Decreased parathyroid hormone secretion in chronic hemodialysis patients without active vitamin D treatment

1991 ◽  
Vol 9 (3) ◽  
pp. 45-48
Author(s):  
Masashi Suzuki ◽  
Yoshihei Hirasawa ◽  
Kidney Center ◽  
Shinrakuen Hospital
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Hemodialysis Patients ◽  
Chronic Hemodialysis ◽  
Active Vitamin ◽  
Active Vitamin D

scholarly journals A Pilot Study of Active Vitamin D Administration and Insulin Resistance in African American Patients Undergoing Chronic Hemodialysis

2013 ◽  
Vol 23 (3) ◽  
pp. 185-193 ◽  
Author(s):  
Adriana M. Hung ◽  
Mary B. Sundell ◽  
Natalia E. Plotnikova ◽  
Aihua Bian ◽  
Ayumi Shintani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
African American ◽  
Pilot Study ◽  
Chronic Hemodialysis ◽  
Active Vitamin ◽  
Active Vitamin D

Calcium homeostasis

2015 ◽  
Author(s):  
Francesco Trepiccione ◽  
Giovambattista Capasso
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Calcium Homeostasis ◽  
Calcineurin Inhibitors ◽  
Blood Levels ◽  
Active Vitamin ◽  
Active Vitamin D

Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.

The Effect of Active Vitamin D Administration on Muscle Mass in Hemodialysis Patients

2013 ◽  
Vol 33 (11) ◽  
pp. 837-846 ◽  
Author(s):  
Atsushi Mori ◽  
Tomoya Nishino ◽  
Yoko Obata ◽  
Masayuki Nakazawa ◽  
Misaki Hirose ◽  
...  
Keyword(s):  
Vitamin D ◽  
Muscle Mass ◽  
Hemodialysis Patients ◽  
Active Vitamin ◽  
Active Vitamin D

scholarly journals The risk of medically uncontrolled secondary hyperparathyroidism depends on parathyroid hormone levels at haemodialysis initiation

2020 ◽  
Vol 36 (1) ◽  
pp. 160-169
Author(s):  
Nahid Tabibzadeh ◽  
Angelo Karaboyas ◽  
Bruce M Robinson ◽  
Philipp A Csomor ◽  
David M Spiegel ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Patient Characteristics ◽  
Risk Difference ◽  
First Year ◽  
Active Vitamin ◽  
Adjusted Risk ◽  
Active Vitamin D ◽  
Dialysis Outcomes

Abstract Background Optimal parathyroid hormone (PTH) control during non-dialysis chronic kidney disease (ND-CKD) might decrease the subsequent risk of parathyroid hyperplasia and uncontrolled secondary hyperparathyroidism (SHPT) on dialysis. However, the evidence for recommending PTH targets and therapeutic strategies is weak for ND-CKD. We evaluated the patient characteristics, treatment patterns and PTH control over the first year of haemodialysis (HD) by PTH prior to HD initiation. Methods We studied 5683 incident HD patients from 21 countries in Dialysis Outcomes and Practice Patterns Study Phases 4–6 (2009–18). We stratified by PTH measured immediately prior to HD initiation and reported the monthly prescription prevalence of active vitamin D and calcimimetics over the first year of HD and risk of PTH >600 pg/mL after 9–12 months on HD. Results The 16% of patients with PTH >600 pg/mL prior to HD initiation were more likely to be prescribed active vitamin D and calcimimetics during the first year of HD. The prevalence of PTH >600 pg/mL 9–12 months after start of HD was greater for patients who initiated HD with PTH >600 (29%) versus 150–300 (7%) pg/mL (adjusted risk difference: 19%; 95% confidence interval : 15%, 23%). The patients with sustained PTH >600 pg/mL after 9–12 months on HD were younger, more likely to be black, and had higher serum phosphorus and estimated glomerular filtration rates at HD initiation. Conclusions Increased PTH before HD start predicted a higher PTH level 9–12 months later, despite greater use of active vitamin D and calcimimetics. More targeted PTH control during ND-CKD may influence outcomes during HD, raising the need for PTH target guidelines in these patients.

scholarly journals Leukaemic Secretion of Calcitriol: A Novel Mechanism of Hypercalcaemia in AML

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5098-5098
Author(s):  
Joshua Misha Lewis Casan ◽  
Sarah Ghotb ◽  
Sue Morgan ◽  
Stephen B Ting
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Rare Complication ◽  
Kidney Injury ◽  
Active Vitamin ◽  
Normal Range ◽  
Lymphoid Malignancies ◽  
Active Vitamin D ◽  
Upper Limit

Abstract Introduction: Whilst relatively common in lymphoid malignancies, hypercalcaemia is an extremely rare complication of acute myeloid leukaemia (AML). Previous case reports have described ectopic parathyroid hormone secretion, leukaemic bony invasion and the release of boneresorptivemediators as causes of hypercalcaemia in AML (GewirtzAM et al. Br JHaematology1983;31(12):1590,ZidarBL, et al.NEJM.1976;295:692). We describe a case of severe hypercalcaemia with acute kidney injury (AKI) accompanying a new diagnosis of AML, subsequently demonstrated to be secondary to leukaemic blast production of active vitamin D (calcitriol) with gross over-expression of vitamin D related genes. This represents a novel pathogenic mechanism causing hypercalcaemia in a myeloid malignancy. Case Report: AA, a 68 year old male presenting with fatigue and found to have circulating blasts was subsequently diagnosed with acutemyelomonocyticleukaemia(78% blasts on bone marrow biopsy). Additionally, he had marked hypercalcaemia (calcium 3.3mmol/L, normal range 2.1-2.6mmol/L) and AKI (creatinine 263umol/L, normal range 60-110umol/L). Given the rarity of AML-associated hypercalcaemia, extensive investigations were undertaken to elucidate the cause. In search of a second concurrent malignancy, AA underwent computed tomography and positron emission tomography scanning, with subsequent biopsy of FDG avid vocal cord nodules; but only benign pathology could be demonstrated. Parathyroid hormone (PTH) levels were appropriately suppressed (0.9pmol/L, normal range 1.6-6.9pmol/L) and levels of PTH-related peptide and serum ACE were normal (<2pmol/L, and 37units/L, normal range 20-70units/L, respectively). Inactive vitamin D, (calcidiol or 25(OH)D3) levels were also normal (88nmol/L, normal range 50-250nmol/L). However, the active vitamin D (calcitriol or 1,25(OH)2D3) level was grossly elevated beyond the upper limit of assay (>500pmol/L, upper limit of normal: 190pmol/L). Both the hypercalcaemia and kidney injury proved refractory to multiple therapeutic strategies including aggressive hydration with an average of over 2.5L of crystalloid per day, as well as intravenouspamidronate. However, as depicted in Figure 1, there was a precipitous response following the initiation of chemotherapy (idarubicinandcytarabine, 7+3 regimen). Within several days, AA's serum calcium levels returned to normal levels, and his kidney function followed a similar pattern of improvement shortly thereafter. The rapid resolution of serum calcium levels also mirrored peripheral blast clearance, and repeat testing of calcitriol levels showed progressive improvement towards a normal concentration. AA achieved complete remission following induction chemotherapy and remains leukaemia free after consolidation chemotherapy and current maintenanceazacitidine. His hypercalcaemia has not recurred and his renal function remains normal. Having excluded other causes of hypercalcaemia and given the dramatic response to chemotherapy, we hypothesised that AA's AML blasts were secreting calcitriol. Accordingly, quantitative PCR was performed on AA's stored leukaemic cells for genes essential to vitamin D metabolism: the vitamin-D receptor (VDR), CYP24A1, and CYP27B1 (1-α-hydroxylase). RNA was extracted from AML cells using the QIAGEN RNeasykit. cDNAwas synthesised from 400ng of RNA using the Roche First Strand cDNASynthesis Kit. Gene expression was assessed by quantitative real-time PCR, relative to the housekeeping gene GAPDH. AA's leukaemia cells demonstrated markedly elevated expression of these vitamin-D related genes compared to healthy control CD34+ cells and four other independent primary AML cells (Figure 2, labelled AML 1-4), which were selected for absence of patient hypercalcaemia from our institution's tissue bank (Figure 2). Conclusion: Hypercalcaemia secondary to secretion of calcitriol can be a manifestation of lymphoid malignancies, however our case is the first documented occurrence of this phenomenon in a myeloid cancer. The PCR studies demonstrated striking overexpression of vitamin D related genes in leukaemia cells, resulting in the patient's hypercalcaemia and AKI. This finding represents a novel mechanism for a rare complication in AML. Figure 1 Figure 1. Figure 2 Figure 2. Disclosures No relevant conflicts of interest to declare.

MO796IMPACT OF ACTIVE VITAMIN D AND CALCIUM PREPARATION ON VASCULAR CALCIFICATION MARKERS IN HEMODIALYSIS PATIENTS WITH HYPOCALCEMIA INDUCED BY CALCIMIMETICS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Yusaku Hashimoto ◽  
Sawako Kato ◽  
Masato Tsuboi ◽  
Makoto Kuro-o ◽  
Yachiyo Kuwatsuka ◽  
...  
Keyword(s):  
Vitamin D ◽  
Treatment Group ◽  
Vascular Calcification ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Hemodialysis Patients ◽  
Active Vitamin ◽  
Oral Calcium ◽  
Active Vitamin D ◽  
Time Point

Abstract Background and Aims Recently, we demonstrated the efficacy of etelcalcetide for control of secondary hyperparathyroidism (SHPT) in the DUET trial; a 12-week multicenter, open-label, randomized (1:1:1), parallel-group study treated with etelcalcetide + active vitamin D (Group E+D), etelcalcetide + oral calcium preparation (Group E+Ca), or control groups (Group C) in 124 subjects undergoing maintenance hemodialysis. Moreover, we also showed that active vitamin D was useful in correcting hypocalcemia induced by calcimimetics, but the oral calcium preparation was superior for suppression of hyperphosphatemia. In this post hoc analysis, we evaluated vascular calcification markers, fibroblast growth factor 23 (FGF23) and calciprotein particles (CPPs), in patients using etelcalcetide (n = 77) extracted from the registrants of the DUET trial. Method Serum levels of FGF23 and CPPs were measured at baseline, 6 weeks and 12 weeks after start of the trial. Skewed data (FGF23 and CPPs) were transformed to natural logarithm to achieve normal distribution prior to statistical analysis. The changes in log CPPs and log FGF23 were estimated in a linear mixed model with each treatment group, time point, and interaction of the treatment group and time point as the fixed effects. We compared these changes between treatment the groups using a linear mixed model and also the Tukey-Kramer method to correct for multiplicity. Additionally, we exploratory examined the correlations among changes of FGF23, CPPs and other biomarkers related to bone mineral metabolisms, iPTH, Ca, P, and calcium-phosphate product, tested by Spearman’s rank correlation coefficient. Results The decreases at the 12-week time point after the trial start in log FGF23 were estimated -1.13 pg/mL in Group E+Ca and -0.10 pg/mL in Group E+D in a linear mixed model, respectively. Similarly, the decreases in CPPs were estimated -1.60 AU in Group E+Ca and -0.82 AU in Group E+D, respectively. Changes of both FGF23 (P = 0.017) and CPPs (P &lt; 0.001) in Group E+Ca significantly decreased compared with those in in Group E+D by Tukey-Kramer multiple-comparison test at 12 weeks after the trial start, while both changes in CPPs and FGF23 could not reach the significant differences between two groups at 6 weeks after the trial start (Figure 1). Reductions in FGF23 positively correlated with reductions in calcium (ρ = 0.42, P &lt; 0.01) and phosphate (ρ = 0.48, P &lt; 0.01) at 6 weeks after the trial start, and in calcium (ρ = 0.30, P &lt; 0.01) and phosphate (ρ =0.70, P &lt; 0.01) at 12 weeks after 6 weeks of the trial start), but there was no correlation with reductions in iPTH at any time point. Reductions in CPPs positively correlated with reductions only in phosphate at 6 weeks after the trial start (ρ = 0.47, P &lt; 0.01) and at 12 weeks after 6 weeks of the trial start (ρ = 0.54, P &lt; 0.01). Conclusion In this analysis, vascular calcification markers were significantly decreased in Group E+Ca compared to those in Group E+D. Further studies should be needed, our study suggests that oral calcium preparation may have an advantage against vascular calcification rather than active vitamin D for the correction of hypocalcemia induced by etelcalcetide in hemodialysis patients with SHPT.

scholarly journals Oral active vitamin D is associated with improved survival in hemodialysis patients

2008 ◽  
Vol 74 (8) ◽  
pp. 1070-1078 ◽  
Author(s):  
Manuel Naves-Díaz ◽  
Daniel Álvarez-Hernández ◽  
Jutta Passlick-Deetjen ◽  
Adrian Guinsburg ◽  
Cristina Marelli ◽  
...  
Keyword(s):  
Vitamin D ◽  
Hemodialysis Patients ◽  
Active Vitamin ◽  
Active Vitamin D
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