Renal divalent cation excretion in secondary hypertension

1. To determine whether abnormal renal calcium excretion is unique to primary genetic hypertension, blood pressure and 24 h urinary excretion of calcium, magnesium, sodium and creatinine were measured in deoxycorticosterone—saline and two-kidney, one-clip Goldblatt hypertensive rats and in their respective controls on low (0.2%) and high (1.8%) dietary calcium intakes. 2. Calcium supplementation lowered blood pressure (P<0.05) in deoxycorticosterone—saline rats and in control saline-loaded rats, raised blood pressure in two-kidney, one clip rats, and had no effect in sham-operated control rats. 3. On both diets, calcium excretion was higher in hypertensive than in normotensive rats. The high calcium diet increased urinary calcium excretion in all rats, but the changes in urinary calcium excretion closely paralleled the diet-induced changes in blood pressure. Thus, urinary calcium excretion in deoxycorticosterone—saline animals, in whom calcium lowered blood pressure the most, rose the least (107%). Urinary calcium excretion rose the most in two-kidney, one-clip animals (1113%), whose blood pressure also rose the most. 4. Urinary magnesium excretion was also abnormal in hypertensive rats compared with normotensive rats, falling on the high compared with the low calcium diet in normotensive rats, but not in either hypertensive strain. Furthermore, urinary magnesium excretion was closely linked to urinary calcium excretion in saline-loaded control rats (r = 0.78; P = 0.008), but was dissociated from urinary calcium excretion in deoxycorticosterone—saline rats (r = 0.02; not significant). 5. We conclude (a) that the renal handling of both calcium and magnesium is altered in secondary hypertension, and (b) that dietary calcium supplementation may have different effects on blood pressure in different forms of hypertensive disease. We hypothesize that elevated blood pressure per se may be responsible for the exaggerated calciuresis of hypertension.

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Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level

Clinical Science ◽

10.1042/cs0930153 ◽

1997 ◽

Vol 93 (2) ◽

pp. 153-157 ◽

Cited By ~ 2

Author(s):

Ryoji Ozono ◽

Tetsuya Oshima ◽

Hideo Matsuura ◽

Katsuhiko Ishibashi ◽

Mitsuaki Watanabe ◽

...

Keyword(s):

Blood Pressure ◽

Calcium Metabolism ◽

Sodium Intake ◽

Urinary Calcium ◽

Urinary Calcium Excretion ◽

Mean Blood Pressure ◽

Calcium Excretion ◽

Sodium Restriction ◽

Sodium Diet ◽

Change In Mean

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

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Estrogen deficiency and low-calcium diet increased bone loss and urinary calcium excretion but did not alter arterial stiffness in young female rats

Journal of Bone and Mineral Metabolism ◽

10.1007/s00774-007-0822-4 ◽

2008 ◽

Vol 26 (3) ◽

pp. 218-225 ◽

Cited By ~ 17

Author(s):

Jong-Hoon Park ◽

Naomi Omi ◽

Toshiya Nosaka ◽

Ayako Kitajima ◽

Ikuko Ezawa

Keyword(s):

Bone Loss ◽

Arterial Stiffness ◽

Young Female ◽

Urinary Calcium ◽

Estrogen Deficiency ◽

Urinary Calcium Excretion ◽

Female Rats ◽

Calcium Excretion ◽

Calcium Diet ◽

Low Calcium Diet

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

Acta Endocrinologica ◽

10.1530/eje-20-0710 ◽

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.

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The relationship between blood pressure and serum parathyroid hormone with special reference to urinary calcium excretion: The Tromsø study

Journal of Endocrinological Investigation ◽

10.1007/bf03345542 ◽

2006 ◽

Vol 29 (3) ◽

pp. 214-220 ◽

Cited By ~ 10

Author(s):

F. Saleh ◽

R. Jorde ◽

J. Svartberg ◽

J. Sundsfjord

Keyword(s):

Blood Pressure ◽

Parathyroid Hormone ◽

Special Reference ◽

Urinary Calcium ◽

Urinary Calcium Excretion ◽

Calcium Excretion ◽

Serum Parathyroid Hormone ◽

The Relationship

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Renal magnesium wasting and hypocalciuria in chronic cis-platinum nephropathy in man

Clinical Science ◽

10.1042/cs0750203 ◽

1988 ◽

Vol 75 (2) ◽

pp. 203-207 ◽

Cited By ~ 30

Author(s):

Viroon Mavichak ◽

Christopher M. L. Coppin ◽

Norman L. M. Wong ◽

John H. Dirks ◽

Valerie Walker ◽

...

Keyword(s):

Serum Magnesium ◽

Normal Subjects ◽

Urinary Calcium ◽

Urinary Calcium Excretion ◽

Total Serum ◽

Calcium Excretion ◽

Total Serum Calcium ◽

Dietary Magnesium ◽

Calcium And Magnesium ◽

Magnesium Excretion

1. The renal handling of calcium and magnesium was studied in six patients with persistent hypomagnesaemia after cis-platinum treatment for testicular tumours. 2. In comparison with normal subjects, the patients showed hypomagnesaemia (mean 0.54 mmol/l), which was associated with a normal urinary magnesium excretion (mean 4.83 mmol/24 h). Urinary calcium excretion was significantly lower in the patients than in the normal subjects (mean 2.05 vs 5.15 mmol/24 h, respectively; P < 0.01), despite slightly higher total serum calcium levels (2.53 vs 2.38 mmol/l, respectively; P < 0.05). During magnesium chloride infusion, when serum magnesium levels were comparable in patients and controls, urinary calcium excretion remained lower in the patients, indicating that hypomagnesaemia was not the cause of the hypocalciuria. 3. Dietary magnesium supplementation resulted in a significant increase in the serum magnesium levels in the patients, while dietary magnesium deprivation resulted in a comparable decrease in urinary magnesium excretion in patients and controls (to 1.46 and 2.00 mmol/day, respectively), although the serum magnesium level fell further (to 0.46 mmol/l) in the patients. 4. The dissociation of renal calcium and magnesium excretion appears to be part of the intrinsic tubular defect caused by cis-platinum. This dissociation of urinary calcium and magnesium excretion, which resembles that seen in Bartter's syndrome, may result from a lesion in the distal convoluted tubule.

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Combined vitamin D and calcium supplementation in vitamin D inadequate patients with urolithiasis: Impact on hypercalciuria and de novo stone formation

Canadian Urological Association Journal ◽

10.5489/cuaj.3332 ◽

2015 ◽

Vol 9 (11-12) ◽

pp. 403 ◽

Cited By ~ 4

Author(s):

Charles Hesswani ◽

Yasser A Noureldin ◽

Mohamed A Elkoushy ◽

Sero Andonian

Keyword(s):

Vitamin D ◽

De Novo ◽

Stone Formation ◽

Calcium Supplementation ◽

Urinary Calcium ◽

Urinary Calcium Excretion ◽

Calcium Excretion ◽

Hydroxyvitamin D ◽

History Of ◽

25 Hydroxyvitamin D

ABSTRACT Introduction: We examined the effect of combined vitamin D and calcium supplementation (VDCS) on urinary calcium excretion and de novo stone formation in vitamin D inadequate (VDI) urolithiasis patients.Methods: We retrospectively reviewed the data of VDI patients (serum 25-hydroxyvitamin D<75 nmol/L) followed at a tertiary stone centre between September 2009 and December 2014. VDI patients with history of urolithiasis, who were placed on VDCS for abnormal bone mineral density or hyperoxaliuria, were included. Hypercalciuric patients and patients on thiazide diuretics were excluded. Metabolic stone workup and two 24-hour urine collections were performed before and after VDCS. Results: In total, we inculded 34 patients, with a mean age of 54.8 years and a mean body mass index of 25.7 kg/m2. After VDCS, there was a significant increase in the mean serum 25-hydroxyvitamin D (52.0 vs. 66.4 nmol/L, p<0.001) and the mean urinary calcium excretion (3.80 vs. 5.64 mmol/d, p<0.001). Eight (23.5%) patients developed de novo hypercalciuria. After a median follow-up of 39 (range: 7-60) months, 50% of hypercalciuric patients developed stones compared with 11.5% of non-hypercalciuric patients (p=0.038).Conclusion: This study showed a significant effect of combined VDCS on mean urinary calcium excretion, de novo hypercalciuria, and stone development in VDI patients with history of urolithiasis. Therefore, VDI urolithiasis patients receiving VDCS are advised to have monitoring with 24-hour urine collections and imaging studies. Although small, the sample size is good enough to validate the statistical outcomes. Prospective studies are needed to confirm these results.

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