Although in the light of all the the ories on the pathogenesis of gout cussed above and of the observations of innumerable investigators, many ques tions regarding the real nature of this complaint are still left unanswered, some facts are nevertheless settled beyond all doubt.
It is proved that in various diseases the blood contains an excess of uric acid and that gout is one of these diseases; secondly, it is certain that an excess of uric acid does not cause the deposit of biurate as long as the kidneys are healthy and their action normal.
In all described cases of gout, in which the post-mortem examination is men tioned, the kidneys have been found dis eased, and in almost all cases they were suffering from granular atrophy. Ebstein reported two clinical cases of gout in which the kidneys had been found healthy, but close investigation revealed the fact that the cases were so incom pletely described as to be utterly value less in that respect.
In all cases of granular atrophy of the kidneys, the power of elimination of the kidneys as regards uric acid, as well as various other substances, is diminished. Charcot found it defective under the administration of turpentine, which does not give the urine the characteristic odor of violets when the kidneys are granular atrophic. The consequence of this de fective elimination of uric acid is its re tention in the blood (von Jaksch), and various observers (Ord and Greenfield, Norman-Moore, Levison, Luff) have demonstrated that in granular atrophy of the kidneys deposits of biurate in the joints are very frequently found, even when no symptom of gout has been mani fest during life.
Lead poisoning resembles gout in giv ing rise to an excess of uric acid in the blood, although it is not accompanied by leucocytes or increased disintegration of whole blood-corpuscles. Now it ap pears from experiments on animals (Charcot, Binet, Coen, and d'Ajutolo), as well as from observations of persons exposed to lead poisoning, that one of the earliest and most constant symptoms of this disease is a pathological change of the renal tubuli conducive in rather short time to granular atrophy of the kidneys. This accords very well with the fact that lead poisoning is very liable to give rise to gout, and that Gar rod, Lancereaux, and various other ob servers have found that a large percent age of their gouty patients suffered also from the consequences of lead poison ing.
In a large number of eases of gout and gouty manifestations, there was a course of severe or perplexing symptoms after one or more attacks of influenza.
It seems probable that influenza tends to adversely modify the perverted metab olism in the goutily disposed. A. E. Sansom (Lancet, Oct. 21, '99).
It has been proved by many experi ments that continued irritation of the kidneys by chemical or mechanical irri tants leads to inflammatory processes and formation of new connective tissue, resulting in granular atrophy. When the kidneys of patients suffering from gravel and calculi for some time are ex amined granular atrophy is always found.
When gouty persons are attacked by an intercurrent disease causing a tem porary hyperproduction of uric acid,— as, for instance, pneumonia,—they are sure to get an attack of acute gout in connection with it.
When all these facts are combined and confronted they seem without exception to point to a theory of gout closely allied to the views proposed by Garrod.
Gout and its principal symptom—the deposition of biurates—occurs when the blood remains for some time overcharged with uric acid which cannot be elimi nated by the kidneys on account of a decrease of their secretory power, which, in turn, is caused (with very few excep tions) by granular atrophy more or less distinctly developed. In all cases of gout the kidneys are diseased, and the gout can never develop as long as the kidneys remain healthy. The morbid state of the kidneys may either be due to inherited predisposition (gout in chil dren, early gout hereditary in families) or be acquired by chronic irritation (lead poisoning, abuse of alcoholic stimulants, uric-acid gravel and calculi). As long as the deposition of biurates progresses very slowly no symptom whatever is caused by it, and it is even possible that the deposits may be redissolved without hav ing caused pain or injury at all; but when the deposits grow too large or when from any cause (excesses of every kind, intercurrent diseases, etc.) the produc tion of uric acid gets very large, the de posits increase quickly, the lymphatics are obstructed, and a genuine attack of acute gout is produced. Injudicious therapeutics, such as the abuse of alka line remedies or springs, are liable to produce attacks of gout by the ingestion of large quantities of sodium salts, which have a distinct deterrent influence on the solution of the quadriurates in the blood.