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

1988 ◽  
Vol 75 (2) ◽  
pp. 203-207 ◽  
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.

Relations between Oxalic Acid, Calcium, Magnesium and Creatinine Excretion in Normal Men and Male Patients with Calcium Oxalate Kidney Stones

1974 ◽  
Vol 46 (3) ◽  
pp. 357-367 ◽  
Author(s):  
A. Hodgkinson
Keyword(s):  
Calcium Oxalate ◽  
Normal Subjects ◽  
Calcium Excretion ◽  
Oxalate Excretion ◽  
Stone Formers ◽  
Calcium Magnesium ◽  
Male Patients ◽  
Calcium And Magnesium ◽  
Magnesium Excretion ◽  
Normal Men

1. The daily excretion of oxalate, calcium, magnesium and creatinine was determined in fifty-two normal men and sixty-five male patients with calcium oxalate-containing renal stones. 2. Direct relationships were found between calcium and oxalate excretion, magnesium and oxalate excretion and calcium and magnesium excretion in both normal subjects and stone-formers. The significance of these relationships is discussed. 3. The mean excretion of calcium and oxalate was significantly higher in the stone-formers, compared with the controls, both calcium and oxalate excretion being raised by about 20%. 4. The effect of oral ingestion of glucose and casein on the rate of excretion of calcium, magnesium, oxalate and phosphate was examined. Glucose increased the rate of calcium and magnesium excretion but had no effect on oxalate excretion and suppressed phosphate excretion. Casein also increased calcium excretion but had little or no effect on magnesium or oxalate excretion, and it increased phosphate excretion. 5. The association of high calcium excretion with high oxalate excretion, in both normal subjects and stone-formers, results in a high degree of supersaturation of the urine with respect to calcium oxalate. The implication of these findings with respect to the cause and treatment of calcium oxalate stones is discussed.

scholarly journals Vitamin D Repletion in Patients with Primary Hyperparathyroidism and Coexistent Vitamin D Insufficiency

2005 ◽  
Vol 90 (4) ◽  
pp. 2122-2126 ◽  
Author(s):  
Andrew Grey ◽  
Jenny Lucas ◽  
Anne Horne ◽  
Greg Gamble ◽  
James S. Davidson ◽  
...  
Keyword(s):  
Vitamin D ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Serum Alkaline Phosphatase ◽  
Vitamin D Insufficiency ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Total Serum ◽  
Calcium Excretion ◽  
Intact Pth

Abstract Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium &lt;12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] &lt;20 μg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 μg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P &lt; 0.01) and 26% at 12 months (P &lt; 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = −0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion.

scholarly journals A Study of Serum Calcium and Magnesium Levels in Idiopathic Epilepsy Patients of Hubli, Karnataka, India

2021 ◽  
Vol 8 (25) ◽  
pp. 2187-2191
Author(s):  
Chandrashekar Kachapur ◽  
Seetaram N. Kallimani ◽  
Gayathri B.H ◽  
Ishwar S. Hasabi ◽  
Zahura M. Devarhoru
Keyword(s):  
Serum Calcium ◽  
Calcium Influx ◽  
Serum Magnesium ◽  
Idiopathic Epilepsy ◽  
Total Serum ◽  
Cross Sectional ◽  
Total Serum Calcium ◽  
Study Results ◽  
Significant Difference ◽  
Calcium And Magnesium

BACKGROUND Magnesium is a potential modulator of seizure activity because of its ability to antagonize the excitatory calcium influx through N-methyl-D-aspartate (NMDA) receptor which is thought to play a role in many human forms of epilepsy. When the extracellular concentration of calcium ion falls below normal, the nervous system becomes more excitable, allowing easy initiation of action potentials. Consequently, hypocalcaemia causes seizures because of its action of increasing excitability in the brain. We wanted to estimate the serum concentration of calcium and magnesium in idiopathic epilepsy patients and its co-relation. METHODS 94 cases of idiopathic epilepsy with breakthrough seizures admitted to KIMS Hospital, Hubli, meeting the inclusion criteria were considered for the study which was for 2-years’ time period. It’s a single centred, time bound and cross sectional study. RESULTS Mean serum calcium was low 8.36 ± 0.45 mg / dL and mean serum magnesium was 1.79 ± 0.28 mg / dL. 64.9 % had total serum calcium less than 8.5 mg / dL and 44.7 % had serum magnesium of < 1.8 mg / dL. 35.1 % had both low calcium and magnesium. There was significant difference in mean serum calcium with respect to number of episodes. There was no significant difference in mean serum magnesium with respect to number of episodes. CONCLUSIONS Serum calcium and magnesium levels which play a role in seizure initiation should be measured in all idiopathic epilepsy patients with breakthrough seizures as a seizure trigger. Considering the role of calcium and magnesium in the pathophysiology of seizures and by evaluating the results from the present study, breakthrough seizure could be provoked by hypocalcaemia and hypomagnesemia. Hence they may be used for the treatment of intractable seizures. KEYWORDS Calcium, Magnesium, Idiopathic Epilepsy

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.

The Relative Importance of Urinary pH and Urinary Content of Citrate, Magnesium and Calcium in the Production of Nephro Calcinosis by Diet and Acetazolamide in the Rat

1970 ◽  
Vol 39 (5) ◽  
pp. 605-623 ◽  
Author(s):  
A. Z. Györy ◽  
K. D. G. Edwards ◽  
J. Robinson ◽  
A. A. Palmer
Keyword(s):  
Calcium Chloride ◽  
Urinary Calcium ◽  
Analysis Of Covariance ◽  
Calcium Excretion ◽  
Urinary Ph ◽  
Experimental Nephrocalcinosis ◽  
Calcium And Magnesium ◽  
Excretion Rates ◽  
Magnesium Excretion ◽  
Urinary Citrate

1. The association of varying levels of urinary pH, urinary citrate and urinary calcium and magnesium excretion rates with kidney citrate, calcium and magnesium concentrations in experimental nephrocalcinosis was examined in twenty-four rats in a 3 × 2 multifactorial experiment with four replicates. All rats received the same synthetic diet for 6 weeks before being killed in the seventh week. In addition the rats received calcium supplements as calcium chloride (diet A), calcium carbonate (diet B), or as an equal mixture of calcium chloride and carbonate (diet N), the content of calcium being kept constant at 6·3 mg per g of diet for all rats. Half of the rats also received 2·5 mg of acetazolamide per g of diet. 2. Diet A produced a systemic acidosis and the most acid urinary pH. Diet B plus acetazolamide produced a more severe systemic acidosis and the most alkaline urinary pH. Urinary magnesium, citrate and calcium excretion rates were generally reduced below normal. Urinary excretion of magnesium and calcium were significantly higher in those rats on diet A than in those on diet B, while urinary citrate excretion was highest in the latter. Acetazolamide caused a further increase in urinary calcium excretion but a decrease in urinary magnesium and citrate excretions. 3. Acetazolamide significantly reduced plasma calcium but elevated plasma magnesium. The changes produced in plasma and urinary calcium and magnesium in the present study were consistent with an action through systemic acidosis for calcium and through urinary pH for magnesium, both being effected at a tubular site. 4. Variation in diet alone as well as acetazolamide administration were significantly associated with variation in the degree of nephrocalcinosis (P < 0·05 and P < 0·005 respectively). Acetazolamide increased nephrocalcinosis by a factor of at least 10. Analysis of covariance showed that acetazolamide was no longer associated with significant nephrocalcinosis when its effects on urinary pH and magnesium were removed from its effect on nephrocalcinosis. Removal of the effect of acetazolamide on urinary citrate excretion did not alter the effect of acetazolamide in producing nephrocalcinosis. Although urinary citrate was reduced to below 10% of normal whenever nephrocalcinosis was severe, it was also reduced to below 10% in rats on diet A which had normal kidney tissue calcium content, the most acid urinary pH and the highest urinary magnesium. 5. Elevation of urinary pH and reduction in urinary magnesium excretion were therefore considered to be of major importance in the causation of experimental nephrocalcinosis; reduction in urinary citrate excretion appeared to be only of secondary importance.

A Study of the Renal Excretion of Calcium by the Production of a Constant Level of Hypercalcemia in Normal and Abnormal Human Subjects

1971 ◽  
Vol 49 (5) ◽  
pp. 469-478 ◽  
Author(s):  
William H. Shaw
Keyword(s):  
Vitamin D ◽  
Serum Calcium ◽  
Incidental Finding ◽  
Human Subjects ◽  
Renal Calculi ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Constant Level ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion

The relationship between urinary calcium excretion and serum calcium was studied at stable serum calcium levels, both normal and elevated. The linearity of this relationship being known, the slope of this line could be determined by sampling only at its lower and upper ends, that is, by measuring urine and serum calcium at a resting level and at a constant level of hypercalcemia produced by a calcium infusion. This method permitted three sets of measurements at each of the two levels, and also tended to eliminate the factor of renal delay time. The procedure was performed with normal subjects, with normals given vitamin D2 or parathyroid extract, and with subjects having hyperparathyroidism, sarcoidosis, and recurrent renal calculi. In the normal subjects the gradient of the slope appeared to indicate that there is no maximal tubular reabsorptive capacity for calcium, in the range sampled at any rate. The slopes of the various abnormal subjects mostly did not differ markedly from those of the normals. One incidental finding was that resting levels of urinary calcium excretion were significantly depressed 24 h following vitamin D2 administration, despite unchanged serum calcium levels.

Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis.

1989 ◽  
Vol 35 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D M Cowley ◽  
B C McWhinney ◽  
J M Brown ◽  
A H Chalmers
Keyword(s):  
Calcium Oxalate ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Molar Ratios ◽  
Oxalate Absorption ◽  
Stone Formers ◽  
Calcium Loading ◽  
High Calcium

Abstract Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.

Renal divalent cation excretion in secondary hypertension

1992 ◽  
Vol 83 (5) ◽  
pp. 561-565 ◽  
Author(s):  
Mario Barbagallo ◽  
Lawrence M. Resnick ◽  
R. Ernest Sosa ◽  
Mary Lou Corbett ◽  
John H. Laragh
Keyword(s):  
Blood Pressure ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Secondary Hypertension ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Hypertensive Rats ◽  
Calcium Diet ◽  
Magnesium Excretion

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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