MECHANISM OF RENAL SECRETION 79 



Group A {uranium nephritis). That uranium salts attack 

 especially the cells of the convoluted tubules we have just seen. 

 The pathology is evidenced by granular and fatty degeneration 

 and by necrosis of large groups of tubules (28). In our experi- 

 ments (K95, K99, KlOO, K98) with uranium the Zenker-fixed 

 material gave similar findings and the glomeruli were normal in 

 appearance. The technique of all the experiments in this series 

 followed a uniform course: An injection, either subcutaneous or 

 intravenous, of a dose of poison big enough to cause a severe 

 acute nephritis (0.02 gram uranium nitrate for a 3 kg. rabbit 

 intravenously), followed twenty-four hours later by an intrave- 

 nous injection of the iron salt. The animals were all kept in 

 metabolism cages and the urine studied after each voiding. 

 In both K95 and KlOO the second injection was the green ferric 

 ammonium citrate, and a great diminution in the amount secreted 

 was noted. In K95 there was only one sample containing iron 

 and that was a mere trace, while in KlOO the iron-positive 

 sample was reported as 'positive (faint).' Normally, the iron 

 appears in liberal amount through two or more specimens of 

 urine at intervals of one to two hours. 



In K99 the animal received sodium ferrocyanide intravenously 

 instead of the ferric salt. The one positive sample contained a 

 considerable quantity of the salt. Following this voiding there 

 was anuria until death, forty-four hours later. From the diffuse 

 nature of the ferrocyanide distribution in the kidney, as else- 

 where, one would expect little interference with its passage into 

 the urine, whatever the pathology. But the distinctly locahzed 

 passage of ferric iron should be greatly inhibited, as was found 

 to be the case. Confirming Richter's observations (84, 85), we 

 observed ascites at autopsy in K95, K99, and KlOO. 



Thus we see a block to the secretion of iron in tubular nephri- 

 tis, as produced by uranium. Similarly, there is a decrease in 

 nitrogen elimination of from 9 to 14 per cent of normal (89) — 

 a reaction the reverse of that found in glomerular nephritis, 

 where the tubules must be hyperactive to compensate. In 

 fact, in arsenic intoxication the urinary nitrogen is increased 

 from 7 to 16 per cent, due to the increase in metabohc rate. 



THE AMEBTCAN JOURNAL OP ANATOMY, VOL. 29, NO. 1 



