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.	9·5	13	1·1	230
	8·4	12	2·2	164
	7·2	17	2·4	200
	6·8	14	1·7
Typical early interstitial nephritis.	9·5	25	2·5	185
	8·0	37	2·7	150
	5·0	37	3·9	130
	7·1	16	2·0
	6·6	24	3·3	185
	6·3	18	2·1
	8·7	20	3·6	100
	7·0	33	2·6	117
	6·3	31	2·1
	6·3	23	2·4	150
Chronic diffuse and chronic interstitial nephritis.	8·0	80	4·8	240
	4·9	17	2·9	170
	8·3	72	3·2	238
	5·3	21	1·9	145
	9·5	44	3·5	210
	2·5	19	1·9	120
	7·7	67	3·1
	6·7	17	1·6	165
	8·3	39	2·9
	6·5	24	3·0	200
Typical fatal chronic interstitial nephritis.	22·4	236	16·7	210
	15·0	240	20·5	225
	14·3	263	22·2	220
	13·0	90	11·1	265
	8·7	144	11·0	225

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

The salient feature of the table is, however, the fact that in early interstitial nephritis the retention of uric acid precedes that of urea or creatinine.

Its importance resides in the reflection that it lends support to those who contend that renal change, leading to failure of excretion of uric acid, is the primary cause of gout; in other words, it gives colour to Magnus Levy’s contention that the phenomena of gout are referable to “a deficient and restricted secretory power of the kidney.” The existence of such a selective excretory incapacity, i.e., for uric acid, does not, he considers, predicate a genuine nephritis. He maintains that such disability on the part of the kidney for uric acid excretion may exist without morphological change; in other words, he thinks it conceivable that a single function of the kidney can become almost exclusively insufficient, though later real damage to the organ and a nephritis frequently follow.

Reflecting on the above theory, it is obvious that, if carried to its logical conclusion, it would appear to postulate that gout is nothing more than a form of renal disorder, marked simply by functional inability to excrete uric acid. The postulate is no mean one, for, as Sir Archibald Garrod says, “If the fault is in the kidneys alone, gout must be removed once and for all from the category of metabolic disorders, and placed among the sequelæ of renal inadequacy, at least in so far as the uric acid phenomena of the disease are concerned.”

Furthermore, Levy’s hypothesis involves the assumption that the excreting functions of the kidney for uric acid and urea are separate and independent of each other, and to discussion of this we now pass on.