Diseases of the kidneys and of the spleen : hemorrhagic diseases / by Dr. H. Senator and Dr. M. Litten ; edited with additions by James B. Herrick ; authorized translation from the German, under the editorial supervision of Alfred Stengel.

  • Senator, H. (Hermann), 1834-1911.
Date:
1905
Catalogue details

Licence: Public Domain Mark

Credit: Diseases of the kidneys and of the spleen : hemorrhagic diseases / by Dr. H. Senator and Dr. M. Litten ; edited with additions by James B. Herrick ; authorized translation from the German, under the editorial supervision of Alfred Stengel. Source: Wellcome Collection.

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    positively proved in the case not only of albumoses and “ peptones,” which have already been discussed on page 22, but also in the case of egg-albumin, casein, gelatin, hemoglobin, and a number of other albu¬ minous bodies.1 With this fact as a basis a number of attempts have been made recently, especially by Semmola, to explain by means of various ingenious hypotheses certain clinical forms of albuminuria, par¬ ticularly so-called Bright’s disease, as caused by such a dyscrasia. Unfortunately, however, in cases of albuminuria in the true sense of the word, none of these or any other foreign albuminous body is found, the albumin consisting always of the normal albumins of the blood—namely, serum-albumin and globulin ; at least, the numerous attempts that have been made up to the present time to demonstrate any material differ¬ ence have resulted in failure ; and so far as our present knowledge goes a dyscrasic or hematogenous albuminuria in this sense still lacks a solid foundation. In addition to these qualitative changes in the albuminous bodies con¬ tained in the blood there are other alterations of a quantitative nature, as well as similar deviations relating to other constituents of the blood, such as the urea, the salts, etc. As changes of this character in the constitution of albumin-containing fluids cannot fail to have their effect on the escape of albumin from such fluids, it must be admitted from the standpoint of the transudate or “ filtration ” theory (see p. 36) that quantitative changes in the proportions of the normal constituents of the blood, the albuminous bodies, the salts, the urea, and others may cause the escape of considerable quantities of albumin and thus lead to the production of albuminuria. A positive decision of this question is exceedingly difficult, because the renal tissue, and particularly the renal epithelium, react at once to any abnormal condition in the blood and are very easily injured in their nutrition and function. Hence, an albuminuria developing after such changes have been brought about by the injection of certain heterogene¬ ous bodies, for example, or the abstraction of certain normal constitu¬ ents of the blood, such as sodium chlorid, may be also due to these renal changes, and therefore actually renal in origin and only indirectly due to a dyscrasia. As with the aid of improved methods of examination more minute structural changes have been found in the kidneys in an ever-increasing number of such cases of albuminuria, which were formerly regarded not as renal but as dyscrasic in nature, the number of the latter has become more and more limited. Another consideration is that all, or at least many, of these alterations in the condition of the blood exert a disturbing influence on the general circulation as well as on that of the kidneys in particular, and may thus indirectly lead to albuminuria. In short, the question is complicated by so many interrelated factors and the conditions are so confused that it cannot be said to have been posi¬ tively demonstrated that a simple “ dyscrasic, hematogenous albuminuria ” 1 S. Senator, Albuminurie, p. 117; and J. Hunk and Lewandowsky, Arch. f. Physiol., 1899, Sup. vol., p. 73.