Abnormal Regulation of Parathyroid Hormone Release by Calcium in Secondary Hyperparathyroidism due to Chronic Renal Failure*

1982 ◽  
Vol 54 (1) ◽  
pp. 172-179 ◽  
Author(s):  
EDWARD M. BROWN ◽  
RICHARD E. WILSON ◽  
RICHARD C. EASTMAN ◽  
JOHANNA PALLOTTA ◽  
SAMUEL P. MARYNICK
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Secondary Hyperparathyroidism ◽  
Hormone Release ◽  
Parathyroid Hormone Release

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.

scholarly journals Calcium-regulated parathyroid hormone release in patients with mild or advanced secondary hyperparathyroidism

1995 ◽  
Vol 48 (5) ◽  
pp. 1553-1558 ◽  
Author(s):  
William G. Goodman ◽  
Tom Belin ◽  
Barbara Gales ◽  
Harald Juppner ◽  
Gino V. Segre ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Hormone Release ◽  
Parathyroid Hormone Release

scholarly journals Study of prevalence of secondary hyperparathyroidism in chronic renal failure in hadoti region

2019 ◽  
Vol 7 (8) ◽  
pp. 2903
Author(s):  
Chiranjee Lal Dayma ◽  
Devendra Ajmera ◽  
Shiv Charan Jelia ◽  
Pankaj Jain
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Secondary Hyperparathyroidism ◽  
Serum Calcium ◽  
Calcium Level ◽  
Serum Calcium Level ◽  
Hormone Level ◽  
Serum Parathyroid Hormone ◽  
The Difference

Background: Secondary hyperparathyroidism is known and early complication of chronic renal failure patients. Aim of this study was to assess the prevalence of secondary hyperparathyroidism and correlation between serum parathyroid hormone level with biochemical parameters in renal failure patients in tertiary care hospital in Kota, Rajasthan.Methods: A cross sectional observational study was carried out in 50 patients who had creatinine clearance of 30ml/min/1.73m2 or less for greater than 6 weeks attended the OPD of department of General Medicine, New Medical College hospital, Kota, Rajasthan from May 2018 to November 2018. Investigations like complete blood count, renal function test, urine routine microscopy and USG abdomen with serum parathyroid hormone, serum phosphorus, serum calcium levels were done. Serum parathyroid hormone level was done by calorimetric method.Results: The prevalence of secondary hyperparathyroidism in our study was 72%.In hyperparathyroidism patient’s serum calcium level was low and the difference was highly significant (p<0.001). There is negative correlation between S.PTH and S. calcium level (r=-0.536). Mean serum calcium level in our study is 1.6mmol/l. In hyperparathyroidism patient’s serum phosphate level was high and the difference was highly significant (p<0.001). There was positive correlation between S.PTH and S.PO4 level (r=0.402). Mean serum phosphorus level in our study is 5.7 mg/dl. Prevalence of hyperparathyroidism was high among CRF patients with normal BP than hypertensive patients and with normal sugar than diabetics but the difference in proportion was not significant (p=0.87, p=0.98 respectively). 90% patients were on haemodialysis while 10% patients were on conservative management.Conclusions: Early detection of secondary hyperparathyroidism in chronic renal failure patients can reduce its complications like bone fracture and cardiovascular complications.

scholarly journals To Study the Association of Parathyroid Hormone with Severe Anaemia in Chronic Renal Failure Patients

2021 ◽  
Vol 10 (10) ◽  
pp. 724-728
Author(s):  
Madhavi Sarkari ◽  
Mahim Mittal ◽  
Ashutosh Kumar Rai
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Clinical History ◽  
Intact Parathyroid Hormone ◽  
Mineral And Bone Disorder ◽  
Cross Sectional

BACKGROUND Chronic kidney disease is defined as abnormalities of kidney structure or function, present for > 3 months, with implications for health. In India, the prevalence of chronic kidney disease (CKD), ranges from 0.79 % to 1.4 %. Secondary hyperparathyroidism (SHPT) is one of the less recognized reasons of anaemia in chronic kidney disease (CKD). In this study, we evaluated the role of SHPT as a cause of anaemia, and correlation of intact parathyroid hormone (iPTH) and haemoglobin (Hb) levels in chronic renal failure (CRF) patients on haemodialysis and also in CRF patients who are not on haemodialysis. METHODS This is an observational cross-sectional study done in the department of medicine in BRD Medical College, Gorakhpur, Uttar Pradesh, India, over a period of one year among a total of 101 patients. All patients underwent detailed clinical history, clinical examination & relevant biochemical investigations. RESULTS Parathyroid hormone level was found elevated in 82.2 % CRF patients in our study; out of these 76.2 % patients were severely anaemic. CONCLUSIONS Anaemia mainly normocytic & normochromic is a common complication of chronic kidney disease. Hormonal failure in CRF patients is very commonly reflected as anaemia & mineral and bone disorder (CKD-MBD). Parathyroid hormone was found elevated in most (82.2 %) of the CRF patients with anaemia. KEY WORDS Chronic Renal Failure (CRF), Intact Parathyroid Hormone (iPTH), Secondary Hyperparathyroidism (SHPT), Chronic Kidney Disease (CKD)

scholarly journals Effect of chronic renal failure on Ca2+ ATPase of brain synaptosomes.

1991 ◽  
Vol 2 (6) ◽  
pp. 1115-1121 ◽  
Author(s):  
S M Hajjar ◽  
M Smogorzewski ◽  
M A Zayed ◽  
G Z Fadda ◽  
S G Massry
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Atpase Activity ◽  
Secondary Hyperparathyroidism ◽  
Cytosolic Calcium ◽  
Calcium Entry ◽  
Blood Levels ◽  
Brain Synaptosomes ◽  
Calcium Extrusion

Chronic renal failure (CRF) is associated with a sustained rise in the concentration of cytosolic calcium [( Ca2+]i) of brain synaptosomes. This was attributed to secondary hyperparathyroidism where the excess blood levels of parathyroid hormone (PTH) augment calcium entry into synaptosomes. However, for such an effect of PTH to cause a sustained rise in [Ca2+]i, calcium extrusion out of synaptosomes should be impaired. The study presented here examined the effect of CRF with and without (CRF-PTX) excess PTH and the treatment of CRF rats with verapamil (V) on the Vmax and Km for calcium of synaptosomal Ca2+ ATPase, an enzyme that plays an important role in pumping calcium out of the synaptosomes. The Vmax of synaptosomal Ca2+ ATPase in CRF rats was significantly (P less than 0.01) lower than that of normal, CRF-PTX, CRF-V, and normal-V rats. However, the values in CRF-V were still below normal (P less than 0.05). There were no significant differences in the Km for calcium of synaptosomal Ca2+ ATPase among the five groups of animals. [Ca2+]i was significantly (P less than 0.01) higher in synaptosomes of CRF rats than in normal, CRF-PTX, CRF-V, and normal-V animals, and the values among the latter four groups were not different. The data demonstrate that the activity of synaptosomal Ca2+ ATPase is reduced in CRF rats, and this derangement is related to the excess PTH. This derangement in Ca2+ ATPase activity plays an important role in the genesis of the sustained elevation of synaptosomal [Ca2+]i in CRF.

scholarly journals Mechanism of Increased Parathyroid Hormone mRNA in Experimental Uremia

1999 ◽  
Vol 10 (12) ◽  
pp. 2562-2568
Author(s):  
CEVDET YALCINDAG ◽  
JUSTIN SILVER ◽  
TALLY NAVEH-MANY
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Protein Binding ◽  
Secondary Hyperparathyroidism ◽  
Mrna Stability ◽  
Rna Degradation ◽  
Cross Linking ◽  
Mrna Levels

Abstract. Patients with chronic renal failure develop secondary hyperparathyroidism with increased synthesis and secretion of parathyroid hormone (PTH) resulting in severe skeletal complications. In rats with secondary hyperparathyroidism due to 5/6 nephrectomy, there are increased PTH mRNA levels, and this mechanism was studied. Parathyroid glands were micro-dissected from control and 5/6 nephrectomy rats and analyzed for PTH mRNA and control genes, and the nuclei were used for nuclear run-on experiments. The cytosolic proteins of the parathyroids were used to study PTH mRNA protein binding by ultraviolet cross-linking and the degradation of the PTH transcript in vitro. Nuclear run-ons showed that the increase in PTH mRNA levels was posttranscriptional. Protein binding to the PTH mRNA 3′-UTR determines PTH mRNA stability and levels. Parathyroid proteins from uremic rats bound PTH mRNA similar to control rats by ultraviolet cross-linking. To determine the effect of uremia on PTH mRNA stability, an in vitro RNA degradation assay was performed with parathyroid proteins from uremic rats. When parathyroid proteins from control rats were incubated with PTH mRNA, there was transcript degradation already at 30 min, reaching 50% at 60 min and 90% at 180 min. With uremic parathyroid proteins, the PTH mRNA was not degraded at all at 120 min and was moderately decreased at 180 min. This decrease in degradation by uremic parathyroid proteins suggests a decrease in parathyroid cytosolic endonuclease activity in uremia resulting in a more stable PTH transcript. The increased PTH mRNA levels would translate into increased PTH synthesis and serum PTH levels, which would lead to metabolic bone disease in many patients with chronic renal failure.

scholarly journals Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism

1997 ◽  
Vol 51 (5) ◽  
pp. 1590-1595 ◽  
Author(s):  
William G. Goodman ◽  
Johannes D. Veldhuis ◽  
Thomas R. Belin ◽  
Harald Juppner ◽  
Isidro B. Salusky
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Suppressive Effect ◽  
Hormone Release ◽  
Parathyroid Hormone Release
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