scholarly journals Modified-Release Calcifediol Effectively Controls Secondary Hyperparathyroidism Associated with Vitamin D Insufficiency in Chronic Kidney Disease

2014 ◽  
Vol 40 (6) ◽  
pp. 535-545 ◽  
Author(s):  
Stuart M. Sprague ◽  
Arnold L. Silva ◽  
Fahd Al-Saghir ◽  
Radhika Damle ◽  
Samir P. Tabash ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Insufficiency ◽  
Modified Release

Use of Extended-Release Calcifediol to Treat Secondary Hyperparathyroidism in Stages 3 and 4 Chronic Kidney Disease

2016 ◽  
Vol 44 (4) ◽  
pp. 316-325 ◽  
Author(s):  
Stuart M. Sprague ◽  
Paul W. Crawford ◽  
Joel Z. Melnick ◽  
Stephen A. Strugnell ◽  
Shaukat Ali ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Extended Release ◽  
Vitamin D Insufficiency ◽  
Double Blind ◽  
Hydroxyvitamin D ◽  
Ckd Stage ◽  
25 Hydroxyvitamin D

Background/Aims: Vitamin D insufficiency and secondary hyperparathyroidism (SHPT) are associated with increased morbidity and mortality in chronic kidney disease (CKD) and are poorly addressed by current treatments. The present clinical studies evaluated extended-release (ER) calcifediol, a novel vitamin D prohormone repletion therapy designed to gradually correct low serum total 25-hydroxyvitamin D, improve SHPT control and minimize the induction of CYP24A1 and FGF23. Methods: Two identical multicenter, randomized, double-blind, placebo-controlled studies enrolled subjects from 89 US sites. A total of 429 subjects, balanced between studies, with stage 3 or 4 CKD, SHPT and vitamin D insufficiency were randomized 2:1 to receive oral ER calcifediol (30 or 60 µg) or placebo once daily at bedtime for 26 weeks. Most subjects (354 or 83%) completed dosing, and 298 (69%) entered a subsequent open-label extension study wherein ER calcifediol was administered without interruption for another 26 weeks. Results: ER calcifediol normalized serum total 25-hydroxyvitamin D concentrations (>30 ng/ml) in >95% of per-protocol subjects and reduced plasma intact parathyroid hormone (iPTH) by at least 10% in 72%. The proportion of subjects receiving ER calcifediol who achieved iPTH reductions of ≥30% increased progressively with treatment duration, reaching 22, 40 and 50% at 12, 26 and 52 weeks, respectively. iPTH lowering with ER calcifediol was independent of CKD stage and significantly greater than with placebo. ER calcifediol had inconsequential impact on serum calcium, phosphorus, FGF23 and adverse events. Conclusion: Oral ER calcifediol is safe and effective in treating SHPT and vitamin D insufficiency in CKD.

scholarly journals Vitamin D insufficiency and deficiency with stages of chronic kidney disease in an Asian population

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
Bancha Satirapoj ◽  
Pokkrong Limwannata ◽  
Amnart Chaiprasert ◽  
Ouppatham Supasyndh ◽  
Panbuppa Choovichian
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Asian Population ◽  
Vitamin D Insufficiency

Prevalence of 25(OH) vitamin D insufficiency and deficiency in chronic kidney disease stage 5 patients on hemodialysis

2007 ◽  
Vol 11 (3) ◽  
pp. 315-321 ◽  
Author(s):  
Elisa DEL VALLE ◽  
Armando L. NEGRI ◽  
Cristina AGUIRRE ◽  
Erich FRADINGER ◽  
Jose R. ZANCHETTA
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Chronic Kidney Disease Stage ◽  
Vitamin D Insufficiency ◽  
Disease Stage ◽  
25 Oh Vitamin D

scholarly journals P0898VITAMIN C STATUS MODIFIES PARATHYROID HORMONE SECRETION IN NON-DIALYZED CHRONIC KIDNEY DISEASE PATIENTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Ryuta Fujimura ◽  
SHOGO SHIBATA ◽  
Takechiyo Tokuda ◽  
Ayako Tanaka ◽  
Aya Mizumoto ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Vitamin C ◽  
Secondary Hyperparathyroidism ◽  
Hormone Secretion ◽  
Serum Vitamin ◽  
Serum Phosphate ◽  
Vitamin C Deficiency

Abstract Background and Aims Among patients with chronic kidney disease (CKD) at predialysis stage, there is a high incidence of secondary hyperparathyroidism. Metabolic changes associated with secondary hyperparathyroidism lead to renal osteodystrophy, including osteitis fibrosa, ectopic calcification, cardiovascular disease, and the risk of death, and serum parathyroid hormone levels are influenced by nutritional variables. Non-dialyzed CKD patients are especially prone to vitamin C deficiency because of dietary restrictions and malnutrition. Vitamin C is an important antioxidant and relates to the development and maintenance of bone tissues. However, the contribution of vitamin C deficiency to parathyroid hormone secretion is unknown. Here, we performed a single-center cross-sectional study in order to assess association of serum vitamin C and parathyroid hormone in non-dialyzed CKD patients. Method We had 280 consecutive patients who underwent serum vitamin C and serum intact parathyroid hormone (iPTH) measurement for screening purposes from January 1st, 2013 to November 30th, 2017. We analysed a total of 128 patients (71.3±11.6 year-old, 80 males) who had an estimated glomerular filtration rate (eGFR) that remained less than 60 mL/min/1.73m2 after 152 patients were excluded because of vitamin C or vitamin D supplementation, age <20 years, dialysis, positive serostatus for HIV, hepatitis B or hepatitis C, chronic infection, or cancer. Results Twenty-three percent of the patients (n=29) had vitamin C levels< 2.0 μg/mL (a range seen in very deficient subjects), 53% (n=68) had levels between 2.0 and 5.5 μg/mL, and 31 patients (24%) had vitamin C levels >5.5 μg/mL, which is considered the upper limit of normal for the healthy population. Log(iPTH) significantly correlated with age (r=-0.238, p=0.00672), log(eGFR) (r=-0.625, p<0.0001), serum calcium (r=-0.609, p<0.0001), and serum phosphate (r=0.41, p<0.0001), and had a tendency to correlate with serum albumin (r=-0.146, p=0.101). Low serum vitamin C was associated with higher serum iPTH (P=0.0005, one-way analysis of variance). In a multiple linear regression model with log(iPTH) as the dependent variable, and age, gender, log(eGFR), serum levels of calcium, phosphate, albumin, and vitamin C as independent variables, the inverse relationship of log(iPTH) and serum vitamin C was confirmed (R2 = 0.568, adjusted R2 = 0.543, P<0.0001), along with other parameters influencing iPTH levels, including age, log(eGFR), serum calcium, and serum phosphate. Low vitamin C levels were also associated with increased serum alkaline phosphatase (r=-0.209, p=0.0179), a further indicator of the impact of vitamin C status on bone metabolism. Conclusion Vitamin C deficiency is prevalent in a significant proportion of non-dialyzed CKD patients. Low vitamin C levels contribute to secondary hyperparathyroidism, leading to increased bone turnover. This novel observation may result from effects of vitamin C on vitamin D metabolism, vitamin D binding in target tissues, and cAMP-linked signalling pathways in bone and parathyroid gland. Therapeutic intervention with supplemental vitamin C for secondary hyperparathyroidism might be a good strategy.

scholarly journals Secondary and tertiary hyperparathyroidism in chronic kidney disease

2017 ◽  
Vol 20 (2) ◽  
pp. 63-68 ◽  
Author(s):  
Lilit V. Egshatyan ◽  
Natalya G. Mokrisheva ◽  
Lyudmila Ya. Rozhinskaya
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Medical Therapy ◽  
Receptor Activation ◽  
Mineral Density ◽  
Tertiary Hyperparathyroidism ◽  
End Stage

In the treatment of secondary hyperparathyroidism of end-stage chronic kidney disease, vitamin D receptor activation and allosteric modulators of the calcium-sensing receptor – inhibit glandular hyperplasia, reduce parathyroid hormone levels, impact on bone turnover and mineral density. But the use of calcimimetic and vitamin D analogs or mimetics did not reduce the need for parathyroidectomy for refractory hyperparathyroidism. The enlarged parathyroid gland and gland nodular transformation became refractory to medical therapy and patient need for parathyroidectomy. Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone after a long period of secondary hyperparathyroidism and renal transplantation. In this article, we present the case of a Caucasian male with chronic kidney disease (end-stage on chronic hemodialysis and after kidney transplantation) and different forms of hyperparathyroidism (secondary and tertiary). Our case study shows that only a multi-interventional strategy is likely to be more effective treatment in cases of severe and refractory to medical therapy hyperparathyroidism.

scholarly journals Insulin Resistance and Vitamin D Deficiency in Patients With Chronic Kidney Disease Stage 2-3

2011 ◽  
pp. 149-155 ◽  
Author(s):  
K. ŠTEFÍKOVÁ ◽  
V. SPUSTOVÁ ◽  
Z. KRIVOŠÍKOVÁ ◽  
A. OKŠA ◽  
K. GAZDÍKOVÁ ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Insulin Sensitivity ◽  
Kidney Disease ◽  
Vitamin D Deficiency ◽  
Chronic Kidney Disease Stage ◽  
Vitamin D Insufficiency ◽  
Disease Stage ◽  
25 Oh Vitamin D

Vitamin D status and the relationship between serum 25(OH) vitamin D concentrations and the components of insulin resistance were examined in 120 patients with chronic kidney disease stage 2 and 3. Insulin sensitivity/resistance was calculated by the quantitative insulin sensitivity check index (QUICKI). In this analysis, the prevalence of insulin resistance was 42 %. Only 17 % of patients had serum 25(OH) vitamin D concentration in the recommended range (≥30 ng/ml), 42 % suffered from vitamin D insufficiency and 41 % had moderate vitamin D deficiency. Insulin resistance significantly correlated with serum 25(OH)D and 1,25(OH)2D concentrations, renal function and protein excretion rate. Our results support the increasing evidence that vitamin D deficiency may be one of the factors participating in the development of insulin resistance already in the early stages of chronic kidney disease.

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