It is reasonable, then, to suppose that if, as testified by Ignatowski and Walker Hall, glycocoll is present in gouty _urine_, it is also present in the _tissue fluids_ of the gouty individual, and so the _precipitation_ of _uric acid_ is favoured. Glycocoll, normally, is almost entirely transmuted into _urea_ by the urea-forming ferment of the liver. Impressed by these considerations, Kionka advances the hypothesis that gout is due to: (1) Functional changes in the liver, a depressed urea-ferment action. (2) A deficient uric acid excretion by the kidney, possibly due to the changed uric acid combinations in the blood. (3) These pathological conditions may be “hereditary” or “acquired,” from overeating, alcohol, lead, etc. In other words, given deficient action of the urea ferment in the liver, then more glycocoll will be present in the blood-stream, and the uric acid may be thrown out of solution.[7] For it is possible, as Kionka suggests, that normally uric acid, on its way to urea, may pass through a _glycocoll_ stage. Now, in the gouty individual the glycocoll may not be entirely transformed to _urea_, and its excess in the _tissue fluids_ may lead to _uric acid deposits_. Perhaps, as Walker Hall observes, “since hepatic deficiency is generally admitted in the gouty, diminished destruction of uric acid and glycocoll may go hand in hand.” In healthy _cartilage_ glycocoll is undemonstrable. But, according to Kionka, if bruised or damaged, a considerable amount thereof is formed. Now, when blood, rich in uric acid, circulates through injured cartilage, the presence of glycocoll favours precipitation of the urates, a possible explanation of the formation of _tophi_. Unfortunately for the valency of this theory, Aberhalden and Schittenhelm show that the methods employed by Frey, to isolate glycocoll from cartilage, were such as yield errors which would quite account for the amount obtained by this worker. They, therefore, deny the presence of glycocoll in damaged cartilages. But, in conclusion, Kionka’s plea for a primary _hepatic functional disability_ derives colour from the fact that the drugs which have gained most approval in the treatment of gout are those which increase the quantity of bile without augmenting the amount of bile acids; and the which are excreted in combination with _glycocoll_, for instance, salicyclic acid combines with glycocoll, and is excreted as salicyluric acid, and benzoic acid, which combines with glycocoll to form hippuric acid. Albeit, we must not overlook the fact that the presence of glycocoll is not peculiar to _gouty_ urine, but, as shown by Walker Hall and Embden, is met with in other disorders. The glycocoll hypothesis as to the origin of gout is, though attractive, therefore still unproven. UREA EXCRETION IN GOUT