scholarly journals Control of hyperparathyroidism with the intravenous calcimimetic etelcalcetide in dialysis patients adherent and non-adherent to oral calcimimetics

2020 ◽  
Author(s):  
Maria Dolores Arenas ◽  
Cristian Rodelo-Haad ◽  
M Victoria Pendón-Ruiz de Mier ◽  
Mariano Rodriguez
Keyword(s):  
Parathyroid Hormone ◽  
Standard Deviation ◽  
Secondary Hyperparathyroidism ◽  
Serum Phosphate ◽  
Dialysis Patients ◽  
Serum Parathyroid Hormone ◽  
Apparent Lack ◽  
Serum Pth ◽  
And Control ◽  
Possible Cause

Abstract Background In dialysis patients, non-adherence to oral cinacalcet adds complexity to the control of secondary hyperparathyroidism. The present study aims to evaluate the use of intravenous calcimimetic, etelcalcetide, in the control of secondary hyperparathyroidism in patients adherent and non-adherent to oral calcimimetics. Method The Simplified Medication Adherence Questionnaire was used to identify non-adherence. Almost half of the patients were non-adherent to the treatment with cinacalcet. Twenty-five patients (15 non-adherent) were switched from cinacalcet to etelcalcetide and were followed-up monthly for 8 months. Results Cinacalcet was discontinued for 1 week before the initiation of etelcalcetide. After this period, the serum PTH levels increased by2-fold in adherent patients, whereas it did not change in non-adherent patients suggesting that they were not taking the medication. Etelcalcetide progressively reduced serum parathyroid hormone (PTH) (mean ± standard deviation) from 818 ± 395 to 367 ± 289 pg/mL (P < 0.001) in non-adherents, and from 496 ± 172 to 228 ± 111 pg/mL (P < 0.01) in adherent patients with a mean dose of 7.0 ± 2.3 and 5.1 ± 1.2 mg in non-adherent and in adherent patients, respectively. Etelcalcetide increased the percentage of patients with PTH on target from 28% to 58%. Patients with serum calcium <8.4 mg/dL increased from 8% to 40%, although they remained asymptomatic. The percent of patients with serum phosphate on target increased from 40% to 65%. Conclusion The lack of adherence to cinacalcet is a possible cause of the apparent lack of response to oral calcimimetic. The use of etelcalcetide ensures compliance and control of secondary hyperparathyroidism in both non-adherent and adherent patients.

Calcitriol therapy and calcium-regulated PTH secretion in patients with secondary hyperparathyroidism

1994 ◽  
Vol 267 (6) ◽  
pp. E961-E967 ◽  
Author(s):  
J. A. Ramirez ◽  
W. G. Goodman ◽  
T. R. Belin ◽  
B. Gales ◽  
G. V. Segre ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Dynamic Tests ◽  
Serum Parathyroid Hormone ◽  
Maximum Increase ◽  
Set Point ◽  
Parathyroid Function ◽  
Before And After ◽  
Intermittent Calcitriol ◽  
Serum Pth

Calcitriol lowers serum parathyroid hormone (PTH) levels in patients with secondary hyperparathyroidism, but its effect on calcium-regulated PTH release remains controversial. Thus 11 patients with secondary hyperparathyroidism underwent dynamic tests of parathyroid function before and after 4 mo of intermittent calcitriol therapy. Serum calcitriol levels rose from 8 +/- 1 to 55 +/- 9 (SE) pg/ml, P < 0.01, serum total and ionized calcium levels increased, and serum PTH levels decreased from 584 +/- 154 to 154 +/- 31 pg/ml, P < 0.05. The maximum increase in serum PTH during hypocalcemia did not differ before (248 +/- 78 pg/ml) or after (280 +/- 100 pg/ml) treatment, but the increase in PTH, expressed as a percentage of preinfusion values, was greater after treatment (329 +/- 73 vs. 132 +/- 10%, P < 0.05). The decreases in serum PTH during calcium infusions did not differ before (70 +/- 5%) or after (73 +/- 5%) therapy, and the set point for PTH release did not change (1.20 +/- 0.03 vs. 1.23 +/- 0.01 mmol/l, not significant). Calcitriol modifies PTH secretion during hypocalcemia in secondary hyperparathyroidism without affecting the set point for PTH release; although calcitriol lowers serum PTH levels, it may also restore the secretory reserve of hyperplastic parathyroid tissues during hypocalcemia.

scholarly journals Low serum parathyroid hormone is a risk factor for peritonitis episodes in incident peritoneal dialysis patients: a retrospective study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yuqi Yang ◽  
Jingjing Da ◽  
Yi Jiang ◽  
Jing Yuan ◽  
Yan Zha
Keyword(s):  
Risk Factor ◽  
Peritoneal Dialysis ◽  
Parathyroid Hormone ◽  
Proportional Hazard ◽  
Serum Parathyroid Hormone ◽  
Cox Proportional Hazard ◽  
Cox Proportional Hazard Regression ◽  
Gram Negative Organisms ◽  
Serum Pth

Abstract Background Serum parathyroid hormone (PTH) levels have been reported to be associated with infectious mortality in peritoneal dialysis (PD) patients. Peritonitis is the most common and fatal infectious complication, resulting in technique failure, hospital admission and mortality. Whether PTH is associated with peritonitis episodes remains unclear. Methods We examined the association of PTH levels and peritonitis incidence in a 7-year cohort of 270 incident PD patients who were maintained on dialysis between January 2012 and December 2018 using Cox proportional hazard regression analyses. Patients were categorized into three groups by serum PTH levels as follows: low-PTH group, PTH < 150 pg/mL; middle-PTH group, PTH 150-300 pg/mL; high-PTH group, PTH > 300 pg/mL. Results During a median follow-up of 29.5 (interquartile range 16–49) months, the incidence rate of peritonitis was 0.10 episodes per patient-year. Gram-positive organisms were the most common causative microorganisms (36.2%), and higher percentage of Gram-negative organisms was noted in patients with low PTH levels. Low PTH levels were associated with older age, higher eGFR, higher hemoglobin, calcium levels and lower phosphate, alkaline phosphatase levels. After multivariate adjustment, lower PTH levels were identified as an independent risk factor for peritonitis episodes [hazard ratio 1.643, 95% confidence interval 1.014–2.663, P = 0.044]. Conclusions Low PTH levels are independently associated with peritonitis in incident PD patients.

scholarly journals Effects of Orai3-Mediated Store-Operated Calcium Entry on Parathyroid Hormone Release in Secondary Hyperparathyroidism

2021 ◽  
Author(s):  
Zhangying Lin ◽  
Shuhao Wang ◽  
Yanxun Han ◽  
Junwei Zhu ◽  
Suwen Bai ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Tumor Development ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Common Complication ◽  
Store Operated Calcium Entry ◽  
Serum Pth ◽  
Parathyroid Hormone Release

Abstract Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease, is characterized by elevated parathyroid hormone (PTH) secretion and Hypocalcemia. Orai3 is a highly selective calcium (Ca2+) channel that plays important roles in tumor development, cardiovascular disease, and autoimmune diseases; however, its role in SHPT is unclear. In the present study, RNA sequencing and western blot assays were used to detect the expression levels of Orai3 in parathyroid tissue from patients with SHPT and from individuals without SHPT. Ca2+ imaging was used to detect the effect of Orai3 channels on Ca2+ signaling in parathyroid gland cells. Enzyme-linked immunosorbent assays were used to detect changes in PTH release. Orai3 knockout rats were used to detect the effect of decreased Orai3 expression on serum PTH levels. We found that the expression of Orai3 in parathyroid tissue obtained from patients with SHPT was significantly higher than that in patients without SHPT. Knockdown of Orai3 in parathyroid cells by transfection with Orai3-specific small inhibitor RNA inhibited store-operated Ca2+ entry (SOCE) in parathyroid cells. Inhibition of SOCE or knockdown of Orai3 significantly inhibited PTH release in parathyroid cells. PTH levels in the blood of Orai3 knockout rat were significantly reduced. Therefore, Orai3 expression and Orai3-mediated Ca2+ signaling may be a mechanism underlying PTH release, and Orai3 may play a role in the development of SHPT.

Seasonal levels of serum parathyroid hormone, calcitonin and alkaline phosphatase in relation to antler cycles in white-tailed deer

1984 ◽  
Vol 106 (2) ◽  
pp. 234-240 ◽  
Author(s):  
Chun Chin Chao ◽  
Robert D. Brown ◽  
Leonard J. Deftos
Keyword(s):  
Alkaline Phosphatase ◽  
Body Weight ◽  
Parathyroid Hormone ◽  
Feed Intake ◽  
Feed Consumption ◽  
Late Winter ◽  
Serum Parathyroid Hormone ◽  
Serum Samples ◽  
Antler Growth ◽  
Serum Pth

Abstract. Seasonal levels of serum parathyroid hormone (PTH), calcitonin (CT), and alkaline phosphatase (AP) were studied in relation to antler growth cycles in 8 male (2.5–6 years old) white-tailed deer. Feed consumption was recorded weekly, whereas body weight was recorded biweekly. Antler length was measured from the pedicle to the tip after velvet growth was initiated. Serum samples were obtained biweekly while animals were tranquilized with xylazine hydrochloride. Serum Ca was significantly (P < 0.05) elevated during the summer. Serum P was significantly (P < 0.05) elevated only during early fall. There was an increase in serum PTH during velvet initiation in April–May, but not thereafter. CT increased during the rapid antler growth period. Serum PTH levels were significantly (P < 0.05) elevated (0.628 vs 0.884 ng/ml) during post-velvet shedding and decreased (0.602 vs 0.346 ng/ml, P < 0.05) during postantler casting. Serum AP activity was highest during rapid velvet antler growth. Feed intake was lowest in early winter, but a compensatory increase was found in late winter. Feed intake peaked in May, then gradually decreased. Body weight was maximum in November and minimum in March. It is concluded that increased PTH during velvet initiation is responsible for Ca absorption and/or mobilization. Increasing PTH levels are related to final mineralization of antlers post-velvet shedding. Higher levels of serum Ca in June–July inhibit continued increase in PTH. Increased CT during rapid antler growth may have prevented excessive bone resorption.

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 &lt;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&lt; 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 &gt;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&lt;0.0001), serum calcium (r=-0.609, p&lt;0.0001), and serum phosphate (r=0.41, p&lt;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&lt;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 Effect of Etelcalcetide vs Cinacalcet on Serum Parathyroid Hormone in Patients Receiving Hemodialysis With Secondary Hyperparathyroidism

JAMA ◽  
2017 ◽  
Vol 317 (2) ◽  
pp. 156 ◽  
Author(s):  
Geoffrey A. Block ◽  
David A. Bushinsky ◽  
Sunfa Cheng ◽  
John Cunningham ◽  
Bastian Dehmel ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Serum Parathyroid Hormone

Altered parathyroid set point to calcium in familial hypocalciuric hypercalcaemia

1984 ◽  
Vol 106 (2) ◽  
pp. 215-218 ◽  
Author(s):  
J. Auwerx ◽  
M. Demedts ◽  
R. Bouillon
Keyword(s):  
Parathyroid Hormone ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Linear Relationship ◽  
Calcium Concentration ◽  
Disodium Edta ◽  
Serum Parathyroid Hormone ◽  
Set Point ◽  
Serum Pth ◽  
The Right

Abstract. Changes in calcium concentration were induced by an infusion of disodium-EDTA or calcium in 2 members of a family suffering from hypocalciuric hypercalcaemia (FHH) associated with interstitial lung disease. These changes in calcium demonstrated an inverse linear relationship with the changes in serum parathyroid hormone (PTH). Infusion of EDTA in control subjects and in patients with an adenoma or hyperplasia of the parathyroid glands also showed inverse relationships between calcium and PTH. The correlation between serum calcium and serum PTH was significant over the range observed during the induced hypo- and/or hypercalcaemia in controls and in patients with FHH or adenoma. The regressions were, however, shifted relative to each other: in comparison with controls, the FHH was displaced upwards and to the right, although not as far as the adenomas. These findings suggest the existence of an elevated set point for extracellular calcium (or calciostat) in FHH.

Skeletal Resistance to Endogenous Parathyroid Hormone in Patients with Early Renal Failure. A Possible Cause for Secondary Hyperparathyroidism

1975 ◽  
Vol 41 (2) ◽  
pp. 339-345 ◽  
Author(s):  
FRANCISCO LLACH ◽  
SHAUL G. MASSRY ◽  
FREDERICK R. SINGER ◽  
KIYOSHI KUROKAWA ◽  
JERRY H. KAYE ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Skeletal Resistance ◽  
Possible Cause

Demonstration of a Diurnal Variation in Serum Parathyroid Hormone in Primary and Secondary Hyperparathyroidism

1975 ◽  
Vol 41 (6) ◽  
pp. 1009-1013 ◽  
Author(s):  
TUSHAR K. SINHA ◽  
SARAH MILLER ◽  
JOHN FLEMING ◽  
RASHID KHAIRI ◽  
JAMES EDMONDSON ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Diurnal Variation ◽  
Serum Parathyroid Hormone
Sign in / Sign up

Export Citation Format

Share Document