THE SUPPRESSION OF URINARY CALCIUM AND MAGNESIUM BY ORAL SODIUM PHYTATE: A PRELIMINARY REPORT

1956 ◽  
Vol 64 (3) ◽  
pp. 343-350 ◽  
Author(s):  
Philip H. Henneman ◽  
Evelyn L. Carroll ◽  
Fuller Albright
Author(s):  
Il Hwan Oh ◽  
Chor Ho Jo ◽  
Sua Kim ◽  
Sungsin Jo ◽  
Sungjin Chung ◽  
...  

Urinary calcium and magnesium wasting is a characteristic feature of metabolic acidosis, and this study focused on the role of the thick ascending limb of Henle's loop in metabolic acidosis-induced hypercalciuria and hypermagnesiuria because thick ascending limb is an important site of paracellular calcium and magnesium reabsorption. Male Sprague-Dawley rats were used to determine the effects of acid loading (by adding NH4Cl 7.2 mmol/220 g BW/d to food slurry for 7 days) on renal expression of claudins and then to evaluate whether the results were reversed by antagonizing calcium-sensing receptor (using NPS-2143). At the end of each animal experiment, the kidneys were harvested for immunoblotting, immunofluorescence microscopy and qPCR analysis of claudins and the calcium-sensing receptor. As expected, NH4Cl loading lowered urinary pH and increased excretion of urinary calcium and magnesium. In NH4Cl-loaded rats, renal protein and mRNA expression of claudin-16, and claudin-19 decreased compared with controls. However, claudin-14 protein and mRNA increased in NH4Cl-loaded rats. Consistently, the calcium-sensing receptor protein and mRNA were upregulated in NH4Cl-loaded rats. All these changes were reversed by NPS-2143 coadministration and were confirmed using immunofluorescence microscopy. Hypercalciuria and hypermagnesiuria in NH4Cl-loaded rats were significantly ameliorated by NPS-2143 coadministration as well. We conclude that in metabolic acidosis, claudin-16 and claudin-19 in the thick ascending limb are downregulated to produce hypercalciuria and hypermagnesiuria via the calcium-sensing receptor.


1969 ◽  
Vol 47 (7) ◽  
pp. 619-626 ◽  
Author(s):  
A. Gonda ◽  
N. Wong ◽  
J. F. Seely ◽  
J. H. Dirks

The effects of unilateral vasodilatation and alterations in the mean arterial pressure upon the renal handling of calcium and magnesium were studied by clearance methods in dogs. Unilateral vasodilatation was produced by infusion of acetylcholine or bradykinin into the left renal artery, while arterial pressure was altered by aortic constriction, carotid occlusion and vagotomy, or by systemic infusion of angiotensin. Urinary electrolyte excretion was increased markedly by the infusion of each vasodilator and also varied directly with the mean arterial pressure, despite the absence of any significant changes in the filtered load. The fractional excretion of both calcium and magnesium correlated significantly with that of sodium. These results indicate that acute changes in renal hemodynamics modify the tubular reabsorption of divalent cations as well as alter sodium reabsorption.


1980 ◽  
Vol 238 (6) ◽  
pp. E573-E578 ◽  
Author(s):  
G. A. Quamme

Renal calcium and magnesium reabsorption was investigated in young, thyroparathyroidectomized rats receiving synthetic salmon calcitonin. Kidney and tubular function was assessed by clearance and in vivo microperfusion techniques, respectively. Calcitonin reduced urinary calcium and magnesium excretion that was attributed to increased reabsorption within the loop of Henle. This enchanced reabsorption was independent of parathyroid hormone; however, it is contingent on a decline in plasma calcium concentration. Prevention of hypocalcemia by CaCl2 infusion in rats acutely administered calcitonin resulted in loop function comparable to animals not receiving the hormone. Calcitonin had little effect on proximal tubule or distal tubule electrolyte reabsorption. These results are consistent with a transport model for calcium and magnesium in the loop of Henle involving a contraluminal transfer step modulated by absolute extracellular calcium or magnesium. Furthermore, these studies suggest that the discrepancies present in the literature concerning renal effects of calcitonin on electrolyte reabsorption are due to variations in observed hormone action, namely, the effect on plasma calcium concentration.


Author(s):  
A. Trinchieri ◽  
A. Mandressi ◽  
G. Zanetti ◽  
E. Patelli ◽  
G. Donghi ◽  
...  

1982 ◽  
Vol 60 (9) ◽  
pp. 1160-1165 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
John H. Dirks

Recollection micropuncture and clearance studies were performed on 21 thyroparathyroidcetomized hamsters to characterize the effect of chlorothiazide on tubular sodium, calcium, and magnesium transport. Acute administration of chlorothiazide resulted in a marked natriuresis while urinary calcium excretion fell and magnesium remained unchanged. The fraction of sodium, calcium, and magnesium remaining at the late proximal tubule increased modestly from 65 ± 4 to 75 ± 3, 68 ± 3 to 75 ± 4, and 78 ± 4 to 85 ± 2%, respectively. Distal tubular fluid to ultrafilterable plasma (TF/UF) sodium concentration rose from 0.24 ± 0.03 to 0.44 ± 0.04 whereas distal TF/UFCa concentration fell from 0.58 ± 0.05 to 0.38 ± 0.06. The fraction of sodium remaining at the distal tubule rose from 4.0 ± 1.4 to 10.0 ± 1.4% while that of calcium decreased from 10.2 ± 1.1 to 7.6 ± 1.2% following administration of chlorothiazide. No change was observed in distal delivery of magnesium. Thus chlorothiazide acted in the distal tubule to decrease sodium reabsorption, enhance calcium transport, and had little effect on distal magnesium reabsorption. These data are consistent with the distal tubular action of chlorothiazide which is independent of parathyroid hormone.


1970 ◽  
Vol 39 (5) ◽  
pp. 605-623 ◽  
Author(s):  
A. Z. Györy ◽  
K. D. G. Edwards ◽  
J. Robinson ◽  
A. A. Palmer

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.


The Lancet ◽  
1969 ◽  
Vol 293 (7607) ◽  
pp. 1214-1215
Author(s):  
MaryG. Mcgeown ◽  
D.G. Oreopoulos ◽  
R.W. White

1988 ◽  
Vol 75 (2) ◽  
pp. 203-207 ◽  
Author(s):  
Viroon Mavichak ◽  
Christopher M. L. Coppin ◽  
Norman L. M. Wong ◽  
John H. Dirks ◽  
Valerie Walker ◽  
...  

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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