Phosphorus administration in patients with profound hypophosphatemia

D. L. Andress, A. J. Felsenfeld, J. B. Vannatta, S. Dokoh, Mark R Haussler, F. Llach

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The influence of severe hypophosphatemia (≤1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (±SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 ± 1.3 vs. 17.8 ± 1.3 ng/ml, P < 0.001). With phosphorus administration, serum phosphorus increased from 0.59 ± 0.07 to 2.58 ± 0.09 mg/dl while 1.25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 ± 4.3 o 14.3 ± 2.9 pg/ml (P < 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggsting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P < 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P < 0.005) and after (r = 0.74, P < 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].

Original languageEnglish (US)
Pages (from-to)551-556
Number of pages6
JournalKidney International
Volume25
Issue number3
StatePublished - 1984
Externally publishedYes

Fingerprint

Hypophosphatemia
Phosphorus
Serum
Calcifediol
Calcitriol
Sterols
Vitamin D
Intravenous Administration
Liver Diseases
Phosphates
Calcium

ASJC Scopus subject areas

  • Nephrology

Cite this

Andress, D. L., Felsenfeld, A. J., Vannatta, J. B., Dokoh, S., Haussler, M. R., & Llach, F. (1984). Phosphorus administration in patients with profound hypophosphatemia. Kidney International, 25(3), 551-556.

Phosphorus administration in patients with profound hypophosphatemia. / Andress, D. L.; Felsenfeld, A. J.; Vannatta, J. B.; Dokoh, S.; Haussler, Mark R; Llach, F.

In: Kidney International, Vol. 25, No. 3, 1984, p. 551-556.

Research output: Contribution to journalArticle

Andress, DL, Felsenfeld, AJ, Vannatta, JB, Dokoh, S, Haussler, MR & Llach, F 1984, 'Phosphorus administration in patients with profound hypophosphatemia', Kidney International, vol. 25, no. 3, pp. 551-556.
Andress DL, Felsenfeld AJ, Vannatta JB, Dokoh S, Haussler MR, Llach F. Phosphorus administration in patients with profound hypophosphatemia. Kidney International. 1984;25(3):551-556.
Andress, D. L. ; Felsenfeld, A. J. ; Vannatta, J. B. ; Dokoh, S. ; Haussler, Mark R ; Llach, F. / Phosphorus administration in patients with profound hypophosphatemia. In: Kidney International. 1984 ; Vol. 25, No. 3. pp. 551-556.
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AU - Andress, D. L.

AU - Felsenfeld, A. J.

AU - Vannatta, J. B.

AU - Dokoh, S.

AU - Haussler, Mark R

AU - Llach, F.

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N2 - The influence of severe hypophosphatemia (≤1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (±SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 ± 1.3 vs. 17.8 ± 1.3 ng/ml, P < 0.001). With phosphorus administration, serum phosphorus increased from 0.59 ± 0.07 to 2.58 ± 0.09 mg/dl while 1.25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 ± 4.3 o 14.3 ± 2.9 pg/ml (P < 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggsting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P < 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P < 0.005) and after (r = 0.74, P < 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].

AB - The influence of severe hypophosphatemia (≤1.0 mg/dl) on vitamin D metabolism was prospectively determined in 11 patients before and after intravenous phosphorus administration. Evidence of liver dysfunction was present in ten patients. The mean (±SE) plasma 25 hydroxycholecalciferol [25(OH)D] was significantly decreased before phosphorus therapy when compared to control subjects (9.4 ± 1.3 vs. 17.8 ± 1.3 ng/ml, P < 0.001). With phosphorus administration, serum phosphorus increased from 0.59 ± 0.07 to 2.58 ± 0.09 mg/dl while 1.25 dihydroxycholecalciferol [1,25(OH)2D] decreased from 34.6 ± 4.3 o 14.3 ± 2.9 pg/ml (P < 0.001). Plasma 25(OH)D, plasma immunoreactive PTH (both amino and carboxyterminal) and serum calcium did not change after phosphorus administration, suggsting that phosphorus alone was responsible for the change in plasma 1,25(OH)2D concentration. An inverse correlation was found between serum phosphorus and plasma 1,25(OH)2D (r = -0.62, P < 0.005). In addition, a direct correlation was observed between plasma 25(OH)D and 1,25(OH)2D both before (r = 0.66, P < 0.005) and after (r = 0.74, P < 0.005) phosphorus administration. Thus, the decrease in 1,25(OH)2D levels with phosphorus therapy suggests a role of serum phosphate in the regulation of this sterol, and hypophosphatemia or phosphorus depletion may change the relationship of substrate [25(OH)D] to product [1,25(OH)2D].

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