Factors Influencing the Urinary Excretion of Calcium**The greater part of this paper is taken from a dissertation submitted by Elizabeth L. Knapp in partial fulfillment of the requirements for the degree of Doctor of Philosophy, in the Department of Chemistry in the Graduate College of the State University of Iowa.

Knapp, Elizabeth L.; Stearns, Genevieve

doi:10.1016/s0002-9378(16)39099-8

Cited by 17 publications

(1 citation statement)

References 18 publications

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“…In children, it may present with other fetures like hematuria and urinary infections [4], In a review [5] of published data of calcium balance studies on 51 patients with idiopathic hypercalciuria [6][7][8][9][10][11][12][13], a negative calcium balance was com mon and recent study also demonstrated an enhanced bone turnover and moderate mineralization defect in some of these patients [14]. While in adults this negative calcium balance is compensated by the large calcium reserve in the skeleton, a severe renal calcium leak in a growing child who needs a positive calcium balance may cause significant hypocalcemia and osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Hypercalciuria Causing Osteoporosis and Hypocalcemia

Wong

Pun²,

Tam³

et al. 1992

Nephron

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Idiopathic hypercalciuria, though a common cause of nephrolithiasis, has not been recognized to cause hypocalcemia and severe bone disease. We describe an adolescent with idiopathic hypercalciuria who presented initially with severe hypocalcemia and osteoporosis and this was later complicated by recurrent renal calculi formation after calcium and vitamin D supplement. After treatment with thiazide, hypercalciuria was controlled and serum biochemistry normalized. While idiopathic renal hypercalciuria may cause a negative calcium balance in adults, a variant of this syndrome with severe renal calcium leak occurring in a growing subject could lead to severe hypocalcemia and osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Idiopathic Hypercalciuria Causing Osteoporosis and Hypocalcemia

Wong

Pun²,

Tam³

et al. 1992

Nephron

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Hypercalciuria Following Poliomyelitis

Dunning¹

1957

AMA Arch Intern Med

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Hypercalciuria and demineralization are frequent sequels to severe paralytic illnesses. Freeman1 and many others * emphasized that osteoporosis and calcium-containing genitourinary calculi commonly complicate traumatic paraplegia. Excess calcium loss also may be inferred to occur in many patients with multiple sclerosis and polyneuritis, since calcium-containing stones often develop during these illnesses. Whedon and Shorr 2 recently demonstrated that every one of seven extensively paralyzed patients developed profound losses of calcium and phosphorus after poliomyelitis.The studies cited above were all performed on patients suffering marked paralysis and immobilization. Except for Whedon and Shorr's investigation, they give relatively little quantitative data on serial patterns of mineral excretion. There are few data available to indicate whether, with paralysis, the intensity or duration of hypercalciuria bears any relationship to the site, degree, or extent of denervation. Few investigations have been directed toward determining whether nervous system illnesses produce decalcification in the absence of immobilization. This lack of analyses perhaps reflects a widespread assumption that demineralization, hypercalciuria, and geni¬ tourinary stone formation are a potential threat only in the presence of severe paralysis and immobility.Patients with widely varying degrees of paralysis due to poliomyelitis were studied in the present investigation. Analyses of urinary calcium, phosphorus, and creatinine excretion were carried out during acute and convalescent illness periods lasting sev¬ eral months. Some of the subjects were almost completely quadriplegic and remained at bed rest for months, while others had little weakness except in bulbar innervated muscle groups and were in bed only a few days. Paralysis and immobilization ranged from mild to severe ; it was, therefore, pos¬ sible to determine whether any relationship existed between the extent and location of paralysis and the intensity and duration of subsequent abnormalities in calcium and phophorus excretion. ProcedureFifty-four males and females, including adults and children, were studied in the Northwest Res¬ pirator Center of the University of Washington for periods lasting from 1 to 12 months during acute and convalescent stages of poliomyelitis.

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Familial Hypophosphatemic Vitamin D Resistant Rickets

Stickler¹,

Hayles²,

Rosevear³

1965

Am J Dis Child

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Cited by 17 publications

References 18 publications

Idiopathic Hypercalciuria Causing Osteoporosis and Hypocalcemia

Idiopathic Hypercalciuria Causing Osteoporosis and Hypocalcemia

Hypercalciuria Following Poliomyelitis

Familial Hypophosphatemic Vitamin D Resistant Rickets

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