Renal Bicarbonate Wasting during Phosphate Depletion A POSSIBLE CAUSE OF ALTERED ACID-BASE HOMEOSTASIS IN HYPERPARATHYROIDISM

Gold, Lawrence W.; Massry, Shaul G.; Arieff, Allen I.; Coburn, Jack W.

doi:10.1172/jci107447

Cited by 101 publications

(31 citation statements)

References 23 publications

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“…Hypophosphatemia in our animals was associated with undetectable plasma PTH and normal total and ionized calcium levels (Table I), findings previously described by other investigators (19). An augmented insulin response to a glucose challenge was noted in the hypophosphatemic state ( Fig.…”

Section: Discussionsupporting

confidence: 89%

“…For example, LeFevre et al (33) have demonstrated that cell membrane phospholipid is critical in the transport process of all monosaccharides. Recently, phosphate depletion has been shown to lead to intracellular alkalosis (19), which may cause an altered intracellular sodium:potassium ratio produced by the efflux of potassium. By so doing, however, one would expect augmented glucose uptake (34,35).…”

Section: Discussionmentioning

confidence: 99%

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The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release.

Harter¹,

Santiago²,

Rutherford³

et al. 1976

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release.

Harter¹,

Santiago²,

Rutherford³

et al. 1976

J. Clin. Invest.

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“…A decrease in the net tubular reabsorption of magnesium during PD is not surprising because others have reported tubular reabsorptive defects of other substances such as calcium (10), bicarbonate (28), glucose (29), and sodium (30).…”

Section: Discussionmentioning

confidence: 99%

Effect of Phosphate Depletion on Magnesium Homeostasis in Rats

Kreußer¹,

Kurokawa²,

Aznar³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The effects of phosphate depletion on magniesiumni (NMg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell signiificantly (P < 0.01) from 10.1+0.27 (SE) to 5.0±0.54 mgIl00 ml within 1 day and conitiniued to fall gradually to a level of 1.2±0.21 mg/100 ml by the end of the 8th wk. A signiificant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46±2.7 to 126±24 ,ueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300±+24 pieq/24 h by the 3rd day and remained high ranging between 150-300 ,ueq/24 h, thereafter. The magnittude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2±0.02 to 0.79±0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which becarmie evident by the 3rd wk of phosphate depletion. Mg contenit of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral contenit because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 ,ueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or veight of the animals.Our results indicate that phosphate depletion is Dr. Kreusser is a Fellow of the Deutsche Forschungsgemeinschaft.Dr. Aznar is a Fellow of the Del Amo Foundation.

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“…Other investigators (28)(29)(30) have attributed the changes in bicarbonate homeostasis in hyperparathyroidism to phosphate depletion induced by PTH rather than to the direct action of the hormone on RHcos.…”

Section: Discussionmentioning

confidence: 99%

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

et al. 1974

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A B S T R A C T The role of parathyroid hormone (PTH) and of Ca++ in the regulation of bicarbonate absorption (RHCO3) and its response to extracellular volume expansion (VE) was studied in HC03-loaded dogs.VE lowered RHCO3 in both intact (from 24.8 to 22.0 mmol/liter GFR, P < 0.01) and thyroparathyroidectomized (TPTX) (from 24.5 to 18.0 mmol/liter GFR, P < 0.001) dogs; glomerular filtration rate (GFR) and filtered HCOi-did not change. Both groups showed a significant increase in the fractional excretion of sodium (CNa X 100/GFR), calcium (CCa X 100/ GFR), and chloride (Cci X 100/GFR) and a decrease in phosphorus reabsorption. Fractional clearance of phosphate (CP X 100/GFR) rose in both groups but did not achieve significance.Infusion of purified parathyroid extract (PTE) decreased RHCOs in intact dogs (from 24.6 to 22.5 mmol/ liter GFR, P < 0.025) and in TPTX dogs (from 26.9 to 22.6 mmol/liter GFR, P < 0.05). No Infusion of Ca++ raised ultrafilterable Ca++ from 5.7 to 7.9 mg/100 ml in intact and from 4.9 to 7.2 mg/ 100 ml in TPTX dogs; RHCOs increased in intact (from 22.9 to 26.9 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.6 to 28.6 mmol/liter GFR, P <0.05). The GFR, RBF, and the fractional excretion of sodium, chloride, and calcium did not change in either group. The reabsorbed phosphate increased in both groups, and fractional phosphorus clearance fell in the intact group but did not change significantly in the TPTX group.Superimposition of PTE on hypercalcemia in TPTX dogs resulted in a decrease in RHco8 (from 27.3 to 23.9 mmol/liter GFR, P < 0.001), which was accompanied by an increase in the fractional excretion of phosphate and a decrease in the reabsorbed phosphate. In this group of TPTX dogs hypercalcemia caused a drop in RBF from 135.6 to 105.8 ml/min with no change in GFR. The RBF returned to control value with PTE infusion.It is concluded that: (a) the lowering of RHCO3 by VE is not dependent solely on stimulation of PTH by the lowered Ca', (b) PTE acts directly on the renal tubules to lower RHCOs, (c) Ca' enhances RHcos and this effect is exerted in the absence of PTH and calcitonin, (d) neither the effects of CaZ nor of PTH appear to be mediated by altered hemodynamics, although this cannot be excluded in Ca^-infused TPTX dogs, (e) Ca' enhanced phosphate reabsorption in the absence of PTH; this may be a specific effect of hypercalcemia on phosphate reabsorption or the nonspecific consequence of the rise in serum phosphorus.

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Renal Bicarbonate Wasting during Phosphate Depletion A POSSIBLE CAUSE OF ALTERED ACID-BASE HOMEOSTASIS IN HYPERPARATHYROIDISM

Abstract: A B S T R A

Cited by 101 publications

References 23 publications

The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release.

The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release.

Effect of Phosphate Depletion on Magnesium Homeostasis in Rats

Effects of Volume Expansion, Purified Parathyroid Extract, and Calcium on Renal Bicarbonate Absorption in the Dog

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