The anatomic histological processes of Bright's disease and their relation to the functional changes : lectures delivered in the Russell Sage Institute of Pathology, City Hospital, New York, during the winter of 1909 / by Horst Oertel.

Horst Oertel

Date:: 1910

Credit: The anatomic histological processes of Bright's disease and their relation to the functional changes : lectures delivered in the Russell Sage Institute of Pathology, City Hospital, New York, during the winter of 1909 / by Horst Oertel. Source: Wellcome Collection.

Provider: This material has been provided by the Augustus C. Long Health Sciences Library at Columbia University and Columbia University Libraries/Information Services, through the Medical Heritage Library. The original may be consulted at the the Augustus C. Long Health Sciences Library at Columbia University and Columbia University.

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$We know ;i tminhci' of kidney lesions associated with extensive, alt liou.i;li slowly |)i'o,iiressin<i;, desl ruction of the epithelium. Accej)t ini;- I leidenliain's \'ie\vs of a ])urely secretory function of the epitlieliuni, one sliould reasonably expect a gradual diminu- tion in tiie amount of urin(^ in those lesions. But the facts speak differently. Patholo<;ists and clinicians have known for a lon<;- time that in certain types of productive nephritis, and in the amyloid kidney, the amount of mine, instead of bein<^' diminished, is actually markedly increased. The gradual loss of epithelium of glomeruli and tubules does not seem to have the slightest relation to the urine output. How, asks Senator, can this be regarded as the active product of the epithelium? Senator, in conjunction with Munk, began, therefore, to in- vestigate that point further.''^ They were aided by a discover}% made shortly before by Roy and others, namely, that it is possible to have kidneys functionate after they have been removed from the body. Taking advantage of this method, they transfused defibrinated blood through kidneys, and were able to observe closely the results of changing pressure and rapidity of flow brought about artificially in transfusion. They found the fol- lowing facts: In active hypersemia—in other words, when the pressure as well as the velocity of the flow is increased—the quantity of urine excreted increases. The quantity of nitrogen increases, while that of the sodium chlorid shows very little va- riation from the normal. That latter point is interesting and important to remember. Then they did the opposite, diminishing the quantity and the pressure through the kidney, with these results, that the amount of urine decreased decidedly, that the amount of nitrogenous material also decreased decidedly, while the amount of sodium chlorid showed no difference from the normal. Incidentalh', I$