How does this work out in actual daily life? he asks. “0·5 gram, in a _normal_ adult, represents the _average daily endogenous uric acid excretion_ in the urine, while that of a _gouty_ subject is about 0·45 gram. Now, assuming that the type and extent of the endogenous metabolism is identical in each instance, then the balance, _i.e._, 0·05 gram, is distributed between the uric acid pent up in the tissues and the uratic deposits, _i.e._, tophi.” Walker Hall tells us it has been stated that about 0·01 gram suffices to cover the amount deposited as _tophi_ every twenty-four hours. The residual 0·04 gram runs to swell the amount in the blood and lymph-streams. “The increase is 0·0114 to 0·0118 gram per litre of blood; in other words, the actual increase of uric acid circulating through the kidneys is about 0·00047 per hour,” which, as Walker Hall contends, “seems to be a very trifling difference, especially as it is one of amount and not a type.” In other words, it is _quantitative_, not qualitative. But, trivial as the disparity is, to what may it be referred? To Walker Hall’s mind, if we are to appreciate the standpoint of those who maintain that the gouty _uricæmia_ is referable to _renal inadequacy_, it is necessary to postulate _the presence of a poison acting upon the renal tubules specifically_. In the gouty uric acid excretion is maintained at a “_low physiological level to the very end_,” and it is easier, he thinks, to adopt the above hypothesis as to its cause than “to conceive of a poison acting upon the _nuclear_ processes in such a way as to induce a persistently low uniform level” of purin excretion. This view, viz., of a _toxin_ acting specifically upon the uric acid excreting cells of the kidney, seems to be the only reasonable assumption available. But even this is difficult of adherence when we recall the fact that the effect of the toxin is so readily neutralised by a few grains of _atophan_. Always we have to recollect, too, that under _normal_ conditions, even given a _constant_ diet, the elimination of uric acid displays _wide variations_. Also the uric acid output in the subjects of _chronic gout_, when placed on a _fixed_ diet, differs but little from that of _normal_ individuals on a like dietary. At most the excretion but tends to fall to, or slightly below, the lower normal limits of uric acid elimination. From the foregoing considerations it is but too obvious that those who render obeisance to the primary renal origin of gout have not only yet to prove that the functions of the kidney are defective, but also upon them lies the _onus probandi why_ gouty subjects should exhibit, or acquire, such a disability. URATIC DEPOSITS IN NEPHRITIS