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PHILIP FREEDMAN, M.D.; JOHN H. PETERS, M.D.; ROBERT M. KARK, F.R.C.P.

AMA Arch Intern Med. 1960;105(4):524-535.

	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

Although the histology of the end-stage kidney, as seen post mortem, rarely conveys evidence of the pathogenesis or etiology of the disease process which damaged it, recognition of the different forms of nephritis is slowly unfolding. Through study of the natural histories of renal disease, augmented by serial renal biopsies, it is becoming increasingly clear that "glomerulonephritis" is not a single unique disease. Its development depends on several distinct etiologies and a variety of pathogenetic mechanisms, among which are some which possibly result from immunological reactions. In recent years the concept that the kidney may be damaged by immunological reactions has received considerable support from experimental studies in animals. In man, at least two disorders of the kidney, acute streptococcal glomerulonephritis and lupus nephritis, seem to develop as a result of immunological reactions involving the organ.

If an immunological reaction were proceeding within the renal tissues, it would seem . . . [Full Text PDF of this Article]

Author Affiliations
Chicago

From the Departments of Medicine, University of Illinois, and the Research and Educational, Presbyterian-St. Luke's, and Cook County Hospitals. Bilton Pollard Fellow of University College Hospital Medical School, London, and Research Fellow in Medicine, University of Illinois (Dr. Freedman); Research Fellow in Medicine, University of Illinois (Dr. Peters), and Professor of Medicine, University of Illinois, and Attending Physician, Presbyterian-St. Luke's, Research and Educational, and Cook County Hospitals (Dr. Kark).

Footnotes
Submitted for publication Sept. 29, 1959.

Supported in part by grants from the U.S. Army (Contract DA-49-007-MD-637) and the U.S. Public Health Service (H-2253).

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