Renal Function in Man 31 



evaluate the number of normal active nephrons by glucose- 

 Tm, since the maximal quantity of glucose in mgm. per min- 

 ute which the kidneys will absorb is determined by the num- 

 ber of nephrons which are both receiving glomerular filtrate 

 and capable of reabsorbing glucose from this filtrate. If the 

 glomerulus of a particular nephron closes, converting it to 

 an aglomerular tubule, or if the tubule itself is rendered in- 

 active by ischemia, it will cease to contribute to glucose-Tm, 

 and this figure will be decreased accordingly. Glucose-Tm 

 will also be decreased by destruction of the reabsorption ca- 

 pacity of the tubule, even though the glomeruli remain open; 

 in this case the nephron enters that category which we have 

 called impotent. Though it is impossible at the moment to 

 distinguish in the diseased kidney which of these three causes 

 — glomerular ischemia, tubular ischemia or tubular injury 

 — may be responsible for reducing glucose-Tm in the diseased 

 kidney, this measurement can be used to determine whether 

 the number of active normal nephrons in the kidney of a 

 particular individual can be increased or decreased by any 

 method. 



Diodrast-Tm serves to measure the number of active ex- 

 cretory tubules, whether glomerular! or aglomerular; it af- 

 fords therefore a measurement of the total quantity of in- 

 tact, tubular excretory tissue in the kidney, which may be 

 designated as the tubular excretory mass.*^ We infer that this 

 tubular excretory mass is identical with the quantity of 

 physiologically intact proximal tubular tissue, since the evi- 

 dence indicates that it is only by the proximal tubule that 

 diodrast is excreted. Within wide limits both glucose-Tm 

 and diodrast-Tm will, under appropriate plasma concentra- 

 tions of glucose and diodrast, be independent of the rate of 

 filtration or the rate of blood flow. That is, they afford us 



