Injecting uric acid intravenously into _gouty_ subjects, Umber noted that at times the whole was retained, but on some occasions was excreted in fractional portions. On the other hand, a _normal_ individual under similar circumstances eliminates it completely. In explanation thereof, he proffered the opinion that this failure on the part of gouty persons to excrete exogenous uric acid was due to a _special affinity of their tissues for uric acid_. As to intravenous injection of uric acid, however, modern investigation has established that, both in normal as well as gouty subjects, its excretion is spread over several days, and the _whole_ is _not_ recoverable from the urine. Now this incomplete excretion or _retention_ of uric acid was attributed to _defective elimination by the renal cells_; but, as shown in a previous chapter, this conception fails of demonstration. Nor, for that matter is there any proof either that the retention is due to _fixation of the uric acid in the blood serum_. Accordingly, to our minds, it is permissible then to canvass the further possibility adumbrated by Umber, viz., that an _increased affinity of the tissues for uric acid_ may haply account for the diminished purin excretion, the excess of uric acid in the blood, lymph, and tissues, and that these same may lead to _uratic deposition_. This last hypothesis derives colour from the findings of Schmoll, Magnus Levy, Vogt, Reach and Bloch, who noted that, after giving thymus to _gouty_ persons, they found far less uric acid in the urine than in the case of normal subjects. Also, that the ingestion of thymus by the victims of _chronic_ gout repeatedly resulted in acute outbursts of the disease. Moreover, as we saw when discussing the _sources_ of uric acid, there are cogent reasons for avoiding a too restricted conception which would make the leucocytes, the muscles, or the digestive glands alone responsible for the _endogenous production of uric acid_; in other words, that a more catholic attitude on our part is indicated, one which would envisage it as the outcome of continuous and _general cellular_ wear and tear. That an _increased cellular destruction_, as induced experimentally, _e.g._, by exposure to Röntgen rays, is capable of raising the _blood content_ of _uric acid_ in a _gouty_ subject, and of precipitating a gouty paroxysm, may be inferred from the researches of P. Linsen. RETENTION CAPACITY OF TISSUES FOR URIC ACID