Vitamin D-Resistant Rickets: The Effect of Calcium Infusion on Phosphate Reabsorption *

Field, Morton H.; Reiss, Eric

doi:10.1172/jci104204

Cited by 40 publications

(7 citation statements)

References 13 publications

(12 reference statements)

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“…They confirmed previous observations that experimental hypercalcemia is attended by an increase in the value of TRP (8)(9)(10)(11), and interpreted this as evidence that induced hypercalcemia per se increased renal phosphate reabsorption via a transport system independent of that normally responsive to PTH. Yet, an increased renal responsiveness to the phosphaturic effect of normal (3) (or even reduced, [4]) concentrations of circulating PTH could explain the characteristic reduction of TRP in patients with FHR (12) as well as the increase in TRP that attends sustained experimental hypercalcemia in these patients (8)(9)(10)(11) (13,14).…”

supporting

confidence: 88%

Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets.

Short¹,

Morris²,

Sebastián³

et al. 1976

J. Clin. Invest.

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A B S T R A C T To determine whether the phosphaturic response to circulating parathyroid hormone (PTH) is exaggerated in patients with familial x-linked hypophosphatemic vitamin D-resistant rickets (FHR), we examined the phosphaturic response to parathyroid extract (PTE) (administered intravenously in the posthypercalcemic state) in two unrelated adult hemizygotes with FHR. In these two patients whose plasma concentration of PTH was normal (determined by radioimmunoassay), neither vitamin D nor phosphate therapy had been given during the past 10 yr. Two normal men and a hypophosphatemic man with intestinal malabsorption, hypocalcemia, and osteomalacia served as control subjects. In all subjects, calcium gluconate was administered intravenously from 6 p.m. to 12 midnight at a rate that maintained the concentration of serum calcium at 13-15 mg/ 100 ml during the administration of calcium. When normocalcemia had recurred the next morning, and the plasma PTH concentration and urinary excretion of cyclic 3',5'-AMP were reduced, PTE was administered intravenously at successively increasing rates of 0.1, 0.4, and 0.8 U/kg per h, each rate lasting 90 min. Minutes after the initiation of PTE in the affected hemizygotes, fractional excretion of filtered phosphate increased from negligible values to values strikingly greater than those of similarly studied control subjects and plateaued at strikingly greater values throughout further administration of PTE. This phenomenon of exaggerated phosphaturia could not be attributed to volume expansion, decreases in serum concentration of calcium during the study, differences in percent of administered calcium Dr. Short's current address is the Department of Medicine, Stanford University, Palo Alto, Calif. 94305.

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supporting

confidence: 88%

Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets.

Short¹,

Morris²,

Sebastián³

et al. 1976

J. Clin. Invest.

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“…First, Albright et al (4) proposed that decreased gut absorption ofcalcium initiates a form of secondary hyperparathyroidism. Evidence in favor of this concept includes principally the demonstration of decreased gut calcium absorption (5) and the normalization of phosphate excretion in patients with VDRR when parathyroid hormone (PTH) is suppressed by calcium infusion (6)(7)(8). Unfortunately, recent measurements of circulating PTH levels in untreated patients with this disorder have been conflicting, and mildly elevated (9)(10)(11), normal (12)(13)(14)(15), and low (16) values have been reported.…”

mentioning

confidence: 99%

Evidence for an Intrinsic Renal Tubular Defect in Mice with Genetic Hypophosphatemic Rickets

Cowgill¹,

Goldfarb²,

Lau³

et al. 1979

J. Clin. Invest.

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A B S T R A C T To investigate the role of parathyroid hormone (PTH) and(or) an intrinsic renal tubular reabsorptive defect for phosphate in mice with hereditary hypophosphatemic rickets, we performed clearance and micropuncture studies in hypophosphatemic mutants and nonaffected littermate controls. Increased fractional excretion ofphosphate in mutants (47.2 +4 vs. 30.8+2% in controls) was associated with reduced fractional and absolute reabsorption in the proximal convoluted tubule and more distal sites. Acute thyroparathyroidectomy (TPTX) increased phosphate reabsorption in both mutants and controls with a fall in fractional phosphate excretion to _7.5% in both groups indicating that PTH modified the degree of phosphaturia in the intact mutants. Absolute reabsorption in the proximal tubule and beyond remained reduced in the mutants, however, possibly because ofthe reduced filtered load. Serum PTH levels were the same in intact mutants and normals as was renal cortical adenylate cyclase activity both before and after PTH stimulation.To evaluate the possibility that the phosphate wasting was caused by an intrinsic tubular defect that was masked by TPTX, glomerular fluid phosphate concentration was raised by phosphate infusion in TPTX mutants to levels approaching those of control mice. Phosphate excretion rose markedly and fractional reabsorption fell, but there was no change in absolute phos-

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“…The contribution of hyperparathyroidism to the phosphate wasting gained further support from the observations of Field and Reiss [152], Falls et al [153], Fraseret al [154], and Blackardet al [155] who demonstra ted that when hypercalcemia was induced in these pa tients, the phosphaturia diminished, which suggested an inhibition of PTH secretion by the hypercalcemia [63]. Later, when radioimmunoassay of serum PTH became available, it was possible to document that PTH was elevated above normal only in a few patients [156][157][158].…”

Section: X-linked Dominant Hypophosphatémie Ricketsmentioning

confidence: 87%

Tubular Disorders of Acid-Base and Phosphate Metabolism

Chan¹,

Alon²

1985

Nephron

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Vitamin D-Resistant Rickets: The Effect of Calcium Infusion on Phosphate Reabsorption *

Cited by 40 publications

References 13 publications

Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets.

Exaggerated phosphaturic response to circulating parathyroid hormone in patients with familial X-linked hypophosphatemic rickets.

Evidence for an Intrinsic Renal Tubular Defect in Mice with Genetic Hypophosphatemic Rickets

Tubular Disorders of Acid-Base and Phosphate Metabolism

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