Now in leukæmia the cause of the uricæmia is over-production of uric acid, but in this instance the same is correlated with an increased elimination of uric acid by the kidneys.
Turning to lead poisoning, the medicinal administration of lead acetate results in a great diminution of uric acid excretion, a response consistent with the view that lead inhibits the excretory power of the kidney for uric acid, the change, at first functional, becoming later organic; for it is held that the uricæmia, associated with plumbism, proves that the action of the lead is not due to inhibition of the formation of uric acid.
Lastly, as to gout, opinion still wavers as to whether or not the excretion of uric acid in this disorder is appreciably lowered. On the other hand, it is significant that the reverse is never claimed, viz., that in gout the uric acid output is abnormally raised. Now, as we saw in leukæmia, the high uric acid blood content is accompanied by a correspondingly high uric acid output; but, on the contrary, in gout, despite the accumulation of uric acid in the blood, there is no parallel increase in its elimination.
Reflecting on the above considerations, Folin and Denis claim that “the mere fact that the uric acid may accumulate in the blood of the gouty without being accompanied by an increased elimination constitutes definite proof that the gouty kidney is damaged with reference to its ability to eliminate uric acid.”
In all deference, we doubt the legitimacy of the inference, if only for the very excellent reason that, to quote Von Noorden’s words, even to-day “it remains uncertain whether the retention of urate arises because the outlet is blocked, or because the uric acid is held fast by chemical affinities.”
Apart from this, there are several objections to Folin and Denis’ assumption.
Uricæmia not Necessarily Due To Renal Defect
Thus Pratt, in some examples of his cases of gout, found that there was no apparent diminution or delay in the output of exogenous purin in the urine. On the other hand, he observes that “our study of the blood shows that a marked increase in retention of uric acid in the blood may result from the ingestion of purin bases even when no evidence of retention is found on examination of the urine.” This would appear to indicate that the uricæmia, sequential to exogenous purin intake, ensues independently of and apparently despite the absence of any delay or diminution in uric acid elimination.
Again, Walker Hall, discussing the metabolism of exogenous purins, reminds us that a gouty subject excretes an excess thereof as completely as a normal individual, with only this difference, that he takes a longer time to do so; but even this disability is removed by a simultaneous intake of atophan. His comment is that “the gouty kidney, therefore, is not poisoned beyond compensating for and responding to an extra load.” “Perhaps,” he says, “the situation may be summed up in the observation that the uricæmia of the gouty is maintained in spite of a fair renal elimination.”