Effect of renal insufficiency on gastrointestinal transport of calcium

1965 ◽  
Vol 209 (1) ◽  
pp. 141-145 ◽  
Author(s):  
David M. Kessner ◽  
Franklin H. Epstein
Keyword(s):  
Vitamin D ◽  
Metabolic Acidosis ◽  
Renal Insufficiency ◽  
Calcium Transport ◽  
Intestinal Transport ◽  
Chemical Gradient ◽  
Subtotal Nephrectomy ◽  
Solution Bathing ◽  
High Doses ◽  
Isolated Rat

Chronic experimental renal insufficiency induced by subtotal nephrectomy decreased the ability of the isolated rat duodenal gut sac to transport calcium against a chemical gradient. The defect in intestinal transport was not reproduced by metabolic acidosis, uremia of short duration, or addition of urea to the ambient solution bathing the gut sac. The transport of calcium by the intestine of uremic rats was increased by pretreatment with high doses of vitamin D and, at the dose level employed, there was no evidence of "resistance" to vitamin D. Dietary restriction depressed the gastrointestinal transport of calcium and may play a role in producing the defect in calcium transport of chronic uremia.

RENAL TUBULAR DYSFUNCTION COMPLICATING THE NEPHROTIC SYNDROME

PEDIATRICS ◽  
1960 ◽  
Vol 26 (1) ◽  
pp. 75-85
Author(s):  
Gunnar B. Stickler ◽  
Alvin B. Hayles ◽  
Marschelle H. Power ◽  
John A. Ulrich
Keyword(s):  
Vitamin D ◽  
Nephrotic Syndrome ◽  
Metabolic Acidosis ◽  
Renal Insufficiency ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Renal Tubules ◽  
Renal Tubular ◽  
Amino Aciduria ◽  
Unusual Type

Observations on two girls in whom an unusual type of chronic renal insufficiency developed many months after the onset of nephrotic syndrome are reported. Each patient became free of edema in spite of persistent massive proteinuria. Growth was retarded and rickets and attacks of tetany developed. The chemical disturbances of the blood were characterized by hypocalcemia, hypokalemia, azotemia and metabolic acidosis. Hyposthenuria, proteinuria, amino-aciduria, and minimal erythrocyturia, cylindruria and glycosuria were present. Healing of the rickets and cessation of attacks of tetany followed the administration of vitamin D and calcium salts. Prednisone was administered to one patient and thereafter proteinuria decreased and renal tubular function improved. Both girls are relatively asymptomatic 11 and 9 years after the onset of nephrotic syndrome, although they are rather small and still have evidence of renal disease. It is possible that cells of the renal tubules have been damaged as a result of prolonged massive proteinuria.

Duodenal and ileal calcium absorption in the rat and effects of vitamin D

1983 ◽  
Vol 244 (6) ◽  
pp. G695-G700 ◽  
Author(s):  
D. Pansu ◽  
C. Bellaton ◽  
C. Roche ◽  
F. Bronner
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Cytosolic Calcium ◽  
Chemical Gradient ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Loop Procedure ◽  
Proximal Intestine

An in situ ligated loop procedure was applied to dissect transmural calcium transport in the intestine into two components, a saturable and a nonsaturable process. The existence of two such processes was confirmed in the duodenum, but ileal calcium transport was devoid of the saturable component. There was a small saturable component in the upper jejunum. The level of CaBP, the vitamin D-dependent cytosolic calcium-binding protein (Mr, approximately or equal to 9,000), corresponded to the magnitude of the saturable component. No CaBP was detected in the ileum. Vitamin D dependence of the saturable component was established by inducing it in the duodenum of vitamin D-deficient animals following intraperitoneal injection of 1,25-dihydroxyvitamin D3. In these same animals, conversely, the ileum did not respond to exogenous 1,25-dihydroxyvitamin D3. This confirms the absence in the ileum of the saturable component of transmural calcium movement and the fact that the nonsaturable component is not vitamin D dependent. Everted sac experiments also showed that duodenal sacs from vitamin D-replete or -repleted animals transported calcium against a chemical gradient, whereas ileal sacs did not. Vitamin D regulation of intestinal calcium absorption thus occurs only in the proximal intestine, even though calcium is absorbed down its chemical gradient all along the small intestine.

scholarly journals Metabolism and biological activity of 25-fluorocholecalciferol, 24-dehydrocholecalciferol and 25-dehydrocholecalciferol in the rat

1979 ◽  
Vol 182 (1) ◽  
pp. 1-9 ◽  
Author(s):  
B L Onisko ◽  
H K Schnoes ◽  
H F DeLuca ◽  
R S Glover
Keyword(s):  
Vitamin D ◽  
Biological Activity ◽  
Intestinal Transport ◽  
Side Chain ◽  
Biological Responses ◽  
Natural Hormone ◽  
Physiological Dose ◽  
High Doses ◽  
Potential Inhibitors

Three side-chain analogues of cholecalciferol (vitamin D3) modified at C-25, namely 25-fluorocholecalciferol, 24-dehydrocholecalciferol and 25-dehydrocholecalciferol, conceived as potential inhibitors of the cholecalciferol 25-hydroxylase have been prepared and tested in the rat. These compounds markedly diminish conversion in vivo of cholecalciferol into 25-hydroxycholecalciferol, but are not antagonists of vitamin D action, because they themselves possess significant biological activity in vivo. Each compound is capable of stimulating the intestinal transport of calcium and the mobilization of calcium from bone in vitamin D-deficient rats. Biological responses equivalent to those generated by a physiological dose of cholecalciferol (0.05 microgram) are produced, however, only when the analogues are administered at high doses (5-50 microgram). The biological activity of 24-dehydrocholecalciferol and 25-dehydrocholecalciferol is shown to result from conversion, in vivo, to the natural hormone, 1 alpha,25-dihydroxycholecalciferol, whereas 25-fluorocholecalciferol is metabolically activated in the rat by hydroxylation to 1 alpha-hydroxy-25-fluorocholecalciferol. This latter conversion is the first reported example of the 1 alpha-hydroxylation of a vitamin D compound lacking the 25-hydroxy group.

Indirect Inhibition of the Biosynthesis of 1,25-Dihydroxycholecalciferol in Rats Treated with a Diphosphonate

1973 ◽  
Vol 44 (4) ◽  
pp. 335-347 ◽  
Author(s):  
L. F. Hill ◽  
G. A. Lumb ◽  
E. B. Mawer ◽  
S. W. Stanbury
Keyword(s):  
Vitamin D ◽  
Vitamin D3 ◽  
Calcium Transport ◽  
Direct Action ◽  
Intestinal Transport ◽  
Intravenous Dose ◽  
Single Intravenous Dose ◽  
Normal Response ◽  
Intestinal Calcium Transport ◽  
Normal Production

1. Rats treated with disodium ethane-1-hydroxy-1,1-diphosphonate for 14 days developed rickets and impaired intestinal calcium transport, even when receiving large amounts of cholecalciferol (vitamin D3). 2. Vitamin d-deficient rats treated with the diphosphonate, and irrespective of the duration of such treatment, responded initially to a single intravenous dose of cholecalciferol with a normal production of 1,25-dihydroxycholecalciferol. 3. This normal response was followed within 2 days by an apparent inhibition of the renal biosynthesis of 1,25-dihydroxycholecalciferol. It is inferred that the impaired intestinal transport of calcium, in diphosphonate-treated rats receiving vitamin D, is due to a deficiency of this renal metabolite. 4. Inhibition of the synthesis of 1,25-dihydroxycholecalciferol could not be attributed to a direct action of the drug on the renal 1-hydroxylase, but appeared to be determined by the initial normal response to vitamin D. 5. The mechanisms possibly involved in producing this effect are discussed.

Accumulation of Aluminum in a Nondialyzed Uremic Child Receiving Aluminum Hydroxide

PEDIATRICS ◽  
1983 ◽  
Vol 71 (1) ◽  
pp. 56-58
Author(s):  
W. R. Griswold ◽  
V. Reznik ◽  
S. A. Mendoza ◽  
D. Trauner ◽  
A. C. Alfrey
Keyword(s):  
Vitamin D ◽  
Renal Insufficiency ◽  
Aluminum Hydroxide ◽  
Phosphate Binder ◽  
Motor Impairment ◽  
Phosphate Binders ◽  
Aluminum Accumulation ◽  
Aluminum Intoxication

A child with renal insufficiency was treated with the oral phosphate binder aluminum hydroxide from age 6 to 31 months. The prescribed dose of elemental aluminum varied from 31 to 108 mg/kg/d. Concurrently the patient developed vitamin D-resistant osteomalacia which failed to improve with parathyroidectomy. Encephalopathy with myoclonic seizures, loss of speech, and motor impairment also occurred. Serum and bone aluminum levels were elevated at 334 µg/L (normal 7 ± 3 µg/L) and 156 mg/kg (normal 3.3 ± 2.9 mg/kg), respectively. This case demonstrates that aluminum may accumulate in tissue of children receiving oral aluminum hydroxide. The accumulation of aluminum may have contributed to the vitamin D-resistant osteomalacia and the encephaiopathy in this patient. Children receiving aluminum-containing antacids as phosphate binders should be monitored for aluminum accumulation and signs of aluminum intoxication.

THE SMALL INTESTINE IN VITAMIN D DEPENDENT RICKETS

PEDIATRICS ◽  
1970 ◽  
Vol 45 (3) ◽  
pp. 364-373
Author(s):  
Richard Hamilton ◽  
Joan Harrison ◽  
Donald Fraser ◽  
Lngeborg Radde ◽  
Rachel Morecki ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Vitamin D ◽  
Calcium Absorption ◽  
Light And Electron Microscopy ◽  
Intestinal Transport ◽  
Duodenal Mucosa ◽  
Intestinal Function ◽  
Active Vitamin ◽  
Phosphorus Absorption ◽  
Deficiency Rickets

We have demonstrated impaired intestinal absorption of calcium in a child with active vitamin D dependent rickets (hereditary pseudovitamin D deficiency rickets) at a time when the patient had normal anti-rachitic activity in her serum. Calcium absorption improved greatly in response to vitamin D, administered in the massive dosage that was necessary to heal the rachitic lesions. Phosphorus absorption may have been slightly impaired in the same patient, but no other absorptive defect was found. We studied intestinal function in five additional patients after they had been placed on vitamin D therapy. No abnormalities were found. In these treated patients, calcium absorption was not measured. Duodenal mucosa studied by light and electron microscopy was normal in all patients. Future investigation of intestinal transport of calcium in these patients should help to explain the pathogenesis of this disease.

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