25[OH]2D), or calcitriol, the active form of vitamin D, by the 1α-hydroxylase enzyme found in the kidney and other tissues
Low 25(OH)D concentrations contribute to a deficiency of 1,25(OH)2D,9,10 driving an increase in parathyroid hormone (PTH) levels and the development of secondary hyperparathyroidism (SHPT).7 1,25(OH)2D assists in the regulation of mineral homeostasis by mobilizing calcium and phosphate through gastrointestinal absorption
Summary
KDIGO (Kidney Disease: Improving Global Outcomes) recently published an updated guideline concerning the diagnosis, evaluation, prevention, and treatment of chronic kidney disease (CKD)–mineral and bone disorders.[1]. The workshop was structured to allow faculty attendees to examine the current state of knowledge through targeted literature reviews presented to the group by invited speakers related to vitamin D physiology, evaluation, outcomes, and management associated with altered vitamin D metabolism in patients with reduced kidney function. This is a report on the extensive deliberations at the workshop, reviewing the highlights and recommendations. Each section includes a discussion overview and a list of recommended research questions
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