RENAL CALCULI 461 



and therefore names the whole process alkalinurw. The conception of Leo 

 that the production of alkaline urine is a result of increased blood alka- 

 lescence is wrong, since an increased blood alkalescence does not exist. It 

 is certain that the formation of a phosphate sediment takes place in neu- 

 tral and weakly acid urine, whereas freshly voided alkaline urine may be 

 quite clear. It has already been mentioned, that making a normally acid 

 urine alkaline does not produce so abundant a sediment as occurs in 

 phosphaturia. Naming the condition "alkalinuria" does not describe the 

 kernel of the matter. Sendtner found an increase in^calcium excretion of 

 the urine in phosphaturia. Soetbeer, Krieger, and Tobler investigated the 

 calcium metabolism of children with phosphaturia and came to the follow- 

 ing conclusions : 



Soetbeer found in the urine of a sick child 0.382 gm. CaO, in the 

 urine of a normal child on the same diet 0.113 gm. CaO. The phosphates 

 were the same in both. The ratio CaO :P 2 O 5 was 1 :4 in the sick, 1 :12 in 

 the normal child. The phosphaturia patient had a corresponding decrease 

 of calcium in the feces. As the sick child had symptoms of colitis, Soet- 

 beer regarded the increase of calcium in the urine as the result of a dis- 

 turbance of calcium excretion in the large intestine. This conclusion has 

 received no concurrence. Concerning the calcium excretion in a diseased 

 large intestine we know nothing. Tobler's patients, who also had increased 

 calcium output in the urine, had essentially normal stools. Tobler con- 

 firmed Soetbeer's observation. He found in a four day period: 



Normal urine, 0.414 gm. CaO. 



Phosphaturia I., 1.943 gm. CaO. 



Phosphaturia II., 0.763 gm. CaO (three-day period). 



The quantity of phosphoric acid was the same in all, the feces of the 

 normal subject containing more calcium than the feces of the other patient. 



Umber investigated adults suffering from phosphaturia. He found the 

 ratio of P 2 O 5 : CaO was as 29 :1 in the subject with phosphaturia as 42 :1 

 in the normal subject. In phosphaturia there was increased calcium excre- 

 tion in relation to phosphoric acid excretion. In the second period the in- 

 creased calcium feeding did not increase calcium excretion in the phos- 

 phaturia patient as it did in the control subject. 



The patient first retains the calcium. According to Umber the phos- 

 phate sediment is caused by too high a content of alkaline earths in pro- 

 portion to the phosphoric acid content and too low an acidity. In Umber's 

 patient 45.5 or 48.8 per cent of the total calcium was excreted in the urine; 

 in the normal subject, 26.8 or 18.65 per cent. Umber remarks that fur- 

 ther investigations must decide whether this partition follows any law. 

 However, a still higher percentage of total calcium is found in the clear 

 urine of healthy persons ; the highest value obtained by Renwall was 64 

 per cent. 



The ratio of P 2 O 5 to CaO in the urine of subjects with phosphaturia 





