The addition of an excess of inorganic phosphate in the form of orthophosphoric acid, acid, basic or neutral sodium or potassium phosphate to the diet of albino rats results in the development of an interesting and permanent renal lesion. The phosphate renal lesion is characterized by a necrosis of the cells of the convoluted tubules commencing at the terminal end, followed by a regeneration of atypical epithelium and calcification of the necrotic debris that fills the tubules. The entire outer stripe of the outer zone of the medulla is transformed into a zone of distorted structures and there is an increase in the interstitial connective tissue. The adjoining cortex is also involved with cystic dilatation of tubules and collapse. Such areas may reach the free surface of the organ and produce a retracted scar. In the gross the kidneys are enlarged and firm on section with a pebbled surface produced by numerous scars. The maximum changes in the kidney structure are reached after some 15 days although necrosis of the convoluted tubule cells is evident after a single day of phosphate feeding. The renal structure is not restored to its normal form when the excess of phosphate is removed from the diet.

The Idoo(I I ) i t i ( 1~-ivith thrombopenic purpura induced 11)antiplatelet w -u i i i .;h( ) \ \ > ;I moderate decrease in 1)lood viscosity ( directly corrclate(1 I\ ith ;L tlecrcase in total cell volume) and a transient increase in non-protcin iiitrogeii. The venous pressure, plasma iscosity. total ;in(I .l)ccitic colloid osniotic pressure and plasma proteins (lo not unilerqo siqnificant changes. P Hyperalinientation in Normal Animals Produced by ProtamineInsulin. 2

The concentration of urea may be determined more easily and with greater accuracy than that of any other non-protein nitrogenous constituent of the blood. We have shown elsewhere (1) that the blood urea concentration ordinarily increases little above its usual level until the amount of functioning renal tissue has been reduced by more than half. Since a decreased renal function is not of immediate importance to the patient until such a degree (50 per cent) of reduction in the renal substance has taken place, the concentration of urea in the blood becomes an excellent clinical index of renal failure. An increase in the blood urea concentration above the normal range is then of great importance. The small number of subjects in the various series which have been published and the disparity of the results obtained have led us to collect further data relating to the blood urea concentration of normal individuals.In figure 1 the series of normal blood ureas which have been reported in the literature are briefly summarized. Only those groups of observations which were obtained, with two exceptions, from ten or more normal subjects and in which a reasonably reliable blood urea method was used have been included. The earlier and less reliable figures have been summarized by Schwartz and McGill (7).An examination of figure 1 shows a large degree of variation between the "normal range" and the mean values of the different groups of observations. Moreover the number of observations in any single series is too small to draw any conclusions of a general nature.'This work was aided by the Wellington Gregg Fund for the Investigation of Bright's Disease. 295

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