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.

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.

scholarly journals Vitamin D metabolite-mediated hypercalcemia and hypercalciuria patients with AIDS- and non-AIDS-associated lymphoma

Blood ◽  
1989 ◽  
Vol 73 (1) ◽  
pp. 235-239 ◽  
Author(s):  
JS Adams ◽  
M Fernandez ◽  
MA Gacad ◽  
PS Gill ◽  
DB Endres ◽  
...  
Keyword(s):  
Los Angeles ◽  
Medical Center ◽  
Elevated Serum ◽  
Urinary Calcium ◽  
Disease Stage ◽  
Additional Patient ◽  
Calcium Excretion ◽  
Adult T Cell Leukemia ◽  
Severe Hypercalcemia ◽  
Excretion Rates

Abstract Fifteen patients with lymphoma and hypercalcemia (greater than or equal to 11.0 mg/dL) were identified by screening the serum chemistry profile obtained from patients upon admission to the Los Angeles County/USC Medical Center. Seven of the 15 (47%) possessed a frankly elevated serum concentration of 1,25-dihydroxyvitamin D [1,25-(OH)2-D]. An additional patient with severe hypercalcemia (16.2 mg/dL) had a serum 1,25-(OH)2-D concentration in the midnormal range, not a suppressed value. To examine the potential existence of hypercalciuria in absence of overt hypercalcemia, prospective screening of 23 normocalcemic patients with lymphoma was undertaken. Four of the 23 patients (17%) had increased fractional urinary calcium excretion rates (0.35 +/- 0.3 mg calcium/100 mL glomerular filtrate [GF], mean +/- SE; normal, less than 0.16 mg/100 mL GF); two of the hypercalciuric patients had a frankly elevated serum 1,25-(OH)2-D concentration. Of the 19 hypercalcemic/hypercalciuric lymphoma patients identified, none had an elevated serum immunoreactive parathyroid hormone concentration. Fourteen of the 19 hypercalcemic/hypercalciuric patients (74%) suffered from B-cell neoplasms, three had Hodgkin's lymphoma, and two had adult T-cell leukemia/lymphoma. All hypercalcemic/hypercalciuric patients had widespread disease (stage III or IV). Six patients, four with hypercalcemia and two with hypercalciuria, had acquired immunodeficiency syndrome (AIDS). These data suggest that the deregulated synthesis of a 1,25-(OH)2-D-like metabolite is a common cause of hypercalcemia and hypercalciuria in patients with lymphoma including patients with AIDS-associated tumors.

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.

Effect of calcitonin on calcium and magnesium transport in rat nephron

1980 ◽  
Vol 238 (6) ◽  
pp. E573-E578 ◽  
Author(s):  
G. A. Quamme
Keyword(s):  
Calcium Concentration ◽  
Transport Model ◽  
Distal Tubule ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Loop Of Henle ◽  
Plasma Calcium Concentration ◽  
Calcium And Magnesium ◽  
Magnesium Excretion

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.

Endogenous ANP augments fractional excretion of Pi, Ca, and Na in rats with reduced renal mass

1988 ◽  
Vol 255 (6) ◽  
pp. F1091-F1097 ◽  
Author(s):  
F. V. Ortola ◽  
B. J. Ballermann ◽  
B. M. Brenner
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Sodium Phosphate ◽  
Renal Mass ◽  
Sodium Intake ◽  
Fractional Excretion ◽  
Sodium Restriction ◽  
Calcium And Magnesium ◽  
Excretion Rates ◽  
Magnesium Excretion

Atrial natriuretic peptide (ANP) infusion increases fractional excretion of many solutes including sodium, chloride, bicarbonate, phosphate, calcium, and magnesium. Because fractional excretion of these solutes increases with advancing renal disease, and because plasma ANP levels are known to be elevated in chronic renal failure, we sought to determine whether ANP mediates increased solute excretion rates per nephron in rats following extensive renal ablation, a model of chronic renal failure. Because sodium restriction decreases plasma ANP levels in the setting of reduced renal mass, we also determined the effect of sodium restriction on sodium, phosphate, calcium, and magnesium excretion rates in rats with 5/6 nephrectomy (NX). We also assessed whether high endogenous ANP levels influence fractional sodium, phosphate, calcium, and magnesium excretion in rats with 5/6 NX, by inhibiting ANP action via infusion of a high-affinity ANP antiserum. Whole-kidney glomerular filtration rate in 5/6 NX rats averaged approximately one-third that of shams, and plasma ANP levels were significantly elevated in these rats above those of shams, but to a lesser extent in rats on low- vs. high-salt intakes. Fractional sodium, phosphate, and calcium, but not magnesium excretion rates were significantly greater in 5/6 NX rats on the higher sodium intake compared with those in 5/6 NX rats on the lower sodium intake. Moreover, in 5/6 NX rats on the higher sodium intake, ANP antiserum significantly reduced fractional sodium, phosphate, and calcium excretion, but was without effect on magnesium excretion. These data implicate endogenous ANP in promoting the adaptive increase in sodium, phosphate, calcium, but not magnesium excretion per nephron in chronic renal disease.

Acute effect of calcitonin on rat renal electrolyte transport

1981 ◽  
Vol 240 (1) ◽  
pp. F12-F16 ◽  
Author(s):  
S. Carney ◽  
L. Thompson
Keyword(s):  
Physiological Role ◽  
Fractional Excretion ◽  
Fold Increase ◽  
Plasma Calcium ◽  
Electrolyte Transport ◽  
Calcium Excretion ◽  
Phosphate Excretion ◽  
Renal Electrolyte Transport ◽  
Calcium And Magnesium ◽  
Magnesium Excretion

Renal clearance studies were performed on parathyroid-intact and acutely thyroparathyroidectomized (TPTX) rats to clarify calcitonin (CT) action on renal electrolyte transport. Although CT (0.15 U x 100 g body wt-1 x h-1) reduced fractional excretion of calcium and magnesium by 72 and 46%, respectively, in TPTX rats without altering sodium and phosphate excretion, a 10-fold increase in CT (1.5 U) caused a smaller reduction in calcium and magnesium excretion and significantly increased sodium and phosphate excretion. A higher CT dose (15 U) did not alter calcium excretion, increased magnesium excretion, and caused an even greater increase in sodium and phosphate excretion. Results in parathyroid-intact animals were similar. Despite the fall in plasma calcium following CT administration, the filtered calcium load was unaltered due to a concomitant increase in glomerular filtration rate. Calcium infusion prior to CT (0.15 U) prevented a detectable fall in plasma calcium concentration. However, a 45% fall in fractional calcium excretion occurred despite the significant increase in filtered calcium. These data suggest that the physiological role of calcitonin on the nephron is to conserve calcium. Reports of increased electrolyte excretion presumably reflect a depressant effect of pharmacological doses of CT on nephron function.

Effect of chlorothiazide on renal calcium and magnesium handling in the hamster

1982 ◽  
Vol 60 (9) ◽  
pp. 1160-1165 ◽  
Author(s):  
Norman L. M. Wong ◽  
Gary A. Quamme ◽  
John H. Dirks
Keyword(s):  
Distal Tubule ◽  
Sodium Concentration ◽  
Urinary Calcium ◽  
Sodium Reabsorption ◽  
Calcium Excretion ◽  
Acute Administration ◽  
Sodium Calcium ◽  
Clearance Studies ◽  
Calcium And Magnesium ◽  
Distal Delivery

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.

scholarly journals STANNIECTOMY INCREASES RENAL MAGNESIUM AND CALCIUM EXCRETION IN FRESHWATER NORTH AMERICAN EELS (ANGUILLA ROSTRATA)

1993 ◽  
Vol 181 (1) ◽  
pp. 107-118
Author(s):  
D. G. Butler
Keyword(s):  
North American ◽  
Calcium Concentration ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Magnesium Concentration ◽  
Calcium Excretion ◽  
Plasma Calcium Concentration ◽  
Magnesium Excretion ◽  
Plasma Magnesium ◽  
American Eels

The corpuscles of Stannius are linked to the renal transport of magnesium in freshwater North American eels. The urinary magnesium concentration and rate of magnesium excretion increased 3 days after the corpuscles had been removed, a trend which continued throughout a 14 day observation period. There was no overall change in urine flow rates except for a brief 50 % reduction 2 days after stanniectomy. Plasma magnesium concentrations drifted downward after stanniectomy. In contrast, plasma calcium concentrations increased significantly within 2 days following stanniectomy and they continued to increase thereafter. Urinary calcium concentrations and the rate of urinary calcium excretion increased 7 days after stanniectomy, implying that the renal response was subject to the increase in plasma calcium concentration: the urine/plasma calcium ratio remained constant. Even though the urinary calcium concentration increased after stanniectomy, the increase in urinary magnesium concentration was proportionally greater.

scholarly journals Calcium sensitivity of dicarboxylate transport in cultured proximal tubule cells

2011 ◽  
Vol 300 (2) ◽  
pp. F425-F432 ◽  
Author(s):  
Kathleen S. Hering-Smith ◽  
Faith R. Schiro ◽  
Ana M. Pajor ◽  
L. Lee Hamm
Keyword(s):  
Proximal Tubule ◽  
Transport Process ◽  
Urinary Calcium ◽  
Extracellular Calcium ◽  
Calcium Excretion ◽  
Proximal Tubule Cells ◽  
Citrate Transport ◽  
Dicarboxylate Transport ◽  
Tubule Cells ◽  
Urinary Citrate

Urinary citrate is an important inhibitor of calcium nephrolithiasis and is primarily determined by proximal tubule reabsorption. The major transporter to reabsorb citrate is Na+-dicarboxylate cotransporter (NaDC1), which transports dicarboxylates, including the divalent form of citrate. We previously found that opossum kidney (OK) proximal tubule cells variably express either divalent or trivalent citrate transport, depending on extracellular calcium. The present studies were performed to delineate the mechanism of the effect of calcium on citrate and succinate transport in these cells. Transport was measured using isotope uptake assays. In some studies, NaDC1 transport was studied in Xenopus oocytes, expressing either the rabbit or opossum ortholog. In the OK cell culture model, lowering extracellular calcium increased both citrate and succinate transport by more than twofold; the effect was specific in that glucose transport was not altered. Citrate and succinate were found to reciprocally inhibit transport at low extracellular calcium (<60 μM), but not at normal calcium (1.2 mM); this mutual inhibition is consistent with dicarboxylate transport. The inhibition varied progressively at intermediate levels of extracellular calcium. In addition to changing the relative magnitude and interaction of citrate and succinate transport, decreasing calcium also increased the affinity of the transport process for various other dicarboxylates. Also, the affinity for succinate, at low concentrations of substrate, was increased by calcium removal. In contrast, in oocytes expressing NaDC1, calcium did not have a similar effect on transport, indicating that NaDC1 could not likely account for the findings in OK cells. In summary, extracellular calcium regulates constitutive citrate and succinate transport in OK proximal tubule cells, probably via a novel transport process that is not NaDC1. The calcium effect on citrate transport parallels in vivo studies that demonstrate the regulation of urinary citrate excretion with urinary calcium excretion, a process that may be important in decreasing urinary calcium stone formation.

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