Alcohol should be absolutely forbidden. In the purely chronic period we may, however, permit a little while wine, red wine or cider diluted with water.
Finally, the physician has an accurate thermometer for guiding him in the alimentation of his patients, namely, the condition of the urine. If the urine reached a litre and a half or two litres (three to four paints), if the urea approaches its normal quantity, of albumin is diminishing, we may relax the diet much. But if, on the contrary, the urine diminishes much, while at the same time the specific gravity falls below 1010, and the albumin increases in quantity, it becomes necessary to return to the absolute milk diet.
The patient should keep up the functions of the skin, and consequently its cleanliness, by washing and by hot baths. He should shun damp cold, and, if it is possible, spend the winter in hot countries. He should take moderate exercise, and should shun prolonged muscular efforts.
Hydrotherapy, which has been advised by several physicians, has has not kept good the promises which were made in its name, and I do not venture to advise its use.
DISCUSSION.
GEO. M. DILLOW, M.D.: I am sorry that circumstances have so shaped themselves as to make it too difficult for me to attend the Congress and thus to fulfil my provisional promise to comment on Dr. P. Jousset’s paper on Bright’s disease. My regret is the greater because the important and ability of the paper should command the highest respect I could offer. I should find it difficult, however, to compress the little that might interest in a ten minutes’ speech, for my views differ in many respects fro those of the learned author of the paper, and I could not express them satisfactory even in a much longer space of time. But I wish to offer something which you can use in part or whole at your pleasure, in case there is no other speaker to fill my place.
Let me say that, as regards the main contention, the presents state of knowledge does not appear to me to warrant restriction of the term, Bright’s disease, to any one of the recognized forms of nephritis, and that it seems less likely to lead to further confusion if we keep the term, as most generally used, in the generic sense, to cover all forms of primitive renal inflammation which suppress the function of the kidney by destruction of its essential element, viz., the glomerulo-tubular system. By whatever name the process may be called, and wherever beginning, this is the ultimate result of every form, of nephritis, and it is to the result, and largely by reason of its gravity, that the term Bright’s disease specially applies.
One has only to be familiar with many authorities and to follow up diagnosis by post-mortem investigation to realize that schematic descriptions do not so often correspond with the anatomical types predicted and pathological processes predicated. Instead of the so-called typical kidneys, we often find many departures; and if, as histologists, we search them all, we find always inflammatory changes involving all the elements of the cortex, tubules, glomerulus, interstitial structure, and bloodvessels, though present in different degrees, combined in different ways, and associated more or less with degenerative lesions.
Whether there are one, two, or more distinct pathological process involved, or whether there is only one, modified by many aetiological factors, which act in such a way as to determine varying evolution, duration, intensity, extent and degeneration, thus giving rise to a varying symptomatology, I do not feel prepared to say, but, as practical clinicians, it is safer to leave the pathologists to fight out their battle to the finish before we preoccupy our minds with the partisan views of any one of the contending authorities.
We cannot say with some that interstitial nephritis only is Bright’s disease; or that others, that parenchymatous nephritis only is Bright’s disease; or that Bright’s disease does not include other intermediate and mixed forms. It is best to regard it as an ensemble of symptoms and lesions, variously combined, differing in evolution, but always presenting a family resemblance in albuminuria and uraemic manifestations, and in glomerular and tubular destruction.
The confusion into which we would be thrown by accepting Dr. Jousset’s position is well illustrated by the effects of lead upon the kidneys. Using the term parenchymatous nephritis in its purely pathological sense, we should understand an inflammation where the initial lesions ar primarily in the tubal epithelia, which we take to be the parenchyma of the kidney. It is a curious fact that the best established example of this parenchymatous process should be the so-called simple interstitial nephritis of lead-poisoning, which Dr. Jousset rules out of the category of Bright’s disease. Charcot and Gambault have demonstrated that the lesions first observed in animals poisoned by repeated fractional doses of white lead are in the epithelia of Henle’s loops, rapidly passing latter into the epithelia of the convoluted tubules and of Bowman’s capsule.
The epithelia swell, flatten through mutual pressure in distended tubules, break down into embryonal (inflammatory) corpuscles; or in other words, proliferate, whence follow atrophy and collapse of the tubes with growth of connective tissue. The large vessels show no lesions. The arterioles, only in the later period, are affected in their outer coat, and the glomerular capillaries remain intact during nearly the whole duration of the experimental disease.
Here, then, is a typical parenchymatous inflammation, the lesion of the glandular structure being primary, and the interstitial and vascular lesions being secondary; and yet here also is the purest type of so-called interstitial nephritis, which end in the small, red, granular kidney, and an inflammation which is also claimed to be dependent upon arteriosclerosis.
Time does not permit me to analyze the author’s descriptions of the two types of nephritis presented, which, of so brief a paper, are most admirably, if too rigorously, summarized. I cannot, however, permit the opportunity to pass without expression of dissent from his view of the relations of the cardio-vascular system to both parenchymatous and interstitial nephritis. In his parenchymatous nephritis (I have to say his to distinguish it from the parenchymatous nephritis of some other authors), which includes the large and small white kidneys and also the mixed forms of kidneys, common in practice, observation of the heart and arterial tension furnishes clues for diagnosis, prognosis, and treatment not second in value to any other source of information.
In his interstitial nephritis, while I recognize that some cases are joined to generalized arteriosclerosis, I believe that oftener the two processes run concurrently under the action of a common cause, and that still more often the renal inflammation precedes the general arterio- sclerosis and cardiac hypertrophy, of which it is the inducing factor. Even upon his own statement the balance of experimental evidence is in favor of the production of cardiac hypertrophy (and so presumably high arterial tension) by trying of the renal artery and removal of a kidney, and if we add to his experiments by ligature of the ureter, we find cardiac hypertrophy following the nephritis thereby induced. But, leaving experiments aside, the clinical facts are against his position.
High arterial tension and dilatation of the heart are common, even almost constant, in certain stages of acute and chronic parenchymatous nephritis; early hypertrophy even occurs in scarletinal nephritis occasionally, and the very statistics cited by Dr. Jousset indicate that hypertrophy was not exceptional in the cases under examination. His appeal to Bamberger’s cases does not sustain his position of exceptional occurrence. Bamberger’s 344 hypertrophied hearts existed in a total of 807 cases of “primitive Bright’s disease,” “acute,” “chronic.” and “atrophic;” 207 of these 344 hypertrophied were with “atrophic” kidneys; 122 with “chronic,” probably large (parenchymatous) kidneys; and 15 with “acute;” but what proportion the several “acute” “chronic,” and “atrophic” cases bore to the whole 807, and in what percentage of each form hypertrophied hearts existed, cannot be inferred.
All that we can say is, that 122 hypertrophies argue not exceptional but frequent occurrence; and that, had we the data for reaching a proper estimate, Bamberger’s statistics probably would show a proportion approximating one-half cardiac hypertrophies to the whole number of parenchymatous cases. But putting aside the argument from Bamberger as not being conclusive, we find that Dr. Jousset has misconceived Galabin’s statistics. Galabin’s 101 cases numbered 65 hypertrophied hearts instead of 34, as the author of the paper asserts; 66 of the 101 were granular kidneys, with 53 cardiac hypertrophies; 22 were example of tubal (parenchymatous) nephritis, of which 11 had cardiac hypertrophy; 13 were waxy kidneys, with 1 hypertrophied heart.
