scholarly journals Role of FGF23 in Pediatric Hypercalciuria

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Maria Goretti Moreira Guimarães Penido ◽  
Marcelo de Sousa Tavares ◽  
Uri Saggie Alon
Keyword(s):  
Urinary Calcium ◽  
Serum Phosphate ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Lower Serum ◽  
Median Plasma ◽  
Registration Number ◽  
Serum Pth ◽  
Lower Urinary

Background. This study explored the possible role of FGF23 in pediatric hypercalciuria. Methods. Plasma FGF23 was measured in 29 controls and 58 children and adolescents with hypercalciuria: 24 before treatment (Pre-Treated) and 34 after 6 months of treatment (Treated). Hypercalciuric patients also measured serum PTH hormone, 25(OH)vitD, phosphate, calcium, creatinine, and 24 h urine calcium, phosphate, and creatinine. Results. There were no differences in age, gender, ethnicity, or body mass index either between controls and patients, or between Pre-Treated and Treated patients. Median plasma FGF23 in controls was 72 compared with all patients, 58 RU/mL (p=0.0019). However, whereas FGF23 in Pre-Treated patients, 73 RU/mL, was not different from controls, in Treated patients it was 50 RU/mL, significantly lower than in both controls (p<0.0001) and Pre-Treated patients (p=0.02). In all patients, there was a correlation between FGF23 and urinary calcium (r=0.325; p=0.0014). Treated patients had significantly lower urinary calcium (p<0.0001), higher TP/GFR (p<0.001), and higher serum phosphate (p=0.007) versus Pre-Treated patients. Conclusions. Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR and serum phosphate concentration, without significant changes in PTH. Further studies are indicated. This trial is registered with Clinical Registration Number RBR 8W27X5.

PTH regulates expression of ClC-5 chloride channel in the kidney

2000 ◽  
Vol 278 (2) ◽  
pp. F238-F245 ◽  
Author(s):  
Ian V. Silva ◽  
Carol J. Blaisdell ◽  
Sandra E. Guggino ◽  
William B. Guggino
Keyword(s):  
Vitamin D ◽  
Protein Expression ◽  
Chloride Channel ◽  
Urinary Calcium ◽  
Kidney Cortex ◽  
Lower Serum ◽  
Protein Levels ◽  
Calcium Reabsorption ◽  
Mrna And Protein Expression ◽  
Serum Pth

Mutations in the chloride channel, ClC-5, have been described in several inherited diseases that result in the formation of kidney stones. To determine whether ClC-5 is also involved in calcium homeostasis, we investigated whether ClC-5 mRNA and protein expression are modulated in rats deficient in 1α,25(OH)2 vitamin D3 with and without thyroparathyroidectomy. Parathyroid hormone (PTH) was replaced in some animals. Vitamin D-deficient, thyroparathyrodectomized rats had lower serum and higher urinary calcium concentrations compared with control animals as well as lower serum PTH and calcitonin concentrations. ClC-5 mRNA and protein levels in the cortex decrease in vitamin D-deficient, thyroparathyroidectomized rats compared with both control and vitamin D-deficient animals. ClC-5 mRNA and protein expression increase near to control levels in vitamin D-deficient, thyroparathyroidectomized rats injected with PTH. No significant changes in ClC-5 mRNA and protein expression in the medulla were detected in any experimental group. Our results suggest that PTH modulates the expression of ClC-5 in the kidney cortex and that neither 1α,25(OH)2 vitamin D3 nor PTH regulates ClC-5 expression in the medulla. The pattern of expression of ClC-5 varies with urinary calcium. Animals with higher urinary calcium concentrations have lower levels of ClC-5 mRNA and protein expression, suggesting that the ClC-5 chloride channel plays a role in calcium reabsorption.

Urinary calcium indices in primary hyperparathyroidism (PHPT) and familial hypocalciuric hypercalcaemia (FHH): which test performs best?

2020 ◽  
pp. postgradmedj-2020-137718
Author(s):  
Muhammad Fahad Arshad ◽  
James McAllister ◽  
Azhar Merchant ◽  
Edmund Rab ◽  
Jacqueline Cook ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
International Workshop ◽  
Significant Proportion ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Clearance Ratio ◽  
Urine Calcium ◽  
Genetic Studies ◽  
Urine Calcium Excretion ◽  
Control Study

AimPrimary hyperparathyroidism (PHPT) is much more common than familial hypocalciuric hypercalcaemia (FHH), but there is considerable overlap in biochemical features. Urine calcium indices help with the differential diagnosis, but their reliability in making this distinction is not clear. The aim of this study was to compare urinary calcium values in patients with PHPT and FHH.MethodsThis was a case–control study of patients with PHPT who had successful surgery and genetically proven FHH between 2011 and 2016. Due to low FHH numbers, patients from neighbouring hospitals and outside study period (2017–2019) were allowed to improve power. Data on demographics and urinary calcium were obtained from electronic records and compared between the two groups.ResultsDuring the study period, 250 patients underwent successful PHPT surgery, while in the FHH arm, 19 genetically proven cases were included. The median (IQR) 24-hour urine calcium excretion (UCE) in the PHPT group was 8.3 (5.6–11.2) mmol/24 hours compared with 3.2 (2.1–6.1) mmol/24 hour in the FHH group (p<0.001). Median (IQR) calcium to creatinine clearance ratio (CCCR) in the PHPT and FHH groups was 0.020 (0.013–0.026) and 0.01 (0.002–0.02), respectively (p=0.001). The sensitivity of urinary tests for PHPT was 96% for UCE (cut-off ≥2.5 mmol/24 hour) and 47% for CCCR (cut-off >0.02). The specificity of the urinary tests for FHH was 29.4% for UCE (cut-off <2.5 mmol/24 hour) and 93% for CCCR (cut-off <0.02).Conclusions24-hour UCE is more sensitive in diagnosing PHPT; however, it is less specific in ruling out FHH as compared with CCCR, when the cut-offs suggested by the International guidelines from the fourth international workshop are used. A significant proportion of patients with PHPT would have also required genetic studies if the guidelines were followed.

scholarly journals The Calcimimetic Cinacalcet Normalizes Serum Calcium in Subjects with Primary Hyperparathyroidism

2003 ◽  
Vol 88 (12) ◽  
pp. 5644-5649 ◽  
Author(s):  
Dolores M. Shoback ◽  
John P. Bilezikian ◽  
Stewart A. Turner ◽  
Laura C. McCary ◽  
Matthew D. Guo ◽  
...  
Keyword(s):  
Placebo Group ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Urinary Calcium ◽  
Dose Finding ◽  
Calcium Excretion ◽  
Normal Range ◽  
Urine Calcium ◽  
Novel Therapy ◽  
Double Blind

Abstract Calcimimetics increase the sensitivity of the calcium-sensing receptor (CaR) to circulating serum calcium, reducing the secretion of PTH and the serum calcium concentration. We evaluated the calcimimetic cinacalcet, a novel therapy for the management of primary hyperparathyroidism. In this randomized, double-blind, dose-finding study, patients (n = 22) with primary hyperparathyroidism were given cinacalcet (30, 40, or 50 mg) or placebo twice daily for 15 d and observed for an additional 7 d. Serum calcium, plasma PTH, and 24-h and fasting urine calcium were measured. Baseline mean serum calcium was 10.6 mg/dl for the combined cinacalcet-treated patients (normal range, 8.4–10.3 mg/dl), compared with 10.4 mg/dl for the placebo group. Mean PTH at baseline was 102 pg/ml (normal range, 10–65 pg/ml) for the combined cinacalcet-treated patients, compared with 100 pg/ml in the placebo group. Serum calcium normalized after the second dose on d 1 and remained normal through d 15 in all cinacalcet dose groups. Maximum decreases in PTH of over 50% occurred 2–4 h after dosing in all cinacalcet-treated groups. The fasting and 24-h urine calcium to creatinine ratios were similar in the cinacalcet and placebo groups. This study demonstrates that cinacalcet safely normalized serum calcium and lowered PTH concentrations without increasing urinary calcium excretion in the study subjects, indicating the potential benefit of cinacalcet as a medical treatment for primary hyperparathyroidism.

scholarly journals Inhibition of calbindin D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria.

1998 ◽  
Vol 9 (8) ◽  
pp. 1416-1426
Author(s):  
C W Yang ◽  
J Kim ◽  
Y H Kim ◽  
J H Cha ◽  
S Y Mim ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Serum Calcium ◽  
Protein Level ◽  
Rat Kidney ◽  
Urinary Calcium ◽  
Calcium Handling ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Calbindin D28k ◽  
Urine Calcium Excretion

A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting.

scholarly journals Bone and Mineral Metabolism in Patients with Primary Aldosteronism

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Luigi Petramala ◽  
Laura Zinnamosca ◽  
Amina Settevendemmie ◽  
Cristiano Marinelli ◽  
Matteo Nardi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Primary Aldosteronism ◽  
Mineral Metabolism ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Mineral Density ◽  
Lower Serum ◽  
Functional Link ◽  
The Impact

Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%;P<0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.

scholarly journals Primary aldosteronism as a cause of secondary osteoporosis

2017 ◽  
Vol 177 (5) ◽  
pp. 431-437 ◽  
Author(s):  
Antonio Stefano Salcuni ◽  
Vincenzo Carnevale ◽  
Claudia Battista ◽  
Serena Palmieri ◽  
Cristina Eller-Vainicher ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Outpatient Basis ◽  
Mineral Density ◽  
Mean Values ◽  
Metabolic Bone ◽  
Confirmatory Tests ◽  
Aldosterone To Renin Ratio ◽  
Serum Pth

Objective Patients with primary aldosteronism (PA) have a high prevalence of osteoporosis (OP) and fractures (Fx). We evaluated the presence of PA in patients admitted to our metabolic bone disease outpatient clinic. Design Study conducted on an in- and outpatient basis in a referral Italian endocrinology unit. Methods A total of 2632 patients were evaluated. 2310 were excluded because they were taking drugs known to affect bone or mineralocorticoids metabolism or were diagnosed to have a secondary cause of osteoporosis. The remaining 322 subjects (304 females, 18 males) took part in the study. Bone mineral density (BMD) and thoracic and lumbar spine vertebral morphometry were performed by dual X-ray absorptiometry. All patients were screened for PA with aldosterone-to-renin ratio. In those who had positive results, confirmatory tests were performed. Results Among 322 subjects, 213 were osteoporotics and 109 were not. PA was diagnosed in eleven out of 213 osteoporotic patients (5.2%) and one out of 109 non-osteoporotic subjects (0.9%, P = 0.066). PA was observed in the 26.1% of patients with the concomitant presence of osteoporosis, hypertension and hypercalciuria. Compared with patients without PA, patients with PA had mean values of urinary calcium excretion, 4.8 ± 2.5 mmol/day vs 7.6 ± 3.2 mmol/day, P < 0.001 and serum PTH levels, 5.4 pmol/L vs 7.3 pmol/L, P < 0.01, significantly higher. Conclusions PA should be considered among the causes of secondary OP.

Mechanism of chronic hypercalciuria with furosemide: increased calcium absorption

1986 ◽  
Vol 251 (1) ◽  
pp. F17-F24 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
C. B. Langman ◽  
F. L. Coe
Keyword(s):  
Calcium Absorption ◽  
Chronic Administration ◽  
Urinary Calcium ◽  
Intestinal Calcium Absorption ◽  
Calcium Excretion ◽  
Calcium Balance ◽  
Urine Calcium ◽  
Calcium Diet ◽  
Filtered Load ◽  
Urine Calcium Excretion

Furosemide produces chronic hypercalciuria. The source of the additional urinary calcium is not known but must be either bone mineral or calcium absorbed by the intestine. Without bone calcium dissolution or increased absorption the filtered load of calcium would fall and urinary calcium excretion would return to pretreatment levels. To determine whether furosemide alters intestinal calcium absorption, we fed furosemide (75 mg . kg body-1 wt . day-1) to 11 rats eating 15 g/day of a 0.60% calcium diet. Compared with 11 control rats, furosemide increased urine calcium (15.6 +/- 0.8 mg/5 days vs. 4.1 +/- 0.3, P less than 0.001). Fecal calcium excretion fell (194 +/- 7 mg/5 days vs. 223 +/- 12, P less than 0.05), indicating an increase in intestinal calcium absorption sufficient to sustain the hypercalciuria. The increase in absorption occurred without an increase in the level of serum 1,25-dihydroxycholecalciferol (180 +/- 20 pg/ml vs. 220 +/- 16, furosemide vs. control, respectively, P = NS). To determine whether the intestinal effect of furosemide persists after the initial sodium diuresis abates, we analyzed only the last 3 days of balance. Again, rats fed furosemide had increased urine excretion and intestinal absorption of calcium, so that net calcium balance was not different from that of controls. Twelve additional rats were fed a 0.02% calcium diet to which 35 mg . kg body wt-1 . day-1 of furosemide was added. Compared with eleven controls, urine calcium increased and fecal calcium excretion again fell, but balance was not different. Chronic administration of furosemide increases intestinal calcium absorption enough to permit urine calcium excretion to remain elevated without the necessity for bone dissolution.

scholarly journals Urine Calcium and Serum Ionized Calcium, Total Calcium and Parathyroid Hormone Concentrations in the Diagnosis of Primary Hyperparathyroidism and Familial Benign Hypercalcaemia

1992 ◽  
Vol 29 (1) ◽  
pp. 52-58 ◽  
Author(s):  
Ian R Gunn ◽  
James R Wallace
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Load Test ◽  
Ionized Calcium ◽  
Calcium Excretion ◽  
Fasting Serum ◽  
Urine Calcium ◽  
Glomerular Filtrate ◽  
Calcium Load ◽  
Serum Pth

A relationship between serum concentrations of ionized calcium and parathyroid hormone (PTH) in persons without parathyroid overactivity was defined by performing an oral calcium load test. As a result, a serum PTH concentration greater than 2·6 pmol/L in a hypercalcaemic patient was regarded as suggestive of hyperparathyroidism. Fasting serum PTH concentrations in 58 patients with surgically and histologically proven primary hyperparathyroidism (PHPT) were all above 2·7 pmol/L (range 3·2–84·5). Thirteen of 20 patients with familial benign hypercalcaemia (FBH) had fasting serum PTH concentrations greater than 2·6 pmol/L (range 1·6–6·1). There was a significant correlation between serum PTH and age in the FBH patients only. Fasting urine calcium excretion (CaE) ranged from 14 to 222 μmol/L of glomerular filtrate in PHPT and 3–34 μmol/L of glomerular filtrate in FBH. The best biochemical discriminant between patients with PHPT and FBH was a plot of fasting serum PTH against CaE. A plot of post-calcium load PTH against post-load CaE showed no further significant advantage in discriminating between the two conditions.

scholarly journals Role of 1,25-Dihydroxy Vitamin D3and Parathyroid Hormone in Urinary Calcium Excretion in Calcium Stone Formers

2014 ◽  
Vol 55 (5) ◽  
pp. 1326 ◽  
Author(s):  
Won Tae Kim ◽  
Yong-June Kim ◽  
Seok Joong Yun ◽  
Kyung-Sub Shin ◽  
Young Deuk Choi ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Calcium Stone ◽  
Stone Formers

The Role of Calcium Utilization of Intestinal Flora in Urinary Calcium Excretion

2007 ◽  
Vol 17 (2) ◽  
pp. 148-150
Author(s):  
Fatma Yurt Lambrecht ◽  
Salih Kavukçu ◽  
Belde Kasap ◽  
Alper Soylu ◽  
Mine Yücesoy ◽  
...  
Keyword(s):  
Intestinal Flora ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Calcium Utilization
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