suitable resolutions, Superintendent Treat, Superintendent Kepford, and Chairman Strief. PROGRAM COMMITTEE REPORT. Report of the program committee for the September conference was given by Superintendent Mogridge, as follows: 1. Mental Diseases of The World War Veterans By George Donohoe, M. D., Superintendent, Cherokee State Hospital, Cherokee, Iowa. 2. The Delinquent Child in the Municipal Court 3. Cause of Delinquency in the Normal Child University of South Dakota, Vermillion, South Dakota. 4. Echoes from the National Conference of Social Work By F. M. Hoeye, State Agent, Board of Control of State Institutions, Des Moines, Iowa. 5. The Outlook for Soldiers' Orphans' Homes, 6. The Outlook for Soldiers' Homes By B. C. Whitehill, Commandant, Iowa Soldiers' Home, Marshalltown, Iowa. The conference adjourned sine die. ACUTE NEPHRITIS. Geo. B. Crow, M. D., Burlington, Ia. According to the 1916 mortality statistics of the Census Bureau nephritis is only exceeded as a cause of death by organic heart disease and tuberculosis. In the registration area in that year the figures for acute nephritis and Bright's disease were 75,316 or 105 per 100,000 population. The figures for heart disease and tuberculosis were 107,475 and 88,666. As these three diseases all tend to chronicity it is readily seen that they not only bulk large as causes of death but also as causes of disability. While all of us have a fairly definite idea of what is meant by nephritis we find considerable difficulty in arriving at a definition that will include all patients that we consider to have the disease and at the same time exclude those with evidences of renal irritation but not considered as cases of nephritis. Osler in his text-book does not define the disease. Rose Bradford in Allbut and Rolleston's system of Medicine says: "Nephritis is usually defined as inflammation of the kidney, although it must be admitted that many of the conditions included under this heading might more correctly be described as due to a toxic action on the renal elements." Herrick in Modern Medicine says: "By nephritis is meant an inflammation of the kidney,and, as the term is commonly employed, a non-suppurative inflammation is implied." Christian, in the Oxford System Of Medicine uses the following definition: "Nephritis is a diffuse, progressive, degenerative, or proliferative lesion involving renal porenchyma or interstital tissue or both". This definition excludes those slight degenerative changes that occur in such conditions as typhoid where with fever we have albuminuria and moderate cylindruria and the kidney is quickly restored to normal after the subsidence of the fever. Volhard and Fahr insist that kidneys showing degeneration of epithelium as the essential change are not to be looked upon as true nephritis; for such a condition they prefer the term nephrosis, and reserve the name nephritis for those cases showing primary vascular changes in the kidney, as they believe that vascular changes always usher in true inflammatory processes. Many classifications of nephritis have been attempted and a large percentage of these have been based upon the anatomical findings at autopsy. These have often been so much at variance with the clinical diagnosis that other bases for classification have been attempted for the use of the clinician. One of the simplest, and quite largely referred to, has been proposed by Christian as follows: 1. Acute nephritis Subacute nephritis 2. Chronic nephritis a. With oedema b. With hypertension c. Mixed or intermediate 3. Essential vascular hypertension progressing into chronic nephritis. 4. Renal arterio-sclerosis progressing into chronic nephritis. It is obviously improper for me to attempt to cover the whole subject of nephritis in this paper, or even to take up fully any subdivision of the subject. I desire to call attention only to certain points connected with the cause, course, and management of those cases which originate as an acute process, usually secondary to infection, and to recite briefly a few cases illustrating some of those points. Bacteria and their toxins cause most of the acute cases. Any sort of an acute infection may at times start an acute nephritis. Ophuls states that the cause of true nephritis is continued bacterial septicaemia and the lesions in the kidneys are probably due to rapid bacteriolysis and incidental liberation of large doses of toxic material in and about affected glomeruli. The streptococcus group of organisms seems the most frequent cause of acute lesions, and infections in the respiratory tract, including the mouth and throat, are especially prone to cause renal disease. Hill places tonsillitis as the most common infection that gives rise to this lesion. According to my observation the laity in general regard tonsillitis as a comparatively trivial disease. We should correct this impression wherever possible and insist on rest in bed until danger from its many complications has passed. Among the exanthems scarlet fever takes first place with measles a much less frequent cause. The incidence of nephritis varies greatly in different epidemics, and everyone has noted that severe nephritis often occurs in the mildest cases of scarlet fever. Here, too, rest in bed, prevention of chilling, and frequent examination of the urine is called for. It is my custom to examine the urine weekly for four weeks after the subsidence of fever in all cases of scarlet fever. Other exanthems are infrequent causes. Curiously enough such a typical respiratory tract infection as influenza rarely leads to acute nephritis. I do not recall such a complication in a single case of more than 3,000 influenza patients admitted to the Norfolk Naval Hospital during the epidemic of 1918-1919. Even feb rile albuminuria was infrequent in those cases. All of us are familiar with the action of such chemicals as mercury and arsenic on the kidneys when taken in poisonous dose but we should not forget that these drugs given in therapeutic dose sometimes produce severe renal irritation and frequent examination of the urine should be made during the treatment of every case of syphilis. Syphilis itself, of course, may produce kidney lesions but careful watch of this factor will often show us the necessity of modifying our treatment. Exposure to cold is often given in the literature as a causative factor in nephritis. The tendency has been to discredit this factor and ascribe the nephritis to an accompanying infection. This is a difficult point to settle. In the etiology of war nephritis, however, many writers insist that exposure to cold and wet was a factor, if not the chief factor. Bruns is quoted as saying that "in seventy per cent of the patients there is a clear history of a chill or exposure to dampness and cold". It seems safe to infer that chilling of the body, if not often the sole cause, may be a frequent contributing and perhaps a determining factor in the etiology of acute nephritis. There is another class of cases that show all the urinary findings typical of acute nephritis, but are lacking in the clinical phenomena associated with the disease. I refer to certain results Jos. H. Barach following severe prolonged physical exertion. after studying the urine of Marathon runners reported that all the cases showed albumin, blood and hyaline and granular casts. Albumin persisted for one week in nearly all cases, and casts persisted for one week in twenty-five per cent. Albumin and casts persisted for three weeks in twelve per cent. He further found that in somewhat less strenuous exertion-baseball and track tryouts, of fifty-seven young men with an average running time of forty-eight minutes distributed over a period of two hours, eightyfive per cent showed increased urinary acidity, seventy-seven per cent showed albuminuria, and seventy-one per cent had hyaline and granular casts. A small percentage showed red blood cells. The amount of albumin was in direct proportion to the severity of the exercise, and the abnormal urinary findings as a whole were in direct relation to the circulatory disturbance as manifested by fall in systolic blood pressure and pulse pressure. I wish here to refer to the findings of recent investigators regarding the pathological histology of acute nephritis. Loehlein, Fahr, Jungman, Herxheimer and others have added materially to our knowledge. Elwyn of New York has recently reviewed the work of these investigators (A. M. Jr. Med, Sc. No. 612) and I shall call attention to the salient points brought out in the above review: The glomeruli are enlarged, often fllling the capsular space. The loops of the capillaries are especially characterized by their bloodlessness while the infertubular capillaries are filled with blood. The walls of the glomerular capillaries are thickened and the lumen is empty of blood but contains a granular protoplasm in which the proliferated endothelial cells and the leukocytes are embedded. The capsular epithelium shows at this stage cloudy swelling. The convoluted tubules show cloudy and fatty degeneration and in some areas desquamation of cells. In viewing the histological pictures the most important point is the bloodlessness of the glomeruli and the reaction to this bloodlessness, Loehlien, Volhard and Fahr all insist that this is the prime factor and that the changes in the tubules are secondary to it. They believe that all the variations in the histological pictures as well as in the clinical pictures depends upon these factors. (1) The duration and intensity of the bloodlessness. (2) The extent of the proliferative and infiltrative reaction consequent upon it. (3) The extent to which the capillaries of the glomeruli can again become filled with blood. Volhard believes that the starting point of this bloodlessness is a spastic contraction of the arteries above the afferent artery to the glomerulus. The arterial narrowing is at first functional and not the result of organic change but if this contraction persists organic changes result in the vessel below the choking as well as in the glomeruli. Changes in the vessel wall below the point of choking are of the nature of a proliferative endarteritis. Once such changes are well established the vessels become permanently narrowed to a greater or less extent. The clinical picture will vary with the intensity and duration of the bloodlessness. If it is extreme no blood enters the glomeruli and anuria results. The amount of water and nitrogenous substances retained makes the clinical picture, severe or mild. It is believed that the primary angiospasm is of vaso-motor origin. The primary stimulus may vary and is not known. It may be reflex from chilling, from the action of bacterial toxins, or perhaps it may be an anaphylactic phenomenon. Acute nephritis is essentially a disease of childhood and young adult life, and because of this fact the picture differs materially from a similar lesion in older people for the reason that we are here dealing with a condition that suddenly strikes previously healthy kidneys-kidneys that have not been subjected to the wear and tear of years and, too, without the cardiac and vessel changes so often seen in older people. The recuperative powers of the kidney in young people are great, and Hill believes that nephritis in children should not be considered as chronic until albuminuria has persisted for at least one year. Frothingham places this period at six or more months. Indeed, Hill states that cases may recover after several years albuminuria. On the other hand severe and fatal nephritis with large amounts of albumin and oedema may supervene or contracted kidney may develop |