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DAVID S. NEWCOMBE, MD; ALAN S. COHEN, MD

Arch Intern Med. 1963;112(5):738-741.

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

Introduction

At the time of his historic discovery of hyperuricemia in gout, A. B. Garrod stated that "Gout would thus appear, at least partly, to depend on a loss of power (temporary or permanent) in the uric acid-excreting function of the kidneys." ¹ Thus began a century of interest and controversy over the role of the kidney in the pathogenesis of gout. The fact that renal mechanisms, as well as metabolic considerations, are important in some cases of gout has been demonstrated by several investigators and accepted by most workers in the field.² In addition, the kidney is one of the major sites for the deposition of uric acid crystals.^3-6 Nonspecific findings such as proteinuria, a decrease in the ability of the kidney to concentrate the urine, and a decrease of phenolsulfonphthalein (PSP) excretion by the kidney are the early manifestations of this derangement.

In recent years uricosuric . . . [Full Text PDF of this Article]

Author Affiliations
BOSTON

Assistant in Medicine, Massachusetts Memorial Hospitals, Special Fellow, National Institutes of Health, Bethesda, Md (Dr. Newcombe); Associate Professor of Medicine, Boston University School of Medicine, Director, Arthritis and Connective Tissue Disease Section, Massachusetts Memorial Hospitals (Dr. Cohen).

From the Robert Dawson Evans Department of Clinical Research, Massachusetts Memorial Hospitals, and the Department of Medicine, Boston University School of Medicine, Boston University Medical Center.

Footnotes
Received for publication Feb 4, 1963; accepted March 4.

Grants in support of portions of this investigation have been received from the United States Public Health Service (T1 AM 5285-02), The Medical Foundation, Inc., and the New England Chapter of the Arthritis and Rheumatism Foundation.

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