From the foregoing it will be seen that we stand in urgent need of further studies of early or oncoming gout and of early nephritis before we can with certitude impeach the kidneys as responsible for the delay in exogenous purin output. Meanwhile, too, we must be careful not to overlook the further disconcerting fact, previously adverted to, that the retardation and diminution of exogenous purin output is not invariable in gout. Nor, for that matter, is it peculiar to gout, considerations both of which, if confirmed, will still further discount the diagnostic significance of this phenomenon.

Uricæmia in Nephritis

Von Jaksch and Klemperer noted long since that in chronic interstitial nephritis urates are always present in the blood. Now, according to Folin and Denis, human blood contains 1·5-2·5 mg. of uric acid per 100 c.c.; but if the eliminating powers of the kidney be deficient, the uric acid content thereof rises, sometimes to as high as from 15-20 mg. per 100 c.c.

But more interesting still the fact noted by Fine, viz., that even in early interstitial nephritis the same feature is well marked, i.e., the blood may contain 4-8 mg. of uric acid per 100 c.c. Indeed, according to this authority, increase in the uric acid content of the blood is the first signal of impaired renal efficiency. This, be it noted, without any coincident proportional increase in the blood content of urea or creatinine. The sequence would appear to indicate that the damaged organ encounters greater difficulty in excreting uric acid than these other metabolites.

But, pari passu with the advance of the renal disease, retention of urea is superadded, and still later creatinine. So constant, indeed, the sequence that, by determining the percentage amount of these three metabolites in the blood, the measure of the renal mischief may be gauged.

But of striking significance is the further point established by Myers and Fine, viz., that the blood content, in respect of uric acid, urea, and creatinine, in early nephritis, is an almost exact replica of that met with in typical cases of gout. The same is well illustrated in the following table, in which the blood content, in respect of these three metabolites, in cases of gout and early and late nephritis is contrasted. The percentage of the retained metabolites in relation to the severity of the case is gauged by the blood pressure findings.

Uric Acid, Urea N, and Creatinine of Blood in Gout and Early and Late Nephritis

Diagnosis.Uric
acid.
Urea N.
Mg. to
100 c.c. blood.
Creatinine.Systolic
blood
pressure.
Typical cases of gout.9·5131·1230
8·4122·2164
7·2172·4200
6·8141·7
Typical early interstitial nephritis.9·5252·5185
8·0372·7150
5·0373·9130
7·1162·0
6·6243·3185
6·3182·1
8·7203·6100
7·0332·6117
6·3312·1
6·3232·4150
Chronic diffuse and chronic interstitial nephritis.8·0804·8240
4·9172·9170
8·3723·2238
5·3211·9145
9·5443·5210
2·5191·9120
7·7673·1
6·7171·6165
8·3392·9
6·5243·0200
Typical fatal chronic interstitial nephritis.22·423616·7210
15·024020·5225
14·326322·2220
13·09011·1265
8·714411·0225

(Myers and Fine: “Arch. Int. Med.,” 1916.)