MADAME PRESIDENT and fellow-practitioners: My line of thought for some time past has been turned rather persistently in the direction of albuminuria. At the present time medical opinion appears to me to be in somewhat of a transition stage in regard to the pathology of diseases of the genito-urinary organs. A good many ancient (and Allopathic) fallacies have been exposed and dropped, and we, the Homoeopathists, are building up newer views upon surer foundations. The process will be show (it is hardly more than begun), for the problems to be solved are so very numerous. I have endeavored to look at the subject of my paper in the light of present knowledge only, and not to go on step beyond what that state of knowledge would seem to justify.
I have kept rigidly before my mind, too, the fact that childhood only, at the present time, is my sphere and, as a consequence, I can only touch upon such point in the general pathology of albuminuria as are within the limits of this restriction. Albuminuria, we know, may be produced in children from a variety of causes; the rarest causation, however, is, I think, due to pressure on the renal veins; but let the causative agent be what it may, I believe albuminuria should always be viewed with gravity.
If I might occupy a few moments of time with a hasty review of the physiology of the kidneys, I should be glad, as I think it will freshen our memories and assist us in the discussion of this subject-a subject I am most anxious to have discussed both bore and now; for I am assured that a finer opportunity for eliciting important truths from a conflict of fine minds will never arise.
Physiology of the Kidneys: Gaze with a retrospective eye, if you please, and we find that the membranous covering of the internal surface of the secretory cells of the kidney is really a true protective organ, keeping from the protoplasm of the cells any substances likely to interfere with their functions. We remember, too, that this membrane varies in its structure, and the variation is due to the degree of functional activity of the epithelium.
In conditions of repose this membrane is homogenous; in conditions of activity it is peculiarly marked, having a quantity of clear streaks running through it, and taking on the appearance of a structure formed of small straight rods, these being held together or separated by an intermediate substance of a clear fluid character. After some great functional excitation a remarkable change takes place; the collected urine detaches and pushes away this membrane from the protoplasm.
The products of the renal secretion collect within the epithelial cells in the form of liquid masses, having either a rounded or elongated appearance, and clear, like the contents of the tubules. This fluid percolates through openings in the limiting membrane, sometimes, breaking through the latter to gain the interior of the canaliculi, often detaching and carrying it away.
A great advance has been made in our study of aetiology, proven by the fact of our knowing that a micro-organismal factor exerts its most prominent pathological influence upon the kidneys.
Within the past year or two some notable contributions have been made to the literature of this disease, notably, that of Clifford Mitchell, whose able exposition of the relation of urinary analysis to diet is of untold value; of Mannaberg, upon the relation of acute nephritis and the streptococci found in endocarditis. In eleven cases of acute nephritis, Mannaberg found the urine to contain streptococci, which disappeared from the exertion with the disappearance of the symptoms of disease.
In patients affected by other maladies, and in healthy individuals, this micro-organism is not to be found, although searched for in a long series of urines. Mannaberg has cultivated this streptococcus in question and separated it, by peculiarities in its cultivation, from other varieties of streptococci. These do not appear to select the kidneys as an especial position for growth; they probably multiply in the blood and tissues generally; and in their escape through the renal structures, produce their series consequences.
This, undoubtedly, is a form of blood-poisoning specially involving the kidneys. As I before said, a great many old fallacies have been dropped; the trend of thought and study to-day is carrying us still further and further from the old lines of thought; views formerly held are either passing into desuetude or becoming very much restricted; causes of disease, formerly hardly conjectured, are being added to the list, and some factors of causation, such as exposure to dampness, cold, etc., are dropped out.
I might occupy your time by citing almost numberless cases, published both abroad and at home by adherents of both schools,,where there is no apparent causation of renal disease from exposure to dampness or cold. I will merely cite from Letzerich. He observed a number of cases of renal inflammation, due to characteristic bacillus, from cultures of which he could reproduce nephritis in rabbits. The symptoms he found in general similar to those in other cases of nephritis, somewhat mild in form, but showing a predominance of gastric phenomena.
He found the spleen apt to be swollen, with considerable fever, and often rapidly developing oedema and effusion into the serous cavities. The urine contained short, straight or curved rods, in large numbers. These symptoms, finding no history of exposure to dampness or cold, make the suggestion of a micro- organism exceedingly relevant, especially so, when taking into consideration the manner of onset, the involvement of the lungs, and the prostration accompanying the affection. The affection in question was found most commonly in children, and in cases which came to post-mortem section, it was found that the bacilli developed only in the interstitial structure of the kidney; the spores were, however, found generally throughout the body.
At no previous time has the question of the infections nature of the renal affection, known as Bright’s disease, been so forcibly placed before the profession; and there can be no doubt whatever as to the prominence which will hereafter be accorded to infections influences in the production of the malady. An exceedingly interesting and instructive paper, published by Agnes Bluhm, upon the aetiology of Bright’s disease, is based upon an analysis of 8442 cases, material derived from clinics during a period of five or six years; and the vast majority of these cases were clearly traced to an infections origin.
We find to-day a good many men in our own school, besides numbers of outsiders, who still pin their faith to a belief in the constant existence of albumin in normal urine. After having made a great number of carefully conducted examination of normal urine, I feel compelled to place in opposition to these. The result of my experiments have proven most satisfactorily to my own mind that the presence of albumin is not characteristic of normal urine. There are some of us who argue, that small amounts occurring in normal urine tentatively is of no significance; that it is only where it reaches any proportion that it should be seriously considered.
I believe that the smallest possible amount should be viewed with gravity, and that under any circumstances whatever, albuminuria means some fault of the epithelial covering of the glomerules. Probably Purdy’s experience along these lines has been as large as any one man’s. He, in a publication of his upon examination of urine for life-insurance, takes this position: “No applicant for life-insurance should be debarred on account of albuminuria, but the time has arrived fro stamping out the idea so prevalent among the profession, that the slighter traces of albumin in the urine are of no significance.
It has been my experience during the past five years to make a large number of analyses of urine, from cases of al sorts, but never once have I met with a single case of albuminuria in which a microscopical examinations have not always returned me the foregoing result, but repeated searching has never failed to disclose pathological evidence, so I have arrived at this conclusion: there is positively no such thing as a physiological albuminuria”.
Physiological albuminuria, however, is a term which has fund so much favor with the profession generally, that whatever the belief may be, it-the term-will, in al probability, remain in vague. I believe that albuminuria is many times the product of an incomplete or pernicious digestion. The incomplete transformation of the albumin leads to the production of a relative albuminuria, and from this, by very evident steps, to a true albuminuria. So, too, the various toxic substances, from a perverted digestion, are brought to the kidneys, in their excretion producing a like train of events.
I think, when we are testing for albumin, we should select the specimen of urine voided at the time when the patient is most fatigued; the amount of albumin, as we know, is greatly influenced by circumstances. Then should begin an exhaustive examination for casts, and if one fail to find them when they are actually present, the result must be a serious error in diagnosis.
