The number of cases of nephritis among gouty patients would be found much greater, even when no trace of albumen is discovered on clinical examination, if the existence of a latent chronic interstitial nephritis were always suspected and characteristic symptoms were taken as proof of the disease. Such indications are: increased pulse tension (higher sphygmometric readings), signs of cardiac hypertrophy, changes in the retinal fields, or defective kidney function. In this connection may be cited some very striking observations from our own experience. In a case of a painter twenty-eight years of age we found a short time after a typical attack of gout a blood pressure of 150 mm. of mercury (Gartner), but no appearance of albuminuria.

In another case - likewise with an etiology of lead poisoning - we have carried on investigations of the metabolism during eight days, the onset of the attack being excluded, and found a conspicuous nitro gen retention without increase of body weight. We have employed the methylene blue test in three cases. In two of these the beginning of the excretion followed ingestion in half an hour, in one case after an hour. In one case the excretion terminated after thirty-six hours, in another after forty hours, and in the third, after ninety-six hours. In two cases a retardation of the excretion could be proved. In four cases we have demonstrated the nitrogen retention, whose significance in, and relation to, chronic nephritis we have stated elsewhere; and at the time of an attack we obtained values of 35, 64, 66, and 83, mg.

In another case which, to be sure, was complicated with chronic interstitial nephritis, we found 61 mg. in the interval between attacks. In two cases we found the molecular concentration normal during an attack (A= - 0.54° and - 0.56°); on the other hand, one case showed a most remarkable result, inasmuch as during an attack when all precautions were taken, a determination was obtained of A== - 0.75°. And three days later (the attack had already subsided considerably) a repeated investigation of the blood serum gave the still remarkable value of A= - 0.76° *.

* The above mentioned results have been already published (Nierenmonographie p. 69), and in spite of the fact that Wald-vogel has more recently reported a similar observation, we hesitated at first, without the existence of further data, to interpret this finding in a direct relation to an attack of gout, because we have found values similar to the foregoing, in two cases, in which the condition was neither one of gout nor nephritis, nor uraemia.

In the ascitic fluid of the case of gout mentioned, also suffering from atrophic kidney and cirrhosis of the liver, and who had a nitrogen retention of 61 mg., we found repeatedly A= - 0.56°, - 057°, - 0.58°, and once = - 0.60°. If we may venture so far as to diagnose a latent nephritis by a single symptom, then we believe that if several of the usual symptoms of a chronic (nephritis occur simultaneously with gout, in spite of the absence of albumen in the urine, one cannot exclude the existence of a chronic nephritis without farther evidence against it. For the modem clinician, nephritis should be diagnosed before there is a demonstrable albuminuria. However, we are fully alive to the fact that there are functional renal disturbances which are not manifested by distinct anatomical lesions. Although we cannot consider every case of gouty diathesis as simply the result of a diseased kidney, we hold - though not so radically as Levison, for example - that a long-continued disturbance of kidney function is etiologically very important for many, though not for all cases, and we will not concede the objection to be of value that in the interval between attacks, the gouty sufferer may show an undiminished excretion of uric acid. It is also true in nephritis that uric acid excretion may be normal, but in spite of the fact, we find a very great increase of uric acid in the blood; which, as we can prove, exhibits only partially the general tendency in nephritis toward retention of nitrogenous metabolism products. This comes about be cause the uric acid value, as we have pointed out, normally varies in such wide limits that a lack of 100 to 150 mg. in the urine per day is scarcely noticed. If we consider how little uric acid is necessary in the blood serum in order to produce an increase in the body fluids of from 5 to 10 mg. of uric acid per 100 cc. of fluid, it will then be understood that by the process of retention a considerable accumulation of uric acid in the blood serum may occur in a comparatively short time, even when the excretion of uric acid is not appreciably interfered with. But it cannot be denied that there is, possibly, another disturbing factor which plays a rôle in the increase of uric acid in the fluids and which tells against the uricolytic power of the kidneys. Moreover, at all events, it appears to me that in numerous, but by no means all, cases of gout we are justified in assuming a more or less close relation between a nephrogenous inhibition of uric acid excretion and the uric acid increase in the blood serum and the fluids. Although in chronic nephritis the kidneys are able to react promptly to an increased production of uric acid by an increased excretion, there may be, nevertheless, an increase of uric acid in the blood in these cases.