The Causes of Hypocalcaemia in Chronic Renal Failure

1971 ◽  
Vol 40 (4) ◽  
pp. 305-315 ◽  
Author(s):  
M. Cochran ◽  
B. E. C. Nordin
Keyword(s):  
Renal Failure ◽  
Serum Calcium ◽  
Sodium Excretion ◽  
Calcium Concentration ◽  
Calcium Absorption ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Serum Calcium Concentration ◽  
Glomerular Filtrate ◽  
Urine Calcium Excretion

1. Serum calcium and phosphate, calcium absorption and calcium excretion were measured in twenty-seven cases of chronic renal failure. 2. Hypocalcaemia was present in thirteen cases and tended to be more severe in patients with the most severe degree of renal failure. 3. The hypocalcaemia could not be attributed to hyperphosphataemia since many of the patients with hypocalcaemia had normal serum phosphate concentrations. 4. Malabsorption of calcium was observed in all but three patients, and was significantly related to the degree of renal failure, but there was only a weak correlation between absorption and the serum calcium concentration. The 24 h calcium excretion was not significantly related to creatinine clearance or to calcium absorption. 5. The relation between serum calcium concentration and fasting urine calcium excretion, expressed in mg per 100 ml of glomerular filtrate, was grossly abnormal. Instead of the positive correlation previously established in normal subjects, plasma calcium and urine calcium expressed in this way were inversely related, signifying a severe reduction in the tubular reabsorption of calcium. 6. Calcium and sodium excretion (each expressed in units per 100 ml of glomerular filtrate) were significantly related, but calcium excretion and serum bicarbonate were not. However, examination of the urine calcium/sodium relationship at urine sodium excretion rates below 1·5 mEq per 100 ml of glomerular filtrate indicated that, within this range, urine calcium excretion was inversely related to serum bicarbonate concentration and positively related to urine sodium excretion. 7. We conclude that there is reduced tubular reabsorption of calcium in renal failure, and this is attributable both to metabolic acidosis and to the increased rate of sodium excretion per nephron, and that it could be a significant contributory factor in the hypocalcaemia which may be observed in renal failure without hyperphosphataemia.

Mechanism of chronic hypocalciuria with chlorthalidone: reduced calcium absorption

1984 ◽  
Vol 247 (5) ◽  
pp. F746-F752 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
F. L. Coe
Keyword(s):  
Serum Calcium ◽  
Calcium Absorption ◽  
Chronic Administration ◽  
Intestinal Calcium Absorption ◽  
Male Rats ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
X 24 ◽  
Filtered Load ◽  
Urine Calcium Excretion

Chlorthalidone, like other benzothiadiazides, lowers urine calcium excretion chronically. If intestinal calcium absorption did not fall or bone accretion did not increase, serum calcium and the filtered load of calcium would increase and urine calcium would return to pretreatment levels. To determine whether overall intestinal calcium absorption fell, we fed chlorthalidone (5 mg X kg body wt-1 X 24 h-1) to 10 adult male rats eating 15 g/day of a 0.6% calcium diet. Compared with 10 control rats, chlorthalidone reduced urine calcium [2.1 +/- 0.1 (SE) vs. 5.8 +/- 0.5 mg/6 days; P less than 0.001]. Fecal calcium rose (307 +/- 9 vs. 257 +/- 12; P less than 0.005) because percent intestinal calcium absorption fell (41 +/- 2 vs. 52 +/- 2; P less than 0.002). Twenty other rats given the same diet were injected subcutaneously with 1,25(OH)2D3 (50 ng/day). In these rats, chlorthalidone reduced urine calcium (23 +/- 3 vs. 59 +/- 3; P less than 0.001) and percent intestinal calcium absorption (60 +/- 1 vs. 66 +/- 1; P less than 0.01). With or without 1,25(OH)2D3, chronic administration of chlorthalidone reduces intestinal calcium absorption, and this reduction seems to be the mechanism that permits urine calcium excretion to remain low.

Calcium Excretion and Serum Calcium Concentration in Adult Intact and Gonadectomized Rats

Endocrinology ◽  
1968 ◽  
Vol 83 (6) ◽  
pp. 1375-1376 ◽  
Author(s):  
BERNARD F. RICE ◽  
ROY PONTHIER ◽  
M. CLINTON MILLER
Keyword(s):  
Serum Calcium ◽  
Calcium Concentration ◽  
Calcium Excretion ◽  
Serum Calcium Concentration

Increased sensitivity to 1,25(OH)2D3 in bone from genetic hypercalciuric rats

1996 ◽  
Vol 271 (1) ◽  
pp. C130-C135 ◽  
Author(s):  
N. S. Krieger ◽  
V. M. Stathopoulos ◽  
D. A. Bushinsky
Keyword(s):  
Bone Resorption ◽  
Calcium Absorption ◽  
Immunoblot Analysis ◽  
Calcium Excretion ◽  
Sprague Dawley ◽  
Urine Calcium ◽  
Fourfold Increase ◽  
Low Calcium Diet ◽  
Slot Blot Analysis ◽  
Urine Calcium Excretion

As a model of human hypercalciuria, we have selectively inbred genetic hypercalciuric stone-forming (GHS) Sprague-Dawley rats whose mean urine calcium excretion is eight to nine times greater than that of controls. A large component of this excess urine calcium excretion is secondary to increased intestinal calcium absorption, which is not due to an elevation in serum 1,25(OH)2D3, but appears to result from an increased number of intestinal 1,25(OH)2D3 receptors (VDR). When GHS rats are fed a low-calcium diet, the hypercalciuria is only partially decreased and urine calcium excretion exceeds intake, suggesting that an additional mechanism contributing to the hypercalciuria is enhanced bone demineralization. To determine if GHS rat bones are more sensitive to exogenous 1,25(OH)2D3, we cultured calvariae from neonatal (2- to 3-day-old) GHS and control rats with or without 1,25(OH)2D3 or parathyroid hormone (PTH) for 48 h at 37 degrees C. There was significant stimulation of calcium efflux from GHS calvariae at 1 and 10 nM 1,25(OH)2D3, whereas control calvariae showed no significant response to 1,25(OH)2D3 at any concentration tested. In contrast, PTH induced similar bone resorption in control and GHS calvariae. Immunoblot analysis demonstrated a fourfold increase in the level of VDR in GHS calvariae compared with control calvariae, similar to the increased intestinal receptors described previously. There was no comparable change in VDR RNA levels as measured by slot blot analysis, suggesting the altered regulation of the VDR occurs posttranscriptionally. That both bone and intestine display an increased amount of VDR suggests that this may be a systemic disorder in the GHS rat and that enhanced bone resorption may be responsible, in part, for the hypercalciuria in the GHS rat.

scholarly journals Inhibition of calbindin D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria.

1998 ◽  
Vol 9 (8) ◽  
pp. 1416-1426
Author(s):  
C W Yang ◽  
J Kim ◽  
Y H Kim ◽  
J H Cha ◽  
S Y Mim ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Serum Calcium ◽  
Protein Level ◽  
Rat Kidney ◽  
Urinary Calcium ◽  
Calcium Handling ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
Calbindin D28k ◽  
Urine Calcium Excretion

A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting.

Mechanism of chronic hypercalciuria with furosemide: increased calcium absorption

1986 ◽  
Vol 251 (1) ◽  
pp. F17-F24 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
C. B. Langman ◽  
F. L. Coe
Keyword(s):  
Calcium Absorption ◽  
Chronic Administration ◽  
Urinary Calcium ◽  
Intestinal Calcium Absorption ◽  
Calcium Excretion ◽  
Calcium Balance ◽  
Urine Calcium ◽  
Calcium Diet ◽  
Filtered Load ◽  
Urine Calcium Excretion

Furosemide produces chronic hypercalciuria. The source of the additional urinary calcium is not known but must be either bone mineral or calcium absorbed by the intestine. Without bone calcium dissolution or increased absorption the filtered load of calcium would fall and urinary calcium excretion would return to pretreatment levels. To determine whether furosemide alters intestinal calcium absorption, we fed furosemide (75 mg . kg body-1 wt . day-1) to 11 rats eating 15 g/day of a 0.60% calcium diet. Compared with 11 control rats, furosemide increased urine calcium (15.6 +/- 0.8 mg/5 days vs. 4.1 +/- 0.3, P less than 0.001). Fecal calcium excretion fell (194 +/- 7 mg/5 days vs. 223 +/- 12, P less than 0.05), indicating an increase in intestinal calcium absorption sufficient to sustain the hypercalciuria. The increase in absorption occurred without an increase in the level of serum 1,25-dihydroxycholecalciferol (180 +/- 20 pg/ml vs. 220 +/- 16, furosemide vs. control, respectively, P = NS). To determine whether the intestinal effect of furosemide persists after the initial sodium diuresis abates, we analyzed only the last 3 days of balance. Again, rats fed furosemide had increased urine excretion and intestinal absorption of calcium, so that net calcium balance was not different from that of controls. Twelve additional rats were fed a 0.02% calcium diet to which 35 mg . kg body wt-1 . day-1 of furosemide was added. Compared with eleven controls, urine calcium increased and fecal calcium excretion again fell, but balance was not different. Chronic administration of furosemide increases intestinal calcium absorption enough to permit urine calcium excretion to remain elevated without the necessity for bone dissolution.

Effect of Diet Cola on Urine Calcium Excretion.

2010 ◽  
pp. P2-198-P2-198
Author(s):  
NS Larson ◽  
R Amin ◽  
C Olsen ◽  
MA Poth
Keyword(s):  
Calcium Excretion ◽  
Urine Calcium ◽  
Urine Calcium Excretion

scholarly journals Effects of Ammonium Chloride Supplements on Serum Calcium Concentration in Pre-parturient Dairy Cows

2002 ◽  
Vol 55 (4) ◽  
pp. 219-222 ◽  
Author(s):  
Naoto SUZUKI ◽  
Akihiro DAIRAKU ◽  
Tomio KATAGAI ◽  
Gensei TSUNODA ◽  
Kazuyuki SUZUKI ◽  
...  
Keyword(s):  
Dairy Cows ◽  
Ammonium Chloride ◽  
Serum Calcium ◽  
Calcium Concentration ◽  
Serum Calcium Concentration
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