NITROGEN RETENTION IN THE BLOOD IN EXPERIMENTAL ACUTE NEPHRITIS OF THE CAT.
It will be seen that uranium nephritis, which involves both tubules and glomeruli, the former more markedly than the latter, produces a marked accumulation of nitrogen in the blood. Chromate nephritis, which involves almost exclusively the tubules, produces only moderate retention of nitrogen. Cantharidin nephritis which involves both tubules and glomeruli, the latter more severely than does uranium, produces a marked accumulation of nitrogen, beginning early and persisting for a considerable period. The experiments were controlled by testing the blood of normal cats kept under the same conditions, these animals showing only slight variations from day to day. This general statement is in accordance with the physiological classification of these nephritides except that the retention in uranium occurs at an early stage, where, according to the physiological studies of Schlayer and his associates, and of Pearce, Hill, and Eisenbrey, the vascular changes have not as yet appeared. It must be noticed that in the three types of nephritis that form the subject of this investigation, anatomical study shows the glomerulus to be distinctly involved in the two forms where accumulation of nitrogen in the blood is most marked, a condition indicating that although almost pure tubular involvement produces only moderate accumulation, the additional involvement of the glomerulus is extremely important in leading to a retention of nitrogenous waste products. The accumulation of non-protein nitrogen in the blood and tissues is not large when compared with the total intake or elimination of nitrogen, and consequently it is practically impossible by means of ordinary nitrogen equilibrium experiments to demonstrate the fact of the retention, to say nothing of determining the degree of accumulation of waste products accompanying nephritis. That both can be demonstrated by the method employed in this research is clearly shown by the figures recorded ablove.
Laboratory of Pathology (Phillips Fund) and the Laboratory of Biological Chemistry of the Harvard Medical School, Boston.
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Folin
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Karsner
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Denis