Calcium metabolism in paravertebral ligamentous ossification

1985 ◽  
Vol 109 (3) ◽  
pp. 428-432 ◽  
Author(s):  
Yoh Takuwa ◽  
Toshio Matsumoto ◽  
Takahide Kurokawa ◽  
Masashi Iizuka ◽  
Yuichi Hoshino ◽  
...  
Keyword(s):  
Calcium Absorption ◽  
Mineral Metabolism ◽  
Normal Serum ◽  
Intestinal Calcium Absorption ◽  
Calcium Excretion ◽  
Baseline Serum ◽  
Oral Calcium ◽  
Significant Difference ◽  
Calcium Load ◽  
Serum Inorganic Phosphate

Abstract. Twenty-eight patients with paravertebral ligamentous ossification (PVLO) and 11 control subjects were studied in an attempt to examine possible involvement of disturbances in mineral metabolism in the development of PVLO. No significant difference in baseline serum calcium and fasting urinary calcium excretion was found between patients with PVLO and controls. Patients with PVLO showed lower serum inorganic phosphate (Pi) and tubular reabsorptive capacity for Pi (TmP/GFR) than controls. Basal nephrogenous cyclic 3',5'-AMP (NcAMP) was elevated in some patients with PVLO. A significant inverse relationship was found between basal TmP/GFR and NcAMP in patients with PVLO (r = −0.50; P < 0.01). Compared with controls, patients with PVLO had significantly lower calciuric responses to an oral calcium load (P < 0.05), suggesting decreased intestinal calcium absorption. Furthermore, a significant inverse correlation was found between basal NcAMP and the calciuric response in patients with PVLO (r = −0.42; P < 0.05). Serum 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D (1,25(OH)2D) levels were not significantly different between the two groups. The size of ossified areas in paravertebral ligaments estimated from spinal radiograms inversely correlated with the calciuric response to the oral calcium load (r = −0.50; P < 0.01). These data demonstrate that the development of PVLO is associated with decreased intestinal calcium absorption in the face of normal serum 1,25(OH)2D level. Thus, together with previous observations showing a high incidence of PVLO in patients with hypoparathyroidism or familial hypophosphataemic rickets/osteo-malacia, the present results suggest that the defect in the action of 1,25(OH)2D may underlie the development of PVLO.

Critical appraisal of oral calcium load test for indirect assessment of intestinal calcium absorption

Urology ◽  
1979 ◽  
Vol 14 (3) ◽  
pp. 251-255 ◽  
Author(s):  
Kashayar Sakhaee ◽  
Roy Peterson ◽  
Cheryl Northcutt ◽  
Charles Y.C. Pak
Keyword(s):  
Critical Appraisal ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption ◽  
Load Test ◽  
Oral Calcium ◽  
Indirect Assessment ◽  
Calcium Load

Hypercalciuria and Hematuria

1986 ◽  
Vol 7 (10) ◽  
pp. 295-318
Keyword(s):  
Urinary Calcium ◽  
Normal Serum ◽  
Urinary Concentration ◽  
Calcium Excretion ◽  
Oral Calcium ◽  
Normal Serum Calcium ◽  
Calcium Reabsorption ◽  
Calcium Load ◽  
Absorptive Hypercalciuria ◽  
Renal Hypercalciuria

Hypercalciuria in children is diagnosed when the urinary calcium excretion is greater than 4.0 mg/kg in 24 hours, the ratio of urinary concentration of calcium to creatinine (UCa/UCr) is greater than 0.20, and there is normal serum calcium. Hypercalciuria may be the result of increased intestinal absorption of calcium (absorptive hypercalciuria) or an impaired proximal tubular defect in calcium reabsorption (renal hypercalciuria). Oral calcium load tests will differentiate the two types of hypercalciuria. Elevated fasting UCa/UCr with normal levels of parathormone (PTH) or urinary cyclic-AMP indicates renal hypercalciuria. After an oral calcium load, the UCa/UCr ratio will be greater than normal in absorptive hypercalciuria. However, Hymes and Warshaw suggest that both subtypes may coexist in some patients.

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.

The Measurement of Intestinal Calcium Absorption by External Radioisotope Counting: Application to Study of Nephrolithiasis

1970 ◽  
Vol 39 (1) ◽  
pp. 95-106 ◽  
Author(s):  
M. R. Wills ◽  
E. Zisman ◽  
J. Wortsman ◽  
R. G. Evens ◽  
C. Y. C. Pak ◽  
...  
Keyword(s):  
Calcium Absorption ◽  
Scintillation Counter ◽  
Renal Stones ◽  
Normal Subjects ◽  
Total Radioactivity ◽  
Urinary Calcium ◽  
Intestinal Calcium Absorption ◽  
Absolute Amount ◽  
Calcium Load ◽  
Fractional Calcium Absorption

1. Gastro-intestinal absorption of calcium was studied in man by the measurement of forearm radioactivity in a large-volume liquid scintillation counter following separate oral and intravenous doses of 47CaCl2. From the ratio of the percentages of total radioactivity appearing in the forearm following these separate determinations the fractional absorption of calcium was estimated. 2. Changes of forearm radioactivity with time following the administration of this isotope were studied; evidence is presented that the radioactivity in the forearm at 4 h after administration of the isotope gives a valid assessment of fractional calcium absorption. 3. Fractional calcium absorption determined by this technique correlated well with the net calcium absorption as determined from stool radioactivity after oral administration of isotope. 4. In normal subjects it was shown that fractional calcium absorption measured by this technique varies inversely with the stable calcium load and that the absolute amount of calcium absorbed from given loads increases with the size of the load in the range 20–1000 mg calcium. 5. Gastro-intestinal calcium absorption was measured at various oral calcium loads in a group of fifteen patients with recurrent calcium-containing renal stones. All the patients were normocalcaemic; some had hypercalciuria. In the patients with hypercalciuria, calcium absorption, fractional and absolute, was significantly increased at all calcium loads as compared to that of patients with normal urinary calcium. 6. It is concluded that hyperabsorption of calcium from the gastro-intestinal tract plays a crucial role in the aetiology of hypercalciuria, probably by causing an increase in the renal filtered calcium load.

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.

scholarly journals Severe hypercalcemia and hypernatremia in a patient treated with canagliflozin

2015 ◽  
Vol 2015 ◽  
Author(s):  
Arshpreet Kaur ◽  
Stephen J Winters
Keyword(s):  
Mental Status ◽  
Water Loss ◽  
Calcium Absorption ◽  
Free Water ◽  
Intestinal Calcium Absorption ◽  
Calcium Excretion ◽  
List Type ◽  
Close Monitoring ◽  
Osmotic Diuresis ◽  
Severe Hypercalcemia

Summary Drugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Inhibition of SGLT2 activity also reduces sodium reabsorption, which together with glycosuria produces a mild diuretic effect with the potential for dehydration and hyperkalemia. We report on a 60-year-old man with uncontrolled type 2 diabetes treated with insulin, glimepiride, metformin and canagliflozin, who was admitted with altered mental status after a syncopal episode. He had a 1-week history of ingestion of Tums for heartburn followed by poor appetite and lethargy. Laboratory work-up showed acute kidney injury, diabetic ketoacidosis (DKA), and parathyroid hormone-independent severe hypercalcemia of 17.4 mg/dl. DKA resolved with insulin treatment, and saline hydration led to improvement in hypercalcemia and renal function over 48 h, but was accompanied by a rapid increase in the serum sodium concentration from 129 to 162 mmol/l despite changing fluids to 0.45% saline. Urine studies were consistent with osmotic diuresis. Hypernatremia was slowly corrected with hypotonic fluids, with improvement in his mental status over the next 2 days. This is the first report of hypercalcemia associated with the use of a SLGT2 inhibitor. Although the exact mechanism is unknown, canagliflozin may predispose to hypercalcemia in patients ingesting excessive calcium because of dehydration from osmotic diuresis, with reduced calcium excretion and possible increased intestinal calcium absorption. Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss. Learning points Canagliflozin, an SGLT2 inhibitor, may cause hypercalcemia in susceptible patients. Although the exact mechanisms are unknown, dehydration from osmotic diuresis and increased intestinal calcium absorption play a role. Close monitoring of serum calcium levels is recommended in patients treated with SGLT2 inhibitors who are elderly, have established hypercalcemia, or take oral calcium supplements. Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss in susceptible patients.

Effects of chlorothiazide on 1,25-dihydroxyvitamin D3, parathyroid hormone, and intestinal calcium absorption in the rat

1982 ◽  
Vol 242 (6) ◽  
pp. G575-G581 ◽  
Author(s):  
M. J. Favus ◽  
F. L. Coe ◽  
S. C. Kathpalia ◽  
A. Porat ◽  
P. K. Sen ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Dihydroxyvitamin D3 ◽  
Ussing Chambers ◽  
1,25 Dihydroxyvitamin D3 ◽  
Descending Colon

Previous studies have shown that thiazide diuretic agents reverse secondary hyperparathyroidism and reduce circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium absorption rates in patients with idiopathic hypercalciuria of the renal-leak variety. We have investigated whether thiazides can reverse the secondary increase in serum parathyroid hormone (PTH) and 1,25(OH)2D3 levels or intestinal calcium absorption induced by feeding rats a diet low in calcium (LCD, 0.02% calcium) but adequate in phosphorus and vitamin D. We found that LCD increased circulating immunoreactive PTH [chow vs. LCD, 0.52 +/- 0.06 vs. 1.06 +2- 0.1 (SE) ng/ml, P less than 0.001], 1,25(OH)2D3 (chow vs. LCD, 101 +/- 15 vs. 325 +/- 38 pg/ml, P less than 0.001), calcium uptake by everted gut sacs from duodenum, ileum, and descending colon, and net calcium absorption by descending colon studied in Ussing chambers in vitro. Chlorothiazide (CTZ) prevented the increase in PTH during LCD (chow + CTZ vs. LCD + CTZ, 0.69 +/- 0.07 vs. 0.73 +/- 0.06, NS) but not the increase in 1,25(OH)2D3 (chow + CTZ vs. LCD + CTZ, 88 +/- 10 vs. 277 +/- 31, P less than 0.002) or intestinal calcium transport. The drug caused no change in serum 1,25(OH)2D3 or intestinal calcium absorption in rats fed normal chow. In rats given exogenous 1,25(OH)2D3 to stimulate intestinal calcium absorption, CTZ reduced urine calcium excretion greatly but did not alter intestinal calcium absorption.

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