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ANWAR SHAH, M.D.; MARGUERITE A. CONSTANT, Ph.D.; BERNARD BECKER, M.D.

AMA Arch Ophthalmol. 1958;59(4):536-540.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Citrate is excreted in comparatively large amounts in human urine, and its excretion varies with age, diet, sex, and other factors from 100 to 1500 mg. per day.^1-4 It is lower in infants and children as compared with adults.^1-3,5-7 Citrate excretion is decreased by acidosis^7-12 (dietary, uremic, and diabetic) and by testosterone administration.¹³ It is increased in alkalosis^7-12 and by the administration of estrogens,^14,15 parathyroid extract,^2,16,17 and vitamin D.^18-22

Previous experimental and clinical studies have suggested that urinary citrate aids in the chelation of calcium into a soluble complex. Low citrate levels in the presence of normal calcium-phosphorous ratios may play a role in the formation of renal calculi.2,23,24 In addition, citrate therapy has been reported to have induced an apparent improvement in a case of nephrocalcinosis.²⁵

In rats, acetazolamide administration has been observed to result in the deposition of calcium . . . [Full Text PDF of this Article]

Author Affiliations
St. Louis

From the Department of Ophthalmology, Washington University School of Medicine, and the Oscar Johnson Institute.

Footnotes
Received for publication July 15, 1957.

Presented in part at the Midwestern Section of the Association for Research in Ophthalmology, Iowa City, March 30, 1957.

The research relating to this study was financed in part under a grant to Washington University School of Medicine made by the Alfred P. Sloan Foundation, Inc. The grant was made upon recommendation of the Council for Research in Glaucoma and Allied Diseases. Neither the Foundation nor the Council assumes any responsibility for the published findings of this study.

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