A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men

1997 ◽  
Vol 83 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
Noriko Ashizawa ◽  
Rei Fujimura ◽  
Kumpei Tokuyama ◽  
Masashige Suzuki
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Bone Resorption ◽  
Resistance Exercise ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Osteoclastic Bone Resorption ◽  
Calcium Excretion ◽  
Repetition Maximum ◽  
Renal Tubular

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, and Masashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men. J. Appl. Physiol. 83(4): 1159–1163, 1997.—Metabolic acidosis increases urinary calcium excretion in humans as a result of administration of ammonium chloride, an increase in dietary protein intake, and fasting-induced ketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as a result of increase in blood lactate concentration. In this study we investigated changes in renal calcium handling, plasma parathyroid hormone concentration, and osteoclastic bone resorption after a single bout of resistance exercise. Ten male subjects completed a bout of resistance exercise with an intensity of 60% of one repetition maximum for the first set and 80% of one repetition maximum for the second and third sets. After exercise, blood and urine pH shifted toward acidity and urinary calcium excretion increased. Hypercalciuria was observed in the presence of an increased fractional calcium excretion and an unchanged filtered load of calcium. Therefore, the observed increase in urinary calcium excretion was due primarily to decrease in renal tubular reabsorption of calcium. Likely causes of the increase in renal excretion of calcium are metabolic acidosis itself and decreased parathyroid hormone. When urinary calcium excretion increased, urinary deoxypyridinoline, a marker of osteoclastic bone resorption, decreased. These results suggest that 1) strenuous resistance exercise increased urinary calcium excretion by decreasing renal tubular calcium reabsorption, 2) urinary calcium excretion increased independently of osteoclast activation, and 3) the mechanism resulting in postexercise hypercalciuria might involve non-cell-mediated physicochemical bone dissolution.

scholarly journals Recombinant human parathyroid hormone (1–84) is effective in CASR-associated hypoparathyroidism

2020 ◽  
Vol 183 (6) ◽  
pp. K13-K21
Author(s):  
Colin Patrick Hawkes ◽  
Dorothy I Shulman ◽  
Michael A Levine
Keyword(s):  
Parathyroid Hormone ◽  
Traditional Approach ◽  
Calcium Supplementation ◽  
Case Series ◽  
Calcium Sensitivity ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Human Parathyroid Hormone

Introduction Gain-of-function mutations in the CASR gene cause Autosomal Dominant Hypocalcemia Type 1 (ADH1), the most common genetic cause of isolated hypoparathyroidism. Subjects have increased calcium sensitivity in the renal tubule, leading to increased urinary calcium excretion, nephrocalcinosis and nephrolithiasis when compared with other causes of hypoparathyroidism. The traditional approach to treatment includes activated vitamin D but this further increases urinary calcium excretion. Methods In this case series, we describe the use of recombinant human parathyroid hormone (rhPTH)1–84 to treat subjects with ADH1, with improved control of serum and urinary calcium levels. Results We describe two children and one adult with ADH1 due to heterozygous CASR mutations who were treated with rhPTH(1–84). Case 1 was a 9.4-year-old female whose 24-h urinary calcium decreased from 7.5 to 3.9 mg/kg at 1 year. Calcitriol and calcium supplementation were discontinued after titration of rhPTH(1–84). Case 2 was a 9.5-year-old male whose 24-h urinary calcium decreased from 11.7 to 1.7 mg/kg at 1 year, and calcitriol was also discontinued. Case 3 was a 24-year-old female whose treatment was switched from multi-dose teriparatide to daily rhPTH(1–84). All three subjects achieved or maintained target serum levels of calcium and normal or improved urinary calcium levels with daily rhPTH(1–84) monotherapy. Conclusions We have described three subjects with ADH1 who were treated effectively with rhPTH(1–84). In all cases, hypercalciuria improved by comparison to treatment with conventional therapy consisting of calcium supplementation and calcitriol.

scholarly journals Effects of calcium-modulating hormones on thiazide receptor density.

1996 ◽  
Vol 7 (7) ◽  
pp. 1052-1057 ◽  
Author(s):  
P Blakely ◽  
D A Vaughn ◽  
D D Fanestil
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Urinary Calcium Excretion ◽  
Ion Concentration ◽  
Calcium Excretion ◽  
Calcitropic Hormones ◽  
Calcium Ion Concentration

Thiazide diuretic drugs act in the distal convoluted tubule (DCT) to inhibit a Na+Cl- cotransporter and enhance reabsorption of luminal calcium. The density of receptors for thiazides in the rat DCT is known to be increased by adrenocortical steroids, furosemide, and bendroflumethiazide, but decreased by ischemia. Because the DCT is a physiologic site of action by calcitonin and parathyroid hormone, this study examined the effects of these calcitropic hormones in thyroparathyroidectomized Sprague-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3H)metolazone to renal membranes, and (2) urinary electrolyte excretion rate. Salmon calcitonin (sCT) (20 to 100 ng/h) (1) increased the density of the renal TZR twofold, an effect that is maximal by 6 h after sCT administration, and (2) decreased urinary calcium excretion rate. Adequate dietary calcium must be provided for the effects of sCT to be observed. Regression analysis demonstrated that renal TZR density correlated negatively with total urinary calcium excretion rate but not with plasma calcium ion concentration. In addition, neither rat calcitonin (rCT), at doses that cause hypocalcemia, nor parathyroid hormone, at doses that cause hypercalcemia, produce direct effects on TZR density in the DCT of the thyroparathyroidectomized rat. Our findings indicate that upregulation of TZR by sCT, which occurs independently of plasma calcium-ion concentration, is likely via a calcitonin-like receptor other than that for rat calcitonin itself.

Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis

2007 ◽  
Vol 292 (1) ◽  
pp. F66-F75 ◽  
Author(s):  
Elaine M. Worcester ◽  
Daniel L. Gillen ◽  
Andrew P. Evan ◽  
Joan H. Parks ◽  
Katrina Wright ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Serum Magnesium ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Calcium Reabsorption ◽  
Renal Tubular ◽  
Filtered Load

Idiopathic hypercalciuria (IH) is common among calcium stone formers (IHSF). The increased urinary calcium arises from increased intestinal absorption of calcium, but it is unclear whether increased filtered load or decreased renal tubular reabsorption of calcium is the main mechanism for the increased renal excretion. To explore this question, 10 IHSF and 7 normal subjects (N) were studied for 1 day. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, and calories. Fasting and fed, ultrafiltrable calcium levels, and filtered load of calcium did not differ between N and IHSF. Urine calcium rose with meals, and fractional reabsorption fell in all subjects, but the change was significantly higher in IHSF. The changes in calcium excretion were independent of sodium excretion. Serum parathyroid hormone levels did not differ between N and IHSF, and they could not account for the greater fall in calcium reabsorption in IHSF. Serum magnesium and phosphorus levels in IHSF were below N throughout the day, and tubule phosphate reabsorption was lower in IHSF than N after meals. The primary mechanism by which kidneys ferry absorbed calcium into the urine after meals is via reduced tubule calcium reabsorption, and IHSF differ from N in the magnitude of the response. Parathyroid hormone is not likely to be a sufficient explanation for this difference.

scholarly journals Renal Tubular Impairment in Children with Idiopathic Hypercalciuria

2006 ◽  
Vol 49 (2) ◽  
pp. 109-111 ◽  
Author(s):  
Sylva Skálová ◽  
Štěpán Kutílek
Keyword(s):  
Reference Data ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Idiopathic Hypercalciuria ◽  
Tubular Damage ◽  
Calcium Excretion ◽  
Spot Urine ◽  
Z Scores ◽  
Proximal Tubular ◽  
Renal Tubular

Idiopathic hypercalciuria (IH) is defined as hypercalciuria that persists after correction of dietary inbalances and has no detectable cause. The excretion of urinary N-acetyl-beta-D-glucosaminidase (U-NAG), a marker of proximal tubular damage, has been previously reported as either increased or normal in children with IH. We evaluated U-NAG in 20 children (13 boys and 7 girls, mean age 10.3 years ± 5.7 SD) with IH (urinary calcium excretion above 0.1 mmol/kg/24 hours, with no detectable cause) and with otherwise normal renal function tests. Ultrasound examination revealed urolithiasis (n = 4) and nephrocalcinosis (n = 1). The U-NAG values were evaluated in the spot urine collected from the second morning void and calculated as the urinary NAG/creatinine ratio (U-NAG/Cr) and expressed in nkat/mmol. The 24-hour urinary calcium excretion (U-Ca/24h) was assessed in a urinary sample from 24-hour collected urine and calculated in mmol/kg. The obtained results of U-Ca/24h and U-NAG/Cr were expressed as Z-scores. When compared to the reference data, the U-Ca/24h and U-NAG/Cr were significantly higher (p=0.0004 and p=0.006, respectively). There was no correlation between the U-NAG/Cr and U-Ca/24h (r = 0.18, p = 0.20). The U-NAG/Cr values were significantly higher in the 5 patients with urolithiasis/nephrocalcinosis, whether compared to the rest of the group (p=0.02), or to the reference data (p=0.01). The U-NAG/Cr activity was higher in 15 children without urolithiasis/nephrocalcinosis when compared to reference data (p < 0.01). There was no difference in U-Ca/24h between the children with and without urolithiasis/nephrocalcinosis (p = 0.58). These findings suggest that tubular impairment, as reflected by U-NAG/Cr, might occur in children with IH, especially in patients with urolithiasis/nephrocalcinosis. There doesn’t seem to be a direct relationship between the U-NAG/Cr activity and the degree of calcium leakage.

SECONDARY HYPERPARATHYROIDISM IN YOUNG RATS GIVEN PROLONGED TREATMENT WITH CALCITONIN

1972 ◽  
Vol 71 (2) ◽  
pp. 313-320 ◽  
Author(s):  
O. Helmer Sørensen ◽  
Inge Hindberg ◽  
S. Nistrup Madsen
Keyword(s):  
Bone Resorption ◽  
Secondary Hyperparathyroidism ◽  
Intestinal Absorption ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Prolonged Treatment ◽  
Calcium Excretion ◽  
Young Rats ◽  
Calcitonin Treatment ◽  
Considerable Loss

ABSTRACT Bone resorption, intestinal absorption of calcium, and urinary calcium excretion were studied in young rats given prolonged calcitonin treatment. The animals soon developed a resistance to the hypocalcaemic effect of calcitonin, probably due to a secondary hyperparathyroidism. In one of the experiments the rats were given 45Ca 2 weeks before the start of the calcitonin treatment in order to label the deep parts of bone. The release of isotope from bone was inhibited after the first injections of the hormone, but even after a few days of calcitonin treatment no differences could be detected between the treated animals and their corresponding controls. An increased release of isotope from bone was registered as soon as the treatment was interrupted, indicating the presence of a secondary hyperparathyroidism. No conclusive changes could be detected in the intestinal absorption of calcium. A transitory reduction in the excretion of calcium in the urine was followed by a considerable loss of calcium.

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 comparative effects of feeding ammonium carbonate, ammonium sulfate, and ammonium chloride on urinary calcium excretion in the rat

1987 ◽  
Vol 65 (11) ◽  
pp. 2202-2204 ◽  
Author(s):  
Susan J. Whiting ◽  
David E. C. Cole
Keyword(s):  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Male Rats ◽  
Calcium Excretion ◽  
Acid Excretion ◽  
Calcium Reabsorption ◽  
Acid Load ◽  
Feeding Trials ◽  
Renal Tubular ◽  
Excretion Rates

When either sulfate or chloride is added to the diet, the resulting acid load causes a rise in urinary calcium excretion. There is, however, the possibility that sulfate, which has been shown to complex renal tubular calcium, will further decrease renal calcium reabsorption and thus produce a greater calciuria than chloride. Because addition of a fixed cation (e.g., sodium) to the diet may also stimulate calciuresis, experiments were conducted using metabolizable ammonium to minimize cation effects. Ammonium salts of sulfate, chloride, and carbonate (control) were added to the diets of male rats at 0.3 mequiv./g weight of diet. Twenty-four hour excretion rates of calcium, sulfate, chloride, and net acid were measured at various intervals up to 1 month. As expected, the chloride and sulfate diets were both associated with significantly elevated urine calcium and net acid excretion as compared with controls. However, those fed sulfate exhibited significantly less calcium and acid excretion and absorbed a smaller proportion of the anion load than those given chloride. In a second experiment, the amounts of supplemental sulfate and chloride were adjusted so that total absorptions were similar. At 2 weeks, both calcium and acid excretions in the fixed anion groups were no longer significantly different. Thus, in chronic feeding trials, there appears to be no measurable difference in the calciuretic properties of sulfate and chloride anions.

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