Selective modulation by vitamin D of renal response to parathyroid hormone: A study in calcitriol-resistant rickets

Lea Even; Yosef Weisman; David Goldray; Ze'ev Hochberg

doi:10.1210/jc.81.8.2836

Selective modulation by vitamin D of renal response to parathyroid hormone: A study in calcitriol-resistant rickets

Lea Even
, Yosef Weisman
, David Goldray
, Ze'ev Hochberg

Bnai-Zion Medical Center
Tel Aviv Sourasky Medical Center
Rambam Health Care Campus Israel
Technion-Israel Institute of Technology

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

Abstract

Calcitriol-resistant rickets (CRR) is an autosomal recessive disease caused by mutated nonfunctioning vitamin D receptors. Because of their lack of biological activity of vitamin D, CRR patients were studied to investigate whether vitamin D modulates the effects of PTH on renal tubules. Five patients with CRR and three controls were studied. After normalization of serum calcium, phosphorus, and PTH levels by oral and iv administration of calcium, exogenous PTH-(1-34) was infused, and timed fractions of urine were collected for measurements of cAMP, sodium, potassium, phosphorus, calcium, and bicarbonate. Serum 1,25-dihydroxyvitamin D₃ [1,25-(OH)₂D₃] was measured before and after PTH-(1-34) infusion. Urinary cAMP and fractional excretion of potassium, phosphorus, and bicarbonate were similar in CRR patients and controls, as was the rise in the serum 1,25-(OH)₂D₃ concentration after PTH-(1-34) infusion. However, urinary excretion of calcium and sodium decreased after PTH-(1-34) infusion in controls, but not in CRR patients. These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)₂D₃ facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1α- hydroxylation of 25-hydroxyvitamin D₃.

Original language	English
Pages (from-to)	2836-2840
Number of pages	5
Journal	Journal of Clinical Endocrinology and Metabolism
Volume	81
Issue number	8
DOIs	https://doi.org/10.1210/jc.81.8.2836
State	Published - Aug 1996
Externally published	Yes

Bibliographical note

Funding Information:
Acknowledgements We thank Marie-Pierre Dufief and Paul Demaret for technical assistance and Michelle Plasch for secretarial assistance. This work was supported by the Belgian National Fund for Scientific Research (F.N.R.S.), the Research Fund of the University of Brussels (U.L.B.), and the Banque Nationale de Belgique. B. Dan is supported by the Fondation Van Goethem-Brichant and the Fondation Lekime-Ropsy.

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SDG 3 Good Health and Well-being

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10.1210/jc.81.8.2836

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title = "Selective modulation by vitamin D of renal response to parathyroid hormone: A study in calcitriol-resistant rickets",

abstract = "Calcitriol-resistant rickets (CRR) is an autosomal recessive disease caused by mutated nonfunctioning vitamin D receptors. Because of their lack of biological activity of vitamin D, CRR patients were studied to investigate whether vitamin D modulates the effects of PTH on renal tubules. Five patients with CRR and three controls were studied. After normalization of serum calcium, phosphorus, and PTH levels by oral and iv administration of calcium, exogenous PTH-(1-34) was infused, and timed fractions of urine were collected for measurements of cAMP, sodium, potassium, phosphorus, calcium, and bicarbonate. Serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] was measured before and after PTH-(1-34) infusion. Urinary cAMP and fractional excretion of potassium, phosphorus, and bicarbonate were similar in CRR patients and controls, as was the rise in the serum 1,25-(OH)2D3 concentration after PTH-(1-34) infusion. However, urinary excretion of calcium and sodium decreased after PTH-(1-34) infusion in controls, but not in CRR patients. These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)2D3 facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1α- hydroxylation of 25-hydroxyvitamin D3.",

author = "Lea Even and Yosef Weisman and David Goldray and Ze'ev Hochberg",

note = "Funding Information: Acknowledgements We thank Marie-Pierre Dufief and Paul Demaret for technical assistance and Michelle Plasch for secretarial assistance. This work was supported by the Belgian National Fund for Scientific Research (F.N.R.S.), the Research Fund of the University of Brussels (U.L.B.), and the Banque Nationale de Belgique. B. Dan is supported by the Fondation Van Goethem-Brichant and the Fondation Lekime-Ropsy.",

year = "1996",

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doi = "10.1210/jc.81.8.2836",

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AU - Goldray, David

AU - Hochberg, Ze'ev

N1 - Funding Information: Acknowledgements We thank Marie-Pierre Dufief and Paul Demaret for technical assistance and Michelle Plasch for secretarial assistance. This work was supported by the Belgian National Fund for Scientific Research (F.N.R.S.), the Research Fund of the University of Brussels (U.L.B.), and the Banque Nationale de Belgique. B. Dan is supported by the Fondation Van Goethem-Brichant and the Fondation Lekime-Ropsy.

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N2 - Calcitriol-resistant rickets (CRR) is an autosomal recessive disease caused by mutated nonfunctioning vitamin D receptors. Because of their lack of biological activity of vitamin D, CRR patients were studied to investigate whether vitamin D modulates the effects of PTH on renal tubules. Five patients with CRR and three controls were studied. After normalization of serum calcium, phosphorus, and PTH levels by oral and iv administration of calcium, exogenous PTH-(1-34) was infused, and timed fractions of urine were collected for measurements of cAMP, sodium, potassium, phosphorus, calcium, and bicarbonate. Serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] was measured before and after PTH-(1-34) infusion. Urinary cAMP and fractional excretion of potassium, phosphorus, and bicarbonate were similar in CRR patients and controls, as was the rise in the serum 1,25-(OH)2D3 concentration after PTH-(1-34) infusion. However, urinary excretion of calcium and sodium decreased after PTH-(1-34) infusion in controls, but not in CRR patients. These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)2D3 facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1α- hydroxylation of 25-hydroxyvitamin D3.

AB - Calcitriol-resistant rickets (CRR) is an autosomal recessive disease caused by mutated nonfunctioning vitamin D receptors. Because of their lack of biological activity of vitamin D, CRR patients were studied to investigate whether vitamin D modulates the effects of PTH on renal tubules. Five patients with CRR and three controls were studied. After normalization of serum calcium, phosphorus, and PTH levels by oral and iv administration of calcium, exogenous PTH-(1-34) was infused, and timed fractions of urine were collected for measurements of cAMP, sodium, potassium, phosphorus, calcium, and bicarbonate. Serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] was measured before and after PTH-(1-34) infusion. Urinary cAMP and fractional excretion of potassium, phosphorus, and bicarbonate were similar in CRR patients and controls, as was the rise in the serum 1,25-(OH)2D3 concentration after PTH-(1-34) infusion. However, urinary excretion of calcium and sodium decreased after PTH-(1-34) infusion in controls, but not in CRR patients. These results suggest a selective modulation by vitamin D of the renal response to PTH; 1,25-(OH)2D3 facilitates PTH-induced calcium and sodium reabsorption, but does not influence PTH-induced cAMP excretion; phosphorus, potassium, and bicarbonate tubular transport, or 1α- hydroxylation of 25-hydroxyvitamin D3.

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IS - 8

ER -

Selective modulation by vitamin D of renal response to parathyroid hormone: A study in calcitriol-resistant rickets

Abstract

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