Tubular Defects in Phosphate Reabsorption in Clinical Medicine

Chesney, Russell W.

doi:10.1007/978-1-4615-9152-8_13

Cited by 6 publications

(1 citation statement)

References 157 publications

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“…The disease in mice and humans is characterized by increased renal excretion of phosphate (P), low plasma P (hypophosphatemia) and osteomalacia {Eicher et al. 1976;Meyer, Jowsey and Meyer 1979;Chesney 1980). The etiology of XLH has not been clearly defined.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Response of X-Linked Hypophosphatemic Mice to Calcitonin

Gm¹,

Ra²

1982

Horm Metab Res

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Other investigations, using the Hyp mouse as an animal model for the human disease X-linked hypophosphatemia (XLH), have demonstrated renal hypersensitivity to calcitonin (CT) using in vitro single renal tubule adenylate cyclase microassays. Renal hypersensitivity to CT may explain the elevated fractional excretion of phosphate (FE-P) and urinary 3'-5'-cyclic AMP (UcAMP) present in Hyp mice. This current study was designed as the in vivo counterpart to the in vitro experiments. CT dose-dependent hypocalcemia when data were constructed in normal and Hyp mice 18 hours after thyroparathyroidectomy (TPTX). Exogenous CT administered to TPTX normal mice resulted in dose-dependent hypocalcemia when data were expressed as the percent change from pretreatment. However, CT did not elicit a hypocalcemic response in TPTX Hyp mice at any dose. Only TPTX normal mice responded to CT with significant hypophosphatemia. FE-P and UcAMP were not significantly changed by CT in either genotype. In a different experiment, a large pharmacologic dose of CT was given to TPTX mice. This dose resulted in a significant but similar elevation of FE-P 1 hour after injection in both Hyp and normal TPTX mice. While UcAMP also rose significantly in both genotypes, the percent increase compared to controls was greater in Hyp mice. In summary, results from these in vivo experiments indicate that Hyp mice are not hypersensitive to physiologic doses of CT, and in fact they seem to be resistant to the hypocalcemic effect of the hormone. The greater increase in UcAMP in TPTX Hyp mice after a pharmacologic dose of CT may be the basis for the earlier in vitro results reported by others. We conclude that renal hypersensitivity to CT does not play a role in the etiology of XLH in the Hyp mouse.

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Section: Introductionmentioning

confidence: 99%

In Vivo Response of X-Linked Hypophosphatemic Mice to Calcitonin

Gm¹,

Ra²

1982

Horm Metab Res

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Kidney and Bone: Physiological and Pathophysiological Relationships

Brown

1992

Comprehensive Physiology

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The sections in this article are: Chemical and Cellular Composition of Bone Extracellular Constituents of Bone Bone Cells Development and Structure of Bone Endochondral Ossification Intramembranous Ossification Skeletal Growth and Modeling Principles of Skeletal Growth Skeletal Modeling Epiphyseal Closure Bone Cell Function and Skeletal Growth and Modeling Bone Turnover and the Remodeling Cycle Skeletal Remodeling Cellular Control of Bone Remodeling Fracture Healing Bone Cell Function and Fracture Repair Interrelationships of Kidney and Bone in Normal Physiology General Considerations Overall Calcium Balance Hormonal Control of Mineral Ion Homeostasis Role of the Parathyroid Glands in the Calcium Homeostatic System Bone Cell Function and Ionic Homeostasis Aspects of Renal Function Essential for Normal Skeletal Structure and Function and Ionic Homeostasis Metabolic Bone Disease Osteitis Fibrosa Osteomalacia Osteoporosis Laboratory Evaluation of Metabolic Bone Disease Direct Assays of Calcium‐Regulating Hormones in Blood Clinical Assessment of the Function of Target Organs for Calcium‐Regulating Hormones Abnormalities in Renal Function Leading to Skeletal Disease Abnormalities in Renal Calcium Handling Abnormalities in Renal Phosphate Handling Hypo‐ and Hypermagnesemia Due to Renal Causes Renal Tubular Acidosis Primary Abnormalities in Vitamin D Metabolism Renal Resistance to PTH : Pseudohypoparathyroidism Chronic Renal Insufficiency Pathophysiology of Renal Osteodystrophy Disorders Affecting the Homeostatic Mechanisms Linking Kidney and Bone Primary Hyperparathyroidism Humoral Hypercalcemia of Malignancy Hypoparathyroidism Deficient Quantities and Action of Vitamin D Hypervitaminosis D Sarcoidosis and Other Granulomatous Diseases Other Hormonal Abnormalities and Drugs Affecting Both Bone and Kidney Calcitonin Growth Hormone Estrogen Glucocorticoids Insulin Thyroid Hormones Miscellaneous Associations Between Bone and Kidney Disorders Affecting Both Kidney and Bone Pharmacological Agents Affecting Both Kidney and Bone Effects of Bone Disease on the Kidney

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Renal Osteodystrophy in Children

Chesney

1985

Chronic Renal Disease

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Tubular Defects in Phosphate Reabsorption in Clinical Medicine

Cited by 6 publications

References 157 publications

In Vivo Response of X-Linked Hypophosphatemic Mice to Calcitonin

In Vivo Response of X-Linked Hypophosphatemic Mice to Calcitonin

Kidney and Bone: Physiological and Pathophysiological Relationships

Renal Osteodystrophy in Children

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