A FURTHER STUDY OF NITROGEN RETENTION IN THE BLOOD IN EXPERIMENTAL ACUTE NEPHRITIS.
These studies, like all studies of the kidney, are difficult of interpretation because of the impossibility of producing a pure glomerular or pure tubular nephritis. Arsenic nephritis in its early stage is physiologically a vascular nephritis, but anatomically tubular, and shows in this stage almost no retention of nitrogen, although studies of urinary nitrogen indicate an increased catabolism. On the other hand, diphtheria nephritis in the early stages is anatomically a nephritis with marked involvement of the glomerulus anatomically, but it is physiologically a tubular form, and in this early stage there is little or no nitrogen retention although studies of metabolism indicate that protein catabolism is increased by the administration of diphtheria toxin. In both cases, however, there appears to come a time when the excreting power of the kidney is exhausted and nitrogen accumulation occurs in the blood. This is much less marked in the arsenic nephritis, with less tubular change, than in diphtheria toxin nephritis with its marked tubular degeneration. This same late accumulation of blood nitrogen is seen in immune serum nephritis, where the tubular changes are persistent and relatively more severe than the glomerular change. It might well be said that this is no argument for the influence of the tubules in the excretion of waste nitrogen because of the general exhaustion of the organism as a whole and of the kidney in particular, and that no positive conclusions can be drawn is indicated by the opening sentence of this summary. Tartrate nephritis was at first considered as purely tubular; but the appearance of occasional glomerular change, as mentioned by Wells in one of his animals, and the fact that the presence of precipitated albumen in the subcapsular space, pointed out by Pearce and Ringer, probably indicates an increased permeability of the tuft capillaries, all lead to the conclusion that although the tubular change predominates, there is, possibly, slight alteration of the glomerulus. This form of nephritis shows the most marked retention of nitrogen, persisting even though the glomeruli show almost no change, tending to clear up with the progress of time and evidently also with the repair of the tubular change, and bearing a direct relation to the dose of tartaric acid and presumably with the degree of tubular change. It must be remembered, however, that the nephritis in the cases of greatest retention is a very severe form, and this again clouds the physiological interpretation of the results. The study shows no reason for altering the conclusions of our earlier studies, but from the interpretation accorded above it appears to throw more stress on tubular change as determining nitrogen retention. It confirms in addition the value of the methods used for studies of this type.
Laboratory of Pathology (Phillips Fund) and the Laboratory of Biological Chemistry of the Harvard Medical School, Boston.
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Karsner
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Denis