The changes in the renal ganglia in bright's disease / by Robert Saundby.

  • Saundby Robert, 1849-1918.
Date:
1883
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Licence: Public Domain Mark

Credit: The changes in the renal ganglia in bright's disease / by Robert Saundby. Source: Wellcome Collection.

Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.

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    [Reprinted for the Author from the British Medical Journal, January 13th, 1883.] THE CHANGES IN THE RENAL GANGLIA IN BRIGHT’S DISEASE.* By ROBERT SAUNDBY, M.D., Member of the Eoyal College of Physicians, and Assistant-Physician to the General Hospital, Birmingham. In the American Journal of Medical Sciences for July 1880, there is a very able paper, by Drs. Da Costa and Longstreth of Philadelphia, entitled “Researches on the State of the Ganglionic Centres in Bright’s Disease.” They give the particulars of nine cases of Bright’s disease, with microscopical details of the changes in the kidneys and semi-lunar ganglia. They divide their cases into three groups : the first includes two cases of well-marked contracting kidney; the second, three cases of the mixed type of chronic Bright’s disease ; and the third, one case of large white kidney, one of recent nephritis after t^hoid fever, and two of chronic Bright’s disease, with large coarse diffusely diseased kidneys. It is impossible to avoid feeling somewhat confused by the heterogeneous composition of these groups; and, in order to place the results of their investigations in a clearer light, I have ventured to summarise the conclusions which I think may be fairly drawn from these nine cases. (a.) In acute or subacute nephritis (Case ix), the only change met with in the ganglia was an increase of the cell-elements of the stroma. (b.) In the large white kidney (Case VIT), the connective tissue of the ganglia was loose and swollen, and its cell-elements in- creased. The ganglionic cells were generally normal, degeuerative changes being present in about one third. .There were no yascular changes. (c.) In the mixed forms (Cases iii, iv, v, VI, and viii), the connective tissue was increased, and its cell elements were nume- rous ; the ganglionic cells were more or less fatty and pigmented; the blood vessels were dilated and thickened in two cases. (d.) In typical contracting kidney (Cases i and ii), the stroma of the ganglia was increased in amount, but contained few cell- elements ; the ganglonic cells were generally shrunken, deformed, fatty, and pigmented; the blood-vessels were dilated and hyper- trophied. After ^ving these descriptions, the authors proceed to consider the relations of the ganghonic lesions to the renal disease; and, after stating that they may be regarded as either causes, concomitants, or results of one another, accept the view that the changes in the gangha stand in some way as causes to certain forms of Bright’s dis- ease, especially the contracting form. In explanation of this view, they propound the following theory of the modus operandi. “ The specific cause, whatever may be its unknown form or character, acts in such a manner on the ganglion-cells presiding as centres of inner- vation to the kidney, and whose fibres, distributed to the vessels of these organs, regulate, not only the calibre of the vascular trunks by changing the state of contraction of their muscular fibres, but also probably the conditions of osmotic action between the blood and the tissues, that the collective phenomena known as Bright’s disease are brought about.” * Bead in the Pathological Section of the British Worcester, August 1882. Medical Association at