This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

H. EUGENE BUTLER, JR., MD; JEAN M. MORGAN, MD; CLEVES McC. SMYTHE, MD

Arch Intern Med. 1965;116(6):853-856.

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

GENERALIZED proximal tubular dysfunction appearing first in adult life is rare. This defect may be either inherited, as in the Fanconi syndrome in children, or acquired. The place of heredity in the appearance of the syndrome in adult life has been questioned.¹ At times an underlying disease process or exposure to a known tubular toxin can be documented. Tubular damage with glycosuria, amino-aciduria, phosphaturia, and acidosis may develop in the nephrotic syndrome in children, but this has been an infrequent finding in adults with nephrosis.^2-4 More recently, outdated tetracycline ⁵ and an antitumor drug, isophthalanilide,* ⁶ have been reported to cause multiple tubular reabsorption defects.

This is a report of an adult with chronic glomerulonephritis and the nephrotic syndrome, who developed proximal tubular dysfunction following treatment with mercaptopurine. A relationship between treatment with mercaptopurine and the emergence of the defects is suggested, since glycosuria and acidosis first occurred . . . [Full Text PDF of this Article]

Author Affiliations
CHARLESTON, SC

From the Department of Medicine, Medical College of South Carolina, Charleston.

Footnotes
Received for publication March 29, 1965; accepted June 1.

Reprint requests to Medical College of South Carolina, 16 Lucas St, Charleston, SC 29416 (Dr. Smythe).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?