Volume 4 — DISEASES OF THE GENITO-URINARY SYSTEM. (continued 3)

It is a matter of great practical importance to determine the cause of these cerebral symptoms, for otherwise there can be no rational treatment of them. It is evident that such cerebral symptoms must depend upon anatomical changes in the brain or its membranes, or upon a change in the composition of the blood which circulates through the brain, or upon the quantity of blood supplied to the brain.

It is to be remembered that such cerebral symptoms occur most frequently with the atrophic form of chronic diffuse nephritis; that they are often the first symptom of renal disease; that the same person may have several such attacks, with no cerebral symptoms during the interval; that the urine is usually, but not always, diminished during the attack, and becomes more abundant when the attack ceases; that such attacks also occur with the chronic congestion of the kidney due to cardiac disease, in pregnant women without kidney disease, and with diseased arteries and high arterial tension without kidney disease.

Anatomical changes in the brain or its membranes do exist in a considerable number of cases of chronic Bright's disease. Chronic meningitis with thickening of the pia mater and an increase of serum is quite common; anæmia and oedema of the brain-tissue are often seen. But there are a great many cases with cerebral symptoms without such lesions, and with such lesions without cerebral symptoms.

The composition of the blood is undoubtedly changed in most of the cases with cerebral symptoms. It is natural to look for such changes as are due to perversion of the excretory function of the kidneys, and to ascribe the cerebral symptoms to the poisoning of the blood by urea, by urea transformed into carbonate of ammonia, or by the other excretory matters which should be eliminated by the urine. Moreover, it has been demonstrated that there is a very marked increase in the amount of urea contained in the blood in such cases. On the other hand, we find that suppression of urine with accumulation of urea in the blood may exist for a long time without cerebral symptoms if the suppression is due to obstruction of the ureters; that with chronic congestion of the kidney, puerperal convulsions, and diseased arteries urea is excreted in fair amount, although cerebral symptoms exist; and that even in cases of cerebral symptoms with chronic diffuse nephritis there may be no increase of urea in the blood.

In most of the cases with cerebral symptoms, however, there are other changes in the composition of the blood, concerning the exact nature of which we are still ignorant. In most cases of chronic Bright's disease the patients become pale and the blood is thin and watery; and this is also often the case with chronic congestion of the kidney and with diseased arteries. In pregnancy the quantity of blood is said to be increased: in cholera a considerable part of the fluid portions of the blood is lost.

Changes in the amount of blood in the brain may be due to lesions of the cerebral arteries or to contraction of these arteries; to changes in the arteries in other parts of the body; to organic disease or functional disorder of the heart; or to a change in the whole amount of blood contained in the body.

It seems to me probable that the so-called uræmic symptoms are most frequently due to disturbances of the circulation of blood. Such disturbances of the circulation produce in the brain cerebral symptoms; in the lungs, dyspnoea; in the stomach, vomiting; in the kidneys, suppression of urine.

With the atrophic form of chronic diffuse nephritis we have all the conditions necessary for an irregular circulation—hypertrophy of the left ventricle, diseased arteries, and hydræmic plethora. In the other cases with cerebral symptoms there are also conditions present capable of interfering with the circulation.

Acute Parenchymatous Nephritis.

PATHOLOGICAL ANATOMY.—The lesions of acute parenchymatous nephritis vary with the intensity of the inflammatory process.

(1) Mild Cases.—The kidneys are of normal size and weight. The capsules are not adherent, the surface of the kidney is smooth, the cortex is of normal color or rather pale. The epithelial cells lining the convoluted tubes are swollen and granular.

(2) More Severe Cases.—The kidneys are increased in size. The cortex is thick and whitish, with white striæ extending in to the bases of the pyramids. The epithelium of both the convoluted and straight tubes and of the Malpighian bodies is swollen and granular. There is cast matter in the tubes.

(3) The Most Severe Cases.—The increase in the size of the kidneys is still more marked. The epithelium of most of the tubes is not only swollen and granular, but is also in many tubes detached from their walls. A great deal of cast-matter, and sometimes blood, is found in the tubes. There are no changes in the stroma or in the blood-vessels of the kidneys.

ETIOLOGY.—Acute parenchymatous nephritis occurs both as a primary and secondary lesion. The idiopathic cases occur without assignable cause or after exposure to cold, and are not very common. The secondary cases are seen very frequently. They complicate a variety of other diseases. With pneumonia, typhus fever, and typhoid fever the nephritis is usually of mild type. With yellow fever and acute atrophy of the liver the nephritis is very severe. With scarlatina, diphtheria, pyæmia, peritonitis, phosphorus- and arsenic-poisoning the severity of the nephritis varies with the different cases.

SYMPTOMS.—(1) The Idiopathic Cases.—The urine is diminished in quantity and may be suppressed; its specific gravity continues nearly normal; it contains albumen, usually in large amounts, sometimes blood: in some cases very few casts are seen, in others there are large numbers of hyaline, granular, and nucleated casts.

As regards the other symptoms, it is convenient to divide the idiopathic cases into three classes. In the first class dropsy and anæmia are the most marked symptoms; with these there are loss of appetite and a depreciation in the general condition of the patient. In the second class cerebral symptoms are more prominent. There will be delirium, convulsions, stupor, coma, and with these persistent vomiting, dyspnoea, and great prostration, but no dropsy. The third class suffer from the symptoms of both the other classes. Dropsy, anæmia, loss of appetite, cerebral symptoms, vomiting, dyspnoea, and prostration are all present.

(2) The Secondary Cases.—The condition of the urine varies with the intensity of the nephritis. In the mild cases the urine is unchanged. In the more severe cases we find the urine diminished in quantity, containing albumen in varying amount, sometimes blood. Hyaline and granular casts are often present, but are not very numerous. Dropsy does not usually occur except with the parenchymatous nephritis of scarlatina. Nausea and vomiting are not infrequent, but it is often difficult to tell whether they are due to the primary disease or to the nephritis. Cerebral symptoms—convulsions, delirium, stupor, and coma—occur with the more severe cases.

DURATION.—(1) The Primary Cases.—The class of cases characterized by cerebral symptoms are of short duration. The bad cases die at the end of a few days, the milder cases recover within a few weeks. The class of cases characterized by dropsy last longer, often for several months.

(2) The Secondary Cases.—The renal symptoms continue during the course of the primary disease, and may disappear with the termination of this disease. But if the nephritis is severe the renal symptoms may continue for months after the primary disease has run its course. Albumen and casts are especially apt to persist for a long time. Such a persistence of the nephritis is especially apt to occur with scarlatina and diphtheria.

PROGNOSIS.—(1) The Primary Cases.—The cases characterized by both dropsy and cerebral symptoms usually end fatally. The cases characterized by cerebral symptoms alone are also very apt to die. The cases characterized by dropsy and anæmia often get well, but the albumen and casts may persist for a long time, and the patient may have several attacks of such a nephritis.

(2) The Secondary Cases.—Here the prognosis varies with the intensity of the nephritis. The more severe forms of the inflammation may add very much to the danger of the primary disease or may persist for a long time afterward.

TREATMENT.—(1) The Primary Cases.—In the cases characterized by dropsy the first indication is to get rid of the dropsy, and this is to be done by the methodical use of diuretics, cathartics, and diaphoretics. It will be found, however, that there is a great difference in the different cases as regards the precise time when these remedies will take effect and the dropsy decrease. Usually it is the best plan during the first few weeks of the disease to keep the patient confined to bed or to the house, and on a milk diet. From time to time efforts should be made to reduce the dropsy, but if these efforts produce no effect they should be discontinued and then tried again. In addition to the dropsy the condition of the stomach and the anæmia require treatment. For the stomach the milk diet is perhaps the most efficacious treatment. For the anæmia iron given by the mouth, combined with daily inhalations of oxygen gas, is of very great service. It is very important in these cases to guard against relapses. If possible, the patients should not return to their ordinary pursuits for a year after their apparent recovery, but should spend that time in travelling and improving their health in every possible way.

In the cases characterized by cerebral symptoms it must be confessed that treatment is not very efficacious. Diuretics have no effect, cathartics seem to do no good. Systematic sweating, the use of pilocarpine in small doses twice a day, inhalations of nitrite of amyl, the administration of chloral hydrate, caffeine, digitalis, and convallaria, and the use of fluid food in small doses, are indicated.

(2) The Secondary Cases.—While the primary disease, to which the nephritis is secondary, is running its course there is little to be done for renal symptoms. If, however, these symptoms persist after the termination of the primary disease, then the main indication is to improve the general health in every possible way.

Chronic Parenchymatous Nephritis.

A good deal of confusion is connected with this name, for the reason that many authors include in this one class all the large white kidneys except the waxy ones, and such kidneys present a variety of lesions. There are, however, a moderate number of cases in which the morbid changes are confined to the epithelium of the tubes and to the Malpighian bodies. All the kidneys, no matter what their gross appearance may be, which present changes in the stroma and blood-vessels, as well as in the tubes, belong properly to the class of chronic diffuse nephritis. I confine the name of chronic parenchymatous nephritis, therefore, to those kidneys in which the inflammatory process runs a chronic course and is confined to the epithelium of the tubes and the Malpighian bodies.

LESIONS.—The kidneys are regularly increased in size, often weighing sixteen or twenty ounces. The capsules are not adherent, the surface of the kidney is smooth. The cortex of the kidney is thick and white, with white striæ running into the bases of the pyramids; the pyramids are large and red. The epithelium of most of the tubes and of the Malpighian capsules is swollen, granular, and detached. Cast-matter is present in the tubes. There may be an increase in the number of the small cells which cover the tufts of vessels in the Malpighian bodies.

ETIOLOGY.—This form of nephritis is not very common. It may follow acute parenchymatous nephritis and chronic congestion of the kidney; it is one of the complications of chronic pulmonary phthisis, and it occurs as an idiopathic disease.

SYMPTOMS.—There is a good deal of variety in the different cases as to the quantity and specific gravity of the urine. Usually the quantity is somewhat diminished, and the specific gravity is between 1020 and 1030.

Albumen is regularly present in considerable quantity, but it may be scanty, and may even disappear altogether for a time. Hyaline and granular casts are usually present, but in small numbers.

Dropsy is a regular symptom, and often goes on to general anasarca, although the degree of the oedema varies from week to week. Occasionally a case will run its course without any dropsy.

The functions of the stomach are disturbed, and the patients suffer from loss of appetite, nausea, and vomiting.

Muscular twitchings, convulsions, stupor, and coma only occur in the very severe cases.

Dyspnoea is often produced by the dropsy, sometimes is simply a nervous phenomenon.

Bronchitis with cough and expectoration may be a complication.

DURATION.—The course of the disease is slow; it lasts for months and years. The cases vary a good deal in the number and severity of the symptoms. Some cases run their course with nothing but the changes in the urine, loss of appetite, and a moderate degree of anæmia. In other cases the dropsy is the most prominent symptom, and in still others the cerebral symptoms predominate. There may be intervals of weeks and months during which all the symptoms, except the changes in the urine, disappear and then come on again.

PROGNOSIS.—The prognosis of chronic parenchymatous nephritis is not good, but still it is not so bad as that of chronic diffuse nephritis: some of the cases recover and never have any further indications of kidney disease.

TREATMENT.—The main indications for treatment are to improve the digestion, remove the dropsy, and restore the blood to a natural condition. It is usually necessary for the patient to give up his ordinary business and if possible to pass the winter months in a warmer climate.

Acute Diffuse Nephritis.

This form of nephritis has been described under a variety of names. It has been called acute Bright's disease, acute desquamative nephritis, acute tubular nephritis, croupous nephritis, acute albuminuria, the first stage of chronic Bright's disease, acute parenchymatous nephritis, glomerulo-nephritis, and acute interstitial nephritis.

MORBID ANATOMY.—The kidneys are increased in size, the capsules are not adherent, the surfaces are smooth. There may be an intense congestion of the entire kidney, including its pelvis, or the cortex is of an opaque white color mottled with red spots, and the pyramids are red. The tissue of the kidney is usually moist and succulent. In the tubes the epithelial cells are swollen, granular, and detached. Cast-matter and blood are found in many of the tubes. In the Malpighian bodies the cells which line the capsules are increased in size and number, sometimes to such an extent as to compress the tuft of vessels. The stroma of the kidney is infiltrated with serum, pus-cells, and blood.

ETIOLOGY.—Most of the cases of acute diffuse nephritis occur after exposure to cold or as a complication of scarlatina.

SYMPTOMS.—(1) The Idiopathic Cases.—Of these we may distinguish two sets of cases. In the first set of cases the invasion of the disease is acute. A person who has previously been usually in good health, after exposure to cold and wet will be suddenly attacked with rigors, a febrile movement, and pain in the back. There will be frequent and painful micturition, the urine being only passed a few drops at a time, or it is completely suppressed.

The urine is bloody or of a brownish smoky color. It is of low specific gravity. It contains a very large amount of albumen, numerous hyaline, granular, epithelial, and blood casts and renal epithelium, and sometimes pus-cells. Later in the disease fatty casts are also present.

The patient soon develops dropsy, the extent of which varies in the different cases. Sometimes it involves only the face, sometimes the hands and feet, or there may be general subcutaneous oedema, serum in the serous cavities, oedema of the lungs and of the glottis. The patients lose their appetite; often there are nausea and vomiting. As a rule, there are cerebral symptoms—headache, drowsiness, stupor, delirium, muscular twitchings, convulsions, and coma. In the milder cases there will be only headache and periods of drowsiness, alternating with periods of irritability. In the severe cases there will be dyspnoea, delirium, repeated convulsions, and coma.

These are the regular symptoms of the disease—symptoms varying in their number and development with the intensity of the nephritis. In the worst cases the cerebral symptoms are developed early and the patients die at the end of a few days. In other cases the symptoms continue for months, and at the end of that time terminate either in the death or recovery of the patient. Albumen and casts in the urine may persist long after all other symptoms have disappeared. In other cases the disease runs a very mild course; the patients are not at any time seriously ill, and they recover completely at the end of two or three weeks. In still other cases the acute inflammation is succeeded by chronic diffuse nephritis. Relapses and repeated attacks of the disease occur in some persons.

The course of the disease may be modified by complicating inflammations. Pericarditis, pleurisy, peritonitis, pneumonia, cystitis, and inflammations of the joints and muscles are not uncommon.

PROGNOSIS.—In the larger number of cases the prognosis is good. The milder cases recover after two or three weeks; more severe cases last for several months. The bad cases die at the end of a few days with cerebral symptoms, or all the symptoms continue and the patient dies at the end of several months, or they pass on to the lesions and symptoms of chronic diffuse nephritis, or they die from some complicating inflammation.

TREATMENT.—In the mild cases but little treatment is required. The patients should be kept in bed, should have a fluid diet, the bowels should be moved, and the restlessness should be quieted by the bromides, chloral hydrate, or opium. If the dropsy is a marked feature, more active purgatives are to be employed, hot-water or hot-air baths are to be used, and jaborandi may be of service. When the urine is very scanty, wet or dry cups over the region of the kidneys and hot fomentation over the same region are of much service. For the more marked cerebral symptoms treatment is not very satisfactory. As the patients get better iron and tonics are usually indicated. Great care must be used to prevent relapses. All exposure to cold must be avoided; the patient is to be kept in the house or sent to a warm climate for some time after he is apparently well. So long as albumen and casts persist in the urine the patients must not be considered well, although they may present no renal symptoms.

(2) In the second set of cases the invasion of the disease is not acute, and the symptoms may at first be so slight that the patient will hardly notice them. Usually the first symptoms are referable to the stomach. The patients lose their appetite, are troubled with nausea, and vomit occasionally. There may be a moderate amount of pain in the back, general languor, and indisposition for mental or physical work. Then they notice a change in the urine; they pass much less than before. The urine remains of its ordinary color or is a little smoky; its specific gravity is less; it contains a good deal of albumen, sometimes a little blood, and large numbers of hyaline, granular, and epithelial casts.

Dropsy makes its appearance at first in the face or feet; it may remain confined to these regions or extend to the rest of the body and become a general dropsy. The cerebral symptoms are slight—headache, irritability, drowsiness. The blood becomes thin and watery and the patients unnaturally pale. There may be dyspnoea either dropsical or nervous. The symptoms continue for weeks or months.

PROGNOSIS.—These cases, as a rule, do well, and recover at the end of a few weeks or months. But in some the symptoms continue and the patients go on to have chronic diffuse nephritis.

TREATMENT.—In the mild cases it is only necessary to keep the patients in the house, put them on a milk diet, keep the bowels open, and after a time give them iron. If the dropsy is more marked, we must try to get rid of it by cathartics, sweating, and diuretics. If the anæmia is marked, inhalations of oxygen must be combined with the administration of iron. In these cases also it is important to guard against relapses.

The Acute Diffuse Nephritis of Scarlatina.

Most cases of scarlatina are complicated either by acute parenchymatous or diffuse nephritis. Some confusion has arisen from the attempt to describe scarlatinal nephritis as if it was one disease, while really there are two anatomical forms of nephritis which occur as complications of scarlatina. When we try to fix the time during the course of scarlatina when the kidney lesions are developed, we meet with the same difficulty—that statistics have been compiled on the supposition that there is only one form of scarlatinal nephritis. If we take all the cases together, we find that kidney symptoms may be developed from the very first day of scarlet fever to the end of the ninth week—that the largest number of cases develop symptoms on the fourteenth day, the next largest on the twenty-first day, and next to this on the seventh day (Tripe). It seems probable that parenchymatous nephritis belongs to the first weeks of the disease, diffuse nephritis to the later weeks.

SYMPTOMS.—The urine is diminished in amount, and may be suppressed. Its specific gravity is low, its color is bloody or smoky; it contains blood, large amounts of albumen, and numerous hyaline, granular, and epithelial casts.

The patients lose their appetites, and suffer from nausea and occasional vomiting. There is a febrile movement, usually not very severe, pain in the back and limbs. They become unnaturally peevish and irritable and complain of headache, the irritability alternating with drowsiness. In the more severe cases delirium, convulsions, and coma are developed. The color of the patients is changed, the skin and mucous membranes becoming pale. Dropsy is developed—sometimes only a little puffiness of the face, hands, or feet, sometimes general anasarca. Synovitis and muscular rheumatism are frequent complications, while pericarditis, pleurisy, and pneumonia occur less often.

The disease runs its course within a moderate length of time, although the changes in the urine often persist long after all the other symptoms have disappeared. The ordinary cases recover after from one to three weeks; the very bad cases die at the end of a few days. In a few cases the symptoms continue and the patient develops chronic diffuse nephritis.

PROGNOSIS.—The prognosis is quite good. The larger number of the cases recover completely. In the more severe cases, however, the patients may die with cerebral symptoms, or all the symptoms will continue and the patient die after several weeks.

TREATMENT.—The indications for treatment are the same as in the idiopathic form of acute diffuse nephritis.

Chronic Diffuse Nephritis.

This is the most common and the most important form of kidney disease. It has been described under a variety of names—chronic Bright's disease, croupous, catarrhal, interstitial, tubal, and parenchymatous nephritis; fatty, granular, atrophied, cirrhotic, and large white kidney.

Although all patients with chronic diffuse nephritis suffer from essentially the same symptoms, yet there is a good deal of difference as to the way in which these symptoms are developed and as to the predominance of some symptoms over others. Although the minute lesions of the kidneys are essentially the same in all cases, yet the gross appearance varies a good deal. There is, therefore, a practical convenience in distinguishing certain varieties of chronic diffuse nephritis. Of late years, however, the tendency to do this has been carried very far, especially as regards the atrophic form of chronic diffuse nephritis. Writers speak as if there were only two forms of chronic diffuse nephritis—the large white kidneys and the atrophied kidneys—and as if each of these had a distinct clinical history. More than this, the changes in the blood-vessels and in the circulation which so often complicate chronic Bright's disease have attracted so much attention that the arterial changes have been regarded as the most important part of the disease, so that we even hear of Bright's disease without any lesion of the kidneys. It is also customary to describe separately those kidneys of which the arteries have undergone waxy infiltrations.

I do not think that either the lesions or the symptoms are such as to justify such views. After separating the true cases of chronic parenchymatous nephritis—cases in which only the epithelium of the tubes and of the Malpighian capsules is changed—all the other kidneys of chronic Bright's disease present essentially the same lesions and give rise to the same symptoms.

We can indeed often tell during the life of the patient whether he has large white or atrophied or waxy kidneys, but in many cases such a diagnosis is impossible.

MORBID ANATOMY.—There is good deal of variety in the gross appearances and size of the kidneys. Most numerous are the so-called atrophied kidneys. These kidneys are usually diminished in weight, the kidneys weighing together three or four ounces, but often they weigh up to ten or twelve ounces. The capsules are adherent, and when they are stripped off portions of the kidney-tissue adhere to them. After stripping off the capsules the surface of the kidney is left finely or coarsely nodular. The cortex is thinned and of a red or grayish mottled color; the pyramids are small or of normal size, sometimes studded with small white concretions of urate of soda. There are often small cysts both in the cortex and pyramids.

Next in frequency come the so-called large white kidneys. Of these a certain number are not examples of chronic diffuse nephritis at all, but of acute or chronic parenchymatous nephritis. Of the large white kidneys which belong to chronic diffuse nephritis we can distinguish three varieties—the simple large white, the waxy large white, and the large white of cardiac disease.

The gross appearance of the kidneys is very much the same whether they are or are not the seat of waxy infiltrations. They are increased in size, weighing together from sixteen to twenty ounces. The capsules are not adherent; the surfaces of the kidneys are smooth and pale, often mottled by large stellate veins. The cortex is thickened, of white or white mottled with red, or yellow or grayish color. In the very waxy kidneys the gray or white color has a semi-translucent appearance. The pyramids are large and red, contrasting with the cortex. We find some kidneys of the same color and general appearance as large white kidneys, but with atrophied cortex and adherent capsules.

The large white kidneys due to cardiac disease are increased in size and weight. The capsules are not adherent, the surfaces are smooth. The cortex is thickened and of a peculiar pinkish-white color; the cortical striæ may still be visible. The pyramids are of a somewhat darker red than the cortex. The whole coloring is entirely different from that of chronic congestion of the kidneys, and the texture, although firm, is not of the stony hardness of that lesion.

Besides the atrophied and the large white kidneys, there are a large number of kidneys which are not diminished in weight and which do not resemble either the large white or the atrophied kidneys. These kidneys weigh together from nine to twenty ounces. The capsules are sometimes adherent, sometimes not. The surface of the cortex may look like that of a normal kidney or be finely or coarsely nodular. The cortex is of normal thickness or thickened; it is of a variety of colors. Sometimes it is not to be distinguished from a normal kidney, or it may be gray or gray mottled with yellow or red or white, or of a diffuse red color. The pyramids are of natural size or large, of red or pale color. I do not know a good name for these kidneys, but their appearance differs altogether from that of the large white or atrophied kidneys.

Still another class may be made of those kidneys which pass from the condition of chronic congestion into that of chronic diffuse nephritis. These kidneys retain the color and the hardness of chronic congestion, but the capsules are adherent, the surfaces finely nodular, and the cortex irregular.

Minute Lesions.—Nearly all the component parts of the kidneys undergo morbid changes. In the tubes the epithelial cells undergo marked changes, especially in the cortex. The epithelial cells are swollen, finely or coarsely granular, or fatty or completely disintegrated, or the seat of hyaline degeneration. They may be detached from the walls of the tubes, or sometimes they are in place, but flattened. The tubes may contain cast-matter, blood, pus-cells, small polygonal cells. The calibre of the tubes is often changed. The tubes may be dilated either in the form of cylindrical or sacculated dilatations; the latter often form cysts of considerable size. Such dilatations regularly affect groups of tubes, as if they were due to obstruction of the large tubes in the pyramids. In other cases the tubes are denuded of epithelium, become smaller, fall together, and look like connective tissue. The membranous wall of the tubules may be thickened or it may undergo waxy degeneration.

The Malpighian bodies are changed. Their capsules may be thickened, contracted, or dilated. The flat cells which line the capsules are increased in size, sometimes in number. The capillary tuft may be dilated or its walls may be thickened; it may be completely obliterated and changed into a ball of fibrous tissue, or it may be the seat of waxy infiltration. Often the Malpighian bodies are much closer together than they are in a normal kidney.

In the stroma, especially in the cortex, there is a new growth of connective tissue. This new connective tissue is in patches of varying size, surrounds Malpighian bodies and blood-vessels, and may be continuous with the capsule of the kidneys.

The arteries are frequently changed. There is a general thickening of all their coats, usually a simple sclerotic thickening.

All these changes, when they have once begun in the kidneys, have a natural tendency to go on and become more and more marked. There is much difference in different kidneys in the predominance of one or more of these changes over others. In one kidney the changes in the tubes will be most marked, in another those in the Malpighian bodies, in another those in the stroma. But there seems no good reason for believing that these changes are developed successively—that there is first a lesion of the stroma, then a lesion of the tubes, or first a lesion of the tubes, and then of the stroma. The earliest examples of chronic diffuse nephritis, obtained from persons dying accidentally of other diseases, show that the lesions are diffuse at the very outset.

In the atrophied kidneys the new connective tissue is in patches. In the earliest stages of the lesion these patches are confined to the region close to the capsule; later in the disease the whole thickness of the cortex is involved. The tubes embraced within these areas of new connective tissue are atrophied and collapsed. The rest of the cortex-tubes exhibit marked degenerative changes in the epithelium, and often cast-matter. Dilatation of the tubes is very common. The Malpighian bodies are usually much altered—the capsules thickened, the tufts atrophied. Occasionally there is waxy degeneration of the Malpighian tufts. There are some atrophied kidneys in which the changes in the stroma are very slight.

In the large white kidneys there is much variety. In some of them one is surprised to find how slight the minute lesions are. In others the principal changes are in the epithelium of the tubes, so that it may be difficult to tell whether they are examples of parenchymatous or of diffuse nephritis. In many others there is a very marked production of new connective tissue either in patches or diffuse. The large white kidneys which are waxy differ from the others only in the addition of the waxy degeneration of the Malpighian tufts and arteries to the other lesions. I have no knowledge of any kidneys in which waxy degeneration exists without the presence of the regular lesions of diffuse nephritis.

In the large white kidneys of cardiac disease the large thickened arteries are a prominent feature.

ETIOLOGY.—Chronic diffuse nephritis is more common in males than in females. It is said to occur at nearly all ages; the maximum liability is in persons between the ages of forty-five and fifty-five years. The disease prevails principally in temperate climates; in New York it is of very common occurrence. Persons who are habitually intemperate, who have constitutional syphilis, who suffer from privation, are very liable to the disease. There is a disposition in certain families to the development of the disease. Not that it is, strictly speaking, hereditary, but there will be a number of examples of it in the same family. A number of brothers and sisters or of more distant relatives in the same family will at different times suffer from the disease. There seems also to be some sort of relationship between chronic diffuse nephritis and pulmonary phthisis. Not only does nephritis complicate phthisis, but in the same family some members have phthisis, others nephritis.

Acute diffuse nephritis and chronic congestion of the kidney may be followed by chronic diffuse nephritis.

Heart disease, emphysema, phthisis, cirrhosis of the liver, chronic inflammation of the bones and joints, gout, rheumatism, and chronic arteritis, are often complicated by the disease.

SYMPTOMS.—It is sometimes impossible to tell which of the varieties of chronic nephritis exists in a given patient, but in other cases the diagnosis can be made. If, however, we correct our clinical diagnosis by post-mortem observations, we find that we may be mistaken about even the (apparently) most characteristic cases. There is more difference in the earlier stages of these cases than in the later ones. In hospitals, where the patients come to die, all the cases of chronic diffuse nephritis are a good deal alike.

The atrophied kidneys present us with a very great variety of clinical histories. It is impossible to describe all the different ways in which the disease may begin and run its course, but we may enumerate some of them:

1. Persons may have atrophied kidneys for a number of years without any renal symptoms; they die from accident or from some other disease, and at the autopsy the kidneys are found to be far advanced in disease.

2. The disease of the kidneys exists, but it gives no symptoms until the patient suffers from some severe accident or is attacked by some acute disease, and then the renal symptoms are suddenly developed.

3. The patient will very slowly lose flesh and strength, the appetite will be capricious, either mental or bodily exertion is an effort, but there are no positive symptoms, except that the urine is of rather low specific gravity, and in the evening urine there will be occasionally a trace of albumen. In this condition these patients may continue for years. They may improve very much under treatment, and finally die from some other disease without ever developing any renal symptoms. Other cases, however, do after a time develop all the characteristic symptoms.

4. For several months the patients do not feel well: the appetite is lost, there is nausea and occasional vomiting, they become pale and anæmic, do not sleep well at night, are irritable and easily worried, are troubled with headache. The urine continues normal or is of low specific gravity or contains a little albumen. Then they suddenly become worse and the regular symptoms are developed.

5. In other cases headache or sleeplessness or dyspnoea or loss of vision may precede all the other symptoms by several weeks.

6. Severe neuralgic pains in different parts of the body, coming on in attacks and very rebellious to treatment, may precede the other symptoms for months.

7. The very first symptoms may be an attack of convulsions. The patient may have been apparently in good health, and while sitting quietly in a room or lying in bed will be seized with a general convulsion. In some of these cases the convulsions are repeated; between them the patient remains partly or completely unconscious, and dies in a few days. In other cases one or two convulsions are followed by the development of the other symptoms of the disease.

8. With valvular disease of the heart and atrophied kidneys we may get the same combination of symptoms which I have described in the section on chronic congestion of the kidneys.

9. The patient may first notice that he is passing too much urine. This urine is of low specific gravity, and occasionally contains a little albumen and hyaline casts. Then the health begins to fail: there are dyspeptic symptoms, headache, occasional oedema of the legs. From time to time the patient becomes worse; the urine is diminished in quantity, the headache is more marked; he cannot sleep, he has dyspnoea, he vomits, the muscles of the face twitch, or there may be general convulsions or delirium or partial or complete coma. Such attacks may last for days or weeks, and then either terminate fatally, or the patient gets better and may be able to return to his ordinary business for a time. In this way the same patient may suffer from a number of such attacks.

10. In some cases dropsy is a prominent feature from the very first and goes on to general anasarca.

The following history would answer for many of the cases of atrophied kidneys: A woman, thirty-eight years old, was in good health, fat and robust, until January, 1873. Then she caught cold; her feet became oedematous; she had headache, pain in the back, vomiting; her eyesight was impaired; her urine was increased in amount and passed more frequently. She continued in this condition and losing flesh and strength until June, 1873, when she came into the hospital. At that time the urine was diminished to eighteen ounces in twenty-four hours; it contained a considerable amount of albumen and hyaline and granular casts. Her color was still good. There was moderate oedema of the feet. After this the urine increased in amount to eighty ounces daily—specific gravity 1002, albumen diminished. The dropsy disappeared, and the patient left the hospital feeling very well on September 29, 1873. In December, 1873, she returned to the hospital with nausea and vomiting, dyspnoea, cough, no dropsy; urine 80 to 100 ounces daily. She had become feeble and anæmic, and there was well-marked hypertrophy of the left ventricle of the heart. She again improved, and was discharged after two weeks. In March, 1874, she returned. The urine was now scanty, and she was troubled with vomiting, dyspnoea, cough, sleeplessness, slight convulsive movements of the voluntary muscles, no dropsy. By the end of April she was again feeling well, and left the hospital. In June, 1874, she returned with all the old symptoms and oedema of the legs. On July 20 she had two general convulsions. After this she again improved for a time, but in September all the symptoms returned, and she was delirious a good deal of the time. Urine 40 to 50 ounces daily, specific gravity 1005, moderate amount of albumen, no casts. By the end of September she again was sleepless, had several slight convulsions, and died October 2. The kidneys were a typical picture of the red atrophied kidneys with thickened arteries.

We may say in general that with the atrophied kidneys the so-called uræmic symptoms—headache, sleeplessness, delirium, convulsions, coma, dyspnoea—are very apt to occur, and that early in the disease. The urine is regularly increased in amount and of low specific gravity, except during the uræmic attacks, when it is diminished; but the uræmic attacks may come on while the patient is passing 30 to 40 ounces of urine of a specific gravity of 1020. Albumen is regularly present only in small amounts, and not constantly, but exceptionally there will be a good deal. Casts are hyaline, not constant, but exceptionally in considerable numbers. Dropsy may be absent throughout the disease, or a little oedema of the face and legs may come and go, or there may be marked general anasarca. Not unfrequently during the uræmic attacks the temperature runs up to 99° to 100°. Hypertrophy of the left ventricle of the heart is a frequent complication, but I have not found it in as large a proportion of cases in New York as it is described by English and German writers.

The duration of the disease is very uncertain. In fact, we seldom know what its real duration is, for the reason that there is no necessary relation between the development of the kidney lesions and the appearance of the symptoms. After the appearance of the kidney symptoms some of the patients die in a few days; others go on for months and years with either constant or intermittent symptoms.

The Large White Kidney.—These cases are more readily recognized than the cases of atrophied kidneys, for the reason that dropsy is more constant and occurs earlier in the disease, and that albumen is regularly present in the urine.

In many of the cases oedema of the face or feet is the first symptom. Often the patients will tell you that it is the only symptom, and that they would feel perfectly well if they could only get rid of the swelling. Closer questioning, however, will usually show that the functions of the stomach are disturbed, that there is occasional headache, that the eyesight is impaired, and that the patient has been passing less urine.

In some cases impairment of vision is the first symptom that attracts the attention of the patient. In some cases disturbances of digestion, or neuralgic pains, or gradual loss of health and strength, or a diminished amount of urine, will be the first symptoms, and may last for weeks before other symptoms are developed. Or the patient may be attacked suddenly as if with acute diffuse nephritis. The urine will contain blood and numerous casts; the dropsy and the other symptoms are rapidly developed. In some of the cases complicated with cardiac disease the history will be that of heart disease rather than that of kidney disease.

When the disease is fairly established the dropsy is always a prominent symptom, often very distressing to the patient. In some patients when once developed it continues to increase steadily up to the time of their death; in others the dropsy comes and goes, sometimes disappearing altogether for weeks and months.

The functions of the stomach are usually disturbed, the patients lose appetite, have nausea and vomiting, oppression after eating, etc. But some persons retain a good appetite for a long time, even though they vomit occasionally. Diarrhoea is often developed; sometimes only enough to carry off part of the dropsy, sometimes profuse, persistent, and uncontrollable. The blood becomes thin and watery, and the skin, the mucous membranes, and the sclerotic assume an unnatural white appearance. The patients lose both mental and bodily vigor, and become less and less fit to carry on their ordinary occupations.

Of the uræmic symptoms, headache and dyspnoea occur at any time in the course of the disease, but convulsions, delirium, and coma belong to its later stages.

The urine is regularly first diminished and afterward increased, but the quantity often varies very much from day to day. The specific gravity is regularly low, albumen is constant and in large amount; casts are usually present in considerable numbers, especially during the exacerbations of the disease, when hyaline, granular, and epithelial casts are found, but in other cases hardly any casts can be found. Blood is sometimes present in the urine during the exacerbations of the nephritis.

The disease varies much in its course and duration. Some cases progress steadily, getting worse from day to day, and die at the end of a few months from the time at which the first symptoms appeared. Other persons go on living for years, the symptoms improving or disappearing for weeks or months, and then coming again. Finally, the patients die—some in an exacerbation of the disease with bloody urine and acute symptoms; some with excessive dropsy; some with delirium, convulsions, and coma; some suddenly; some with complicating disease.

The following histories may serve to illustrate the course of the disease:

A male, thirty years old, of intemperate habits, for one year before his death noticed that his urine was sometimes scanty and high-colored, sometimes abundant and pale, and that his eyesight became impaired. For four months there was occasional nausea and vomiting. For six weeks there was occasional headache, dyspnoea, and oedema of the feet, the urine more scanty. For nine days before death he passed from one to four ounces of urine daily, specific gravity 1014, albumen 50 per cent., numerous hyaline, granular, and epithelial casts. The man was now feeble and anæmic, had headache, was drowsy, vomited occasionally, had twitching of muscles of face; continued drowsy, but with his mental faculties quite clear, so that he was able to transact some business an hour before he died. Death was sudden while lying quietly in bed. The kidneys weighed twenty ounces, surfaces smooth, cortex thick and white, pyramids large and red. The Malpighian bodies showed a marked increase in the size and number of the capsule cells; the cortex-tubes were dilated; in some the epithelium was flattened, in others swollen, granular, and detached; in the pyramid-tubes the epithelium was swollen and detached; there was cast-matter in some of the tubes, both in the cortex and pyramids; there was a very extensive new growth of new connective tissue in the cortex, partly diffuse, partly in patches.

A male, forty-one years old, six years before his death caught cold while bathing, and suffered with dropsy, a febrile movement, prostration, scanty urine which contained albumen, blood, and numerous casts. After a few weeks all the symptoms disappeared and he returned to his business. He continued to enjoy good health for about eighteen months; then in the winter the urine became scanty and contained blood, albumen, and numerous casts. General anasarca was rapidly developed. The dropsy lasted for six months, and then disappeared, but the urine from that time always contained varying amounts of albumen and casts. For nearly two years after this time the man continued to feel well, was actively engaged in business, had no dropsy, but the urine still contained casts and albumen. Then the dropsy returned again, and was very considerable. But the appetite and digestion continued good, there was no headache, the patient was intelligent and cheerful. The dropsy, a moderate diarrhoea, and the change in the urine were the only symptoms. In two months the dropsy had again disappeared and the patient returned to his work. After this time, however, the patient was never as well: a little oedema of the legs was present much of the time; he became gradually more and more anæmic and feeble, and finally died with marked dropsy and anæmia about six years from the time of the first appearance of kidney symptoms.

The Large White Kidneys with Waxy Infiltration.—It is well known that in certain persons a peculiar morbid change takes place in the viscera. The walls of the blood-vessels and some of the glandular cells become infiltrated with a peculiar translucent substance. This morbid change is commonly known by the name of waxy or amyloid infiltration. It is known that such an infiltration occurs regularly in persons who have chronic inflammations of the bones and joints, constitutional syphilis, and pulmonary phthisis. It is also known that this new substance is colored in a special way by iodine and some of the aniline colors. Beyond this we have no real knowledge of what the substance is or how it is produced.

In other parts of the body the waxy infiltration can hardly be said to produce any local symptoms. If one has a waxy liver or spleen, these organs may give the physical evidences of their enlargement, but that is all. We look upon such patients as suffering from some general changes concerning the nature of which we are ignorant, but not as suffering simply from disease of the liver or spleen.

It seems at first sight natural to think of waxy kidneys in the same way—not as examples of kidney disease, but as parts of a general morbid condition. This view has been adopted by most authors. They describe the waxy kidneys as something different from the other forms of nephritis. But really this is an error. In the vast majority of cases the waxy kidneys are simply a variety of chronic diffuse nephritis. It is possible (Cohnheim) to have waxy infiltration of the Malpighian bodies without other lesion of the kidney, but this is a rare exception. The rule is that we find the ordinary lesions of chronic diffuse nephritis; and, more than this, we often find the nephritic lesions very much farther advanced than the waxy infiltration. The association of the lesions is not at all such as to give the idea that the waxy infiltration is produced first and the other lesions afterward. It is also not uncommon to find waxy infiltration of the Malpighian tufts without similar changes in any other part of the body.

The type of the nephritis varies in different cases. Most of the kidneys resemble the large white kidneys, some the atrophied, some those which are neither large white nor atrophied. The clinical history varies in the same way, and is that of a large white or atrophied kidney, as the case may be. The only difference is that in some patients (not in the majority) there is a very large amount of urine passed of low specific gravity.

As a matter of fact, in most cases of waxy kidneys we simply make the diagnosis of chronic diffuse nephritis, and if we add to this that of waxy infiltration it is because the patients have had syphilis or bone or joint disease. Even in this way we are often enough deceived, as in the following case:

A woman, twenty-six years old, came into the hospital on January 25, 1876. She had contracted syphilis five years before. For two years she had suffered from dyspnoea and frontal headache. For seven months there was occasional oedema of the face and feet. At the time of her admission to the hospital she was very pale and anæmic; the urine was of a specific gravity of 1008, abundant, and contained no albumen or casts. The liver was very large and smooth. It was supposed that she had waxy liver and kidneys. She grew steadily weaker, continued to have a little oedema, vomited occasionally, developed the physical signs of bronchitis, with a temperature of 104° Fahr., and died on April 3, 1876. At the autopsy the aortic valves were found thin and insufficient. There was muco-pus in both the large and small bronchi, with irregular spots of red hepatization in the lung. The liver and spleen were large and waxy. The kidneys weighed together four ounces, and presented the ordinary lesions of atrophied kidneys, with only commencing waxy infiltrations of a few of the Malpighian tufts.

The Large White Kidney of Heart Disease.—This variety of chronic diffuse nephritis seems to be secondary to organic disease of the heart, and, less frequently, to emphysema of the lungs. The urine is diminished in amount, sometimes suppressed; it is dark-colored, the specific gravity varies between 1010 and 1030; albumen is absent altogether or present in small amount; hyaline and granular casts may be present, but are not constant. Dropsy may be absent or moderate or excessive. Cerebral symptoms—vomiting, cough, dyspnoea, anæmia—are usually present. Some of the patients die suddenly, some with dropsy, some with urgent dyspnoea.

The examples of chronic diffuse nephritis which are neither atrophied kidneys nor large white kidneys are numerous. Some of them give the clinical history of the large white kidneys, some that of the atrophied kidneys, some do not correspond to that of either; but they all exhibit some of the characteristic symptoms of chronic nephritis—changes in the urine, dyspnoea, vomiting, cerebral symptoms, dropsy, anæmia.

The following histories will show the course of the disease in some of these cases:

Case 1.—A male, forty years old, came into hospital on October 9, 1881. The patient was a beer-drinker, but denied rheumatism and syphilis. He said that he had been perfectly well until fourteen months before; then he had an attack of lobar pneumonia which confined him to the house for four weeks. Since that time he has never felt as well and has had occasional dyspnoea. Nine months ago the dyspnoea became so troublesome that he had to give up work, and he also began to suffer from severe headaches. Three weeks ago the urine became scanty and dropsy appeared in the legs and scrotum. When admitted to the hospital the patient was large and fat. There was dropsy of the legs and of the scrotum, marked dyspnoea, sibillant râles over both lungs; 10 ounces of urine in twenty-four hours, specific gravity 1023, albumen 10 per cent., hyaline and epithelial casts. The urine on Oct. 12 was 13 ounces; on Oct. 14, 42 ounces; on Oct. 18, 54 ounces. On this last day he had several convulsions, became comatose, and died October 19. At the autopsy the pia mater was thickened and there was an increase of serum beneath it. The heart weighed fourteen ounces, the aortic and mitral valves were a little thickened, the walls of the ventricles were unnaturally hard. In the lungs there were a few old hard miliary tubercles. The kidneys weighed sixteen ounces, surfaces smooth, capsules not adherent, cortex and pyramids of red color, urates in the pyramids. The cortex-tubes showed marked changes in their epithelium, but the Malpighian bodies, stroma, and arteries were nearly normal.

Case 2.—A female, forty-five years old, was admitted to the hospital December 5, 1881. Denied rheumatism, syphilis, and intemperance. She had considered herself strong and well until two months before. Then she had a sudden attack of dyspnoea, dizziness, faintness, and cardiac palpitation. After this she was never well, complained of pain about the heart, headache, attacks of dyspnoea, dropsy of the face, hands, and feet. The urine was scanty and dark-colored. She is now emaciated and anæmic, has moderate oedema of the legs, complains of dyspnoea, headache, and nausea. The heart's action is feeble and irregular, and there is a presystolic murmur. On December 19 she vomited blood. On January 2 she had a chill, followed by a temperature of 102°. On January 5 she became drowsy, then had twitchings of the muscles of the face; became semi-comatose, and died January 11. While she was in the hospital the urine varied in amount from 1 to 6 ounces daily; it contained a very large amount of albumen and a few hyaline casts. After death the pia mater looked sodden and finely granular. The walls of its arteries were a little thickened, and there were little clumps of endothelial cells on its outer surface. The mitral valve of the heart was thickened and stenosed. The kidneys were of medium size, their capsules slightly adherent, their surfaces finely nodular, the cortex of normal thickness, red mottled with yellow spots. There was an extensive growth of diffuse connective tissue separating the tubes both in the cortex and pyramids. The tubes were large and contained much cast-matter. Most of the Malpighian bodies were normal.

COMPLICATIONS.—The most frequent complication of chronic diffuse nephritis is disease of the heart. We find cardiac lesions and renal lesions associated in three different ways:

1. Valvular lesions or dilatation of the ventricles produce chronic congestion of the kidney, with its changes into parenchymatous or diffuse nephritis or the large white kidney of cardiac disease.

2. Chronic diffuse nephritis is followed by the development of hypertrophy of the left ventricle. This may occur with all the varieties of chronic diffuse nephritis, but is most common with the atrophied kidneys.

3. Valvular lesions and chronic nephritis occur in the same persons, but neither can be said to depend upon the other.

The arteries are often diseased, the aorta and the arteries throughout the body. There may be a simple sclerosis and thickening of the wall of an artery, or endarteritis deformans, or obliterating arteritis.

Cerebral apoplexy may occur with all the varieties of chronic diffuse nephritis, but much more frequently with atrophied kidneys.

Thickening of the pia mater, with increase of serum beneath it, is often seen.

Dilatation of the lateral ventricles of the brain sometimes occurs, and may give rise to cerebral symptoms.

Pericarditis is seen more frequently with the atrophied kidneys.

Pneumonia is especially apt to be fatal when it occurs in persons already suffering from chronic diffuse nephritis.

Emphysema and chronic bronchitis are often associated with the atrophied kidneys.

Phthisis is found with all the varieties of chronic nephritis.

Peritonitis occurs in a few cases as a complicating inflammation.

Cirrhosis of the liver is found quite frequently.

PROGNOSIS.—In every case of chronic diffuse nephritis the natural course of the morbid changes in the kidney tissue is to become more marked and involve more and more of the kidney. The effect upon the general health of the patient is not in any exact relation to the degree of the kidney lesion. These two facts render the prognosis of chronic diffuse nephritis very uncertain. The disease is always a very serious one, and terminates regularly in destroying life, but the length of time that will elapse before this fatal termination, and the precise way in which death will take place, are difficult to determine beforehand.

TREATMENT.—There seems no good reason for believing that we can directly influence the development of the lesions in the kidneys. It is possible that such a development may be indirectly delayed by improving the general health of the patient.

There is good reason to believe that some of the symptoms which occur regularly in patients who have chronic diffuse nephritis are dependent not upon the nephritis, but upon other causes. We may therefore look for indications for treatment in three different directions:

1. To delay the development of the disease by improving the general health of the patient.

2. To treat those symptoms which are not produced by the kidney disease.

3. To treat those symptoms which are produced by the kidney lesions.

To fulfil the first indication the most potent influences that we have are the giving up of business and of vicious habits and causing the patient to live year after year in the most suitable climates. Generally speaking, warm climates are to be preferred, but the individual disposition of each patient must always be consulted.

Of less efficacy, but still of importance, are the improvement of the digestion by means of drugs and the feeding of the patient.

In every patient suffering from chronic diffuse nephritis there are a number of symptoms which seem to depend directly upon other conditions, and not upon the kidney lesions; for if these conditions are removed the symptoms disappear, although the kidney lesions continue. To this category of symptoms seem to belong the headache, delirium, stupor, coma, and convulsions, the nervous dyspnoea, the vomiting in part, the dropsy in part, the diminution of urine in part. All these symptoms are due to disturbances of the circulation, and the disturbances of the circulation are produced by a number of causes which may act separately or together. Changes in the valves and walls of the heart, in the force and regularity of the heart's contraction, in the walls and size of the arteries and capillaries, and in the volume and composition of the blood, each, separately or associated, may interfere with the proper circulation of the blood, and this interference usually takes the form of too much blood in the veins and too little blood in the arteries.

Anatomical changes in the valves of the heart, in its walls, and in the walls of the arteries and capillaries cannot be influenced by any means at our command. The force and regularity of the contractions of the heart can, however, be very decidedly modified by drugs. Opium in moderate doses makes the heart's action slower and stronger; iodide of potassium makes the heart's action more regular; convallaria makes the heart's action slower and stronger; digitalis increases the force of the heart's action, but at the same time contracts the arterioles; aconite and veratrum viride make the heart's action slower and more feeble.

The size of the arteries and capillaries can also be altered by drugs. Nitrite of amyl and nitro-glycerin relax and dilate the whole arterial and capillary system; chloral hydrate dilates the arterioles (Fothergill).

The volume of the blood can be diminished by bloodletting and by eliminating the plasma of the blood indirectly by sweating, purging, or diuresis.

The symptoms which can be ascribed directly to the presence of the kidney disease are—(1) The changes in the composition of the blood. We have still very little exact knowledge of what these changes are, but we may say generally that there is an increase in the relative quantity of the watery constituents of the blood and of the excrementitious products which should be eliminated by the kidneys. (2) The changes in the quantity of urine probably depend partly on the changes in the circulation, partly on the composition of the blood, and partly upon the structural changes in the kidneys. The albumen and casts seem to be directly due to the kidney lesion. (3) The changes in the nutrition of the patient, the disturbances of digestion, and some of the headaches, all seem to belong directly to the kidney disease.

Now let us try to apply these principles to the practical treatment of the different symptoms.

The Urine.—As regards the presence of albumen and casts, it is doubtful whether we are able to do anything, although it is customary to give the tr. ferri chloridi and the bichloride of mercury in order to diminish the excretion of albumen. As regards the quantity of urine, we must distinguish whether the patient is in the ordinary course of the disease, whether he is having an uræmic attack, or whether he is having an acute exacerbation of the nephritis with congestion of the kidney and blood in the urine. Under the circumstances last mentioned the indications are to apply wet or dry cups over the lumbar region, to use hot fomentations to the back or hot-air baths, to open the bowels freely, to put the patient on a milk diet, and, if the heart's action is too strong, to give aconite in small doses.

If during the ordinary course of the disease the urine is constantly diminished, diuretics are often of good service, although the cases differ as to the particular drugs which answer best. The preparations of digitalis, the diuretic pill of digitalis, squills, and bichloride of mercury, the iodide and acetate of potash, and jaborandi in small doses, are the most reliable agents of this class. Sometimes the frequent use of milk or of water in small quantities (half an ounce or an ounce every half hour) will answer the purpose. There can never be any use in continuing the employment of diuretics in these cases if after a fair trial they do not increase the flow of urine.

During the progress of uræmic attacks diuretics do not act, and the same is often the case with cathartics and diaphoretics. The urine is only to be increased by the same means which are indicated for the relief of the whole uræmic condition, and of these we will speak later.

The dropsy in many cases will vary in amount, and even disappear at times without any treatment. It is regularly most marked with the large white kidneys and with those kidneys which are neither large white nor atrophied, especially when there is complicating heart disease and the patient is anæmic. Generally speaking, it is best to keep dropsical patients in bed most of the day. We attempt to get rid of the oedema by the skin, the bowels, and the kidneys, to regulate the heart's action, and to improve the condition of the blood. Hot-air baths or hot-water baths repeated every day, the milder hydragogue cathartics, and the different diuretics may all be used with advantage. If the dropsy is excessive, it may be necessary to tap the peritoneal or pleural cavities or to puncture the skin of the legs and scrotum. Sometimes bandaging the legs so as to exert moderate pressure seems to assist in getting rid of dropsy. To regulate the heart's action we find that digitalis, convallaria, and the iodide of potash are often of service. To improve the condition of the blood the systematic use of iron and oxygen is indicated. The most hopeless cases are those in which there is complicating heart disease and those in which the dropsy steadily increases, although the patient is passing from 60 to 100 ounces of urine daily.

Disturbances of the stomach are of different kinds and dependent upon different conditions. There may be simply loss of appetite or discomfort after eating, or nausea, flatulence, and vomiting; and these symptoms will be associated with chronic catarrhal gastritis or with a stomach that is anatomically normal. Sometimes, although there is occasional nausea and vomiting, the appetite continues good, or as part of an uræmic attack there will be constant vomiting.

The habitual dyspeptic disturbances are to be treated like other cases of gastric dyspepsia. A regulated diet, the vegetable bitters, the mineral acids, or the alkalies are sometimes of service. The repeated and persistent vomiting of uræmic attacks is a most distressing symptom and one often very difficult to control. The patients must be fed with small quantities of fluid food or of prepared meat. The most efficient remedies are those addressed to the condition of the circulation. Hypodermic injections of morphia, enemata of chloral hydrate, inhalations of nitrite of amyl, convallaria in small doses by the mouth, are all of service.

The anæmia from which the patients suffer is to be combated by the systematic use of iron and oxygen. Any efficient preparation of iron will answer, but it must often be given in considerable doses. Sometimes the bichloride of mercury in small doses answers better than iron. The oxygen should be inhaled for from five to thirty minutes twice a day.

The so-called uræmic attacks, although they have a general similarity, yet vary in their manifestations in different cases. In some cases the patient develops an unnatural restlessness and anxiety, an inability to sleep, now and then a sudden twitch of one of the facial muscles, and headache. Or a patient whose color is still good will only complain of pain in the epigastrium and moderate dyspnoea, and yet will be in bed and evidently seriously ill. Or a patient who has been troubled with dyspeptic symptoms and gradual loss of strength suddenly develops vomiting, intense headache, sleeplessness, a single convulsion followed by facial paralysis. A man with a previous history of chronic Bright's disease becomes persistently anæmic and dropsical; he has constant dyspnoea, cannot lie down, cannot sleep, and yet looks drowsy and stupid; is mildly delirious and has very little intelligence; then gradually becomes unconscious, then comatose, and so dies. Or there are first attacks of dyspnoea, either spasmodic or from exertion, but which are temporary and can be relieved. Then the dyspnoea becomes more constant and severe; the patient cannot lie down at all, all remedies become less and less efficacious, and the dyspnoea only ends with the life of the sufferer. In other cases a patient will suddenly become unconscious, although not comatose; he will lie flat in bed, the skin livid and bathed in perspiration, the respiration labored and rapid, with coarse râles all over the lungs, the heart's action rapid and feeble, the temperature perhaps a little elevated; or sudden and profound coma or noisy delirium or repeated convulsions may be the prominent features.

There is hardly a limit to the variety of the precise manner in which all these symptoms—restlessness, sleeplessness, headache, vomiting, delirium, convulsions, and coma—may present themselves. It is to be remembered that although all these symptoms are always dangerous, and often fatal, yet patients may pass through a number of such attacks before the fatal one arrives.

To relieve these attacks the most effectual remedies are opium, chloral hydrate, nitrite of amyl, convallaria, digitalis, caffeine, bloodletting, purging, sweating, and cathartics.

Opium is a very valuable remedy, but great judgment is required in selecting the preparation and the dose for each case. The old doctrine that opium is a dangerous drug for patients suffering from Bright's disease is perfectly true, but it is equally true that it is also a valuable remedy. Generally speaking, the more marked the uræmic attack the larger the dose of opium that will be borne. It is always well to try to obtain a free movement from the bowels, although this is not always possible.

In the milder cases the fluid extract of convallaria in ten-minim doses will often diminish the frequency of the heart's action, increase the production of urine, and improve the general condition of the patient.

In the earlier stages of dyspnoea five-grain doses of the iodide of potash with a little opium will sometimes keep the patient comfortable for months. For the severe attacks of dyspnoea dry cups over the chest and inhalations of oxygen are of service. In the worst and most uncontrollable dyspnoea it seems justifiable to keep the patient under the influence of ether or chloroform.

SUPPURATIVE NEPHRITIS AND PYELO-NEPHRITIS.

Suppurative inflammation of the tissue of the kidney and of its pelvis and calices occurs under several different conditions: It is the result of injuries; it is due to emboli; it occurs without discoverable causes; it is secondary to cystitis, the cystitis being due to strictures of the urethra, to stone in the bladder, to paraplegia, to operations on the urethra, bladder, and uterus, to gonorrhoea, to enlarged prostate.

Chronic suppurative pyelo-nephritis is often caused by the presence of calculi in the pelvis of the kidney.

1. Suppurative Nephritis from Injury.—Gunshot wounds, incised or punctured wounds, falls, blows, and kicks are the ordinary traumatic causes. If the injury is a very severe one, it causes the death of the patient in a short time; if it is less severe, suppurative inflammation may be developed.

The inflammatory process may be diffuse, so that the whole of one or both kidneys is converted into a soft mass composed of pus, blood, and broken-down tissue, or it is circumscribed, and one or more abscesses are found in the kidney which may communicate with the pelvis.

SYMPTOMS.—Rigors mark the beginning of the suppuration, and are often repeated through its course. A febrile movement is developed which is apt to assume the hectic character with sweatings. There is often vomiting. There may be very severe pain, referred to the region of the inflamed kidneys. The urine is diminished or suppressed; it contains blood alone or blood and pus.

In the bad cases the patients pass into the typhoid condition, become delirious, and die comatose or with a very rapid or febrile pulse. Or the disease is protracted, the patients become more and more emaciated, and finally die exhausted.

In other cases the symptoms abate, the urine returns to its natural condition, and the patients recover.

TREATMENT.—The management of these cases is rather surgical than medical. The external wound is to be treated antiseptically, and the general condition of the patient to be looked after in the ordinary way.

Such traumatic abscesses are of infrequent occurrence. I have no personal knowledge of them.

2. Abscesses produced by Emboli.—In ordinary endocarditis with vegetations on the valves it often happens that fragments of the vegetations become fixed in the branches of the renal arteries. When this is the case infarctions are produced, usually of the white variety.

With malignant endocarditis, with surgical pyæmia, and with the curious cases called idiopathic pyæmia, small emboli seem to find their way into the smallest branches of the renal artery. They do not produce infarctions, but small abscesses. In these cases the kidneys are increased in size and dotted with little white points surrounded by a red zone. These little white points are formed by an infiltration of pus-cells between the tubes, and in the larger foci by a breaking down of the kidney-tissue. Colonies of micrococci are sometimes, but not always, found in the Malpighian tufts, the veins, and the abscesses.

SYMPTOMS.—These embolic abscesses can hardly be said to have any clinical history. Whatever symptoms may belong to them are lost in those of the general disease from which the patient is suffering.

3. Idiopathic Abscesses.—Occasionally cases of abscesses of one of the kidneys are met with. They last a long time, and when the patient dies both the kidney tissue and the pelvis are involved to such an extent as to render the anatomical diagnosis difficult. The greater part of the kidney-tissue is destroyed and replaced by sacs full of pus; the pelvis is dilated and its walls thickened. The surrounding connective tissue is thickened; perforations and sinuses may extend into the surrounding connective tissue, into the large intestine, and through the diaphragm into the lung.

SYMPTOMS.—At first these cases are apt to be very obscure. An irregular febrile movement accompanied with rigors comes and goes, lasting for shorter or longer periods. The patients lose appetite, vomit occasionally, and become emaciated and anæmic. With this there may be pain over the region of one of the kidneys.

After a time a tumor may make its appearance in the position of one kidney—a tumor which can be felt through the anterior abdominal wall. If the abscess communicates with the pelvis of the kidney and the ureter remains pervious, pus and fragments of kidney-tissue are discharged with the urine. The pus is usually discharged at intervals, and at such times the size of the tumor diminishes. In other cases the pus burrows in other directions—into the retro-peritoneal connective tissue, the peritoneal cavity, the colon, or through the diaphragm into the lung. These cases are apt to run a protracted course and terminate fatally.

TREATMENT.—The only plan of treatment likely to cure the patient is a surgical one—either to extirpate the diseased kidney, or to cut down on the abscess and treat it on the antiseptic plan like any deep abscess.

4. Suppurative Pyelo-Nephritis with Cystitis.—LESIONS.—Usually both kidneys are affected. They are increased in size, and both the kidneys and their pelvis are congested. The mucous membrane of the pelvis is thickened and coated with pus or patches of fibrin. Scattered through the kidneys are abscesses and purulent foci of different sizes. The smallest foci are not visible to the naked eye, but with the microscope we find collections of pus-globules between the tubes, with swelling and degeneration of the epithelium within the tubes. The larger purulent foci look like white streaks or wedges running parallel to the tubes and surrounded by zones of congestion. The larger abscesses replace considerable portions of the kidney.

The ureters in some cases are inflamed, their walls thickened, their inner surface coated with pus or fibrin. The bladder presents regularly the lesions of acute or chronic cystitis.

ETIOLOGY.—For the production of this form of nephritis inflammation of the bladder seems to be necessary. How the inflammatory process is transmitted from the bladder to the kidneys is still uncertain, but it seems probable that it is effected by bacteria. The cases of cystitis in which a suppurative nephritis is likely to be developed are those due to strictures of the urethra, stone in the bladder, operations on the urethra, bladder, and uterus, paraplegia, gonorrhoea, and enlarged prostate.

SYMPTOMS.—When the nephritis occurs with cystitis due to stone in the bladder, strictures, or operations on the genito-urinary tract, the symptoms are much the same. The patient has first the symptoms belonging to the cystitis, then he is attacked with rigors, followed by a febrile movement. The rigors are often repeated; the febrile movement is very irregular and often accompanied by profuse sweating. There is a rapid change in the general condition of the patient. He becomes much prostrated and emaciated from day to day. The face is drawn and anxious, the tongue dry and brown, the pulse rapid and feeble, and delirium is developed, and the patient finally dies in a condition resembling that of typhoid fever or of pyæmia. The urine is diminished in amount; it may be suppressed. It contains blood, pus, and mucus. The pus and mucus belong to the cystitis; the blood seems to be derived both from the kidneys and the bladder.

Cases of suppurative nephritis complicating gonorrhoea are fortunately not common, but several of them have been observed. Murchison² describes two cases, in both of which the cerebral symptoms were very marked—delirium, convulsions, and coma. I have seen one such case. The patient was a prostitute who came into the hospital with a specific vaginitis. After a few days she developed symptoms of an acute cystitis; then after a few more days she was attacked with rigors and a febrile movement, passed rapidly into the typhoid condition, and died. At the autopsy there were found acute cystitis, pyelitis, and numerous small abscesses in both kidneys.

² Lancet, 1875, p. 80.

When suppurative nephritis complicates the cystitis due to enlarged prostate, the clinical symptoms are somewhat different. The patients are usually men over fifty. They have generally suffered from the symptoms of enlarged prostate—retention of urine, either constant or intermittent, and more or less cystitis, with pus and mucus in the urine in varying amount. Sometimes, however, no such history is obtained; the patients assert that they have had no previous bladder trouble. The first symptom is diminution in the amount of urine passed and the appearance of blood. The quantity of urine is only a few ounces or it is completely suppressed. The blood is present in considerable amount; often the patients seem to pass pure blood instead of urine. The patients rapidly become prostrated and very anxious. There are usually no rigors, and there may be no febrile movement. After this the prostration becomes more marked, the pulse is rapid and feeble, the skin cold and bathed in perspiration, and the patients die in collapse at the end of a few days.

PROGNOSIS.—Suppurative nephritis secondary to cystitis is a very fatal disease; so far as I know, all the cases die.

TREATMENT.—The treatment for these cases is altogether a preventive one directed to the cystitis. In the cases of paraplegia, stone in the bladder, stricture, and enlarged prostate constant care must be used to prevent the accumulation of urine in the bladder and the development of cystitis.

In all cases of operation on the genito-urinary tract the supervention of cystitis is to be guarded against.

PERINEPHRITIS.

The loose connective tissue which is situated around and beneath the kidney may become the seat of suppurative inflammation, and in this way abscesses of considerable size are formed.

LESIONS.—The connective tissue behind the kidney seems to be the usual point of origin of the inflammatory process, and it is here that the pus first collects. After the abscess has reached a certain size the suppuration seems to have a natural tendency to spread and the pus burrows in different directions—backward through the muscles; downward along the iliac fossa, even as far as the perineum and scrotum or vagina; forward into the peritoneal cavity, the colon, or the bladder; upward through the diaphragm. The kidney is either compressed by the abscess or its tissue also becomes involved in the suppurative process. The soft parts around the abscess become thickened.

ETIOLOGY.—Perinephritis is either secondary or primary. The secondary cases are due to extension of the inflammation from abscesses in the vicinity, such as are formed with caries of the spine, pelvic cellulitis, puerperal parametritis, perityphlitis, suppuration of the kidneys, and pyelo-nephritis. The primary cases occur after exposure to cold, after contusions over the lumbar region, great muscular exertion, and without discoverable cause. The lesion is said to complicate typhus and typhoid fever and smallpox. The disease occurs both in children and adults, most of the cases reported having been between the ages of twenty and forty years.

SYMPTOMS.—The disease begins regularly with pain and tenderness referred to the lumbar region on one side between the lower border of the ribs and the crest of the ilium, sometimes to a point above or below this. At about the same time are developed repeated rigors, a febrile movement with evening exacerbations, sweating, loss of appetite, vomiting, and prostration. These are all the symptoms for from one to two weeks. Then the skin over the lumbar region on one side becomes red and oedematous; the corresponding thigh is kept flexed and rigid, for any movement of it gives pain. Then the lumbar region becomes more and more swollen until fluctuation can be made out, and finally the abscess breaks through the skin. If such cases are left to run their course the abscess may reach a very large size. If the pus does not extend backward, but in some other direction, the symptoms are more obscure, for the local symptoms of an abscess in the back are absent.

If the abscess ruptures into the peritoneal cavity, the symptoms of acute general peritonitis are suddenly developed. If it perforates into the colon or bladder, the pus is discharged with the feces or the urine. If the perforation is through the diaphragm, there will be empyema, or the lung becomes adherent and pus is coughed up from the bronchi. As soon as the abscess is opened and the pus escapes the acute constitutional symptoms subside.

Trousseau believes that the inflammatory process sometimes stops short of the production of pus. In such cases of course there are no evidences of the formation of an abscess.

The disease may terminate in different ways:

1. The inflammation may terminate in resolution (Trousseau).

2. The abscess is opened by operation or spontaneously and the patient recovers.

3. Although the abscess is opened either by the surgeon or spontaneously, the suppurative process continues and the patient dies exhausted, usually with waxy viscera.

4. Perforation into the peritoneum, the pleura, or the lung causes death.

TREATMENT.—The main point in treatment is to discover the abscess and to open it. The longer the suppurative process goes on and the larger the abscess, so much the worse is the prognosis. It is proper to explore with the aspirator after the disease has lasted for a few days, even if no fluctuation can be made out. The abscess is to be opened and treated on antiseptic principles.

HÆMATURIA AND HÆMOGLOBINURIA OR HÆMATINURIA.

BY JAMES TYSON, A.M., M.D.

The above terms are applied, the first to a condition of urine in which, of the constituents of blood, red discs at least are present; the second to that in which, while no corpuscles are found, blood coloring matter is abundant. Each of these conditions has been repeatedly observed as a distinct state at the moment when urine is passed; but it is also to be remembered that a true hæmaturia may, in the course of a few hours, become a hæmatinuria or hæmoglobinuria, by solution or disintegration of the red blood-discs. So far as I know, this subsequent solution and conversion can take place only in an alkaline urine; but as any urine through decomposition may become alkaline, it is evident that any hæmaturia may, in the course of time, become a hæmoglobinuria—a fact sometimes overlooked. I have, for example, known urine to be sent from Southern parts of the United States which, when shipped, contained blood-corpuscles, but which, when received in Philadelphia, contained no blood-discs, only large amounts of blood coloring matter. Especially does this occur in warm weather, when urine decomposes quickly. Such a hæmoglobinuria might be characterized as secondary. Doubtless, too, a more rapid solution is contributed to in some instances by the state of the blood-discs themselves, which are at times disintegrated before or at the moment they leave the blood-vessels, at others are intact, and at others, still, may be just ready to fall to pieces. In the hæmoglobinuria, where the blood-corpuscles have been secondarily dissolved and disintegrated, their remnants may be found in the shape of dark-brown or red granules, which form a sediment of varying bulk.

The immediate cause of this dissolved state of the blood-discs, where not due to the solvent action of an alkaline urine, appears to be the difference in degree of the cachexia which is at the bottom of the renal hemorrhagic tendency.

The term hæmaturia is applied to blood in the urine from whatever part of the urinary passages it may come, whether the bladder, ureters, kidney, or even urethra; whereas the blood in primary hæmoglobinuria always comes directly from the kidney.

In this paper I shall confine myself to the consideration of renal hæmaturia and hæmoglobinuria in the strict sense of the term; nor will I include such renal hæmaturia as constantly occurs in the first stage of acute Bright's disease.

Emphasizing again that all primary hæmoglobinurias are renal, it is important to be able to say of a given hæmaturia whether it is renal or not. Even coarse methods are often sufficient to settle the question. Blood from the kidney, so far as my experience goes, is never discharged in the shape of clots, at least large enough to be recognized as such by the naked eye. More frequently coagula of blood are passed when hemorrhage takes place into the pelvis of the kidney. These coagula generally cause severe pain in their descent, and by this symptom are distinguished from coagula from the lower part of the ureter and bladder.

The smoky hue, which is characteristic of the presence of small quantities of blood in an acid urine, affords presumptive evidence that the blood is renal in its origin, because the conditions which are associated with blood from other parts of the genito-urinary tract are very apt to be associated with an alkaline urine, to which blood imparts a bright-red hue. This is, however, not invariable, as smoke-hued urine may be due to admixture of blood from the bladder and parts of the genito-urinary tract other than the kidney.

The microscope affords valuable assistance in determining the source of blood in the urine. In addition to blood-discs or their molecular débris, tube-casts made up of cemented blood-discs or their débris are very constantly, although not invariably, found in such urine. This evidence is conclusive, and, although sometimes wanting, the invariable absence of clots from blood descended from the kidney, together with the absence of irritation of the bladder, makes it usually quite easy to recognize a renal hæmaturia.

It is scarcely necessary to say that all urine containing blood or hæmoglobin contains albumen, the quantity varying with that of these substances present. Any further deviations from the normal composition of the urine are, in the main, due to admixture of other constituents of blood.

Causes which give rise to Hæmaturia and Hæmoglobinuria.

Hæmaturia is due to a variety of causes, which may be local or general. Local hæmaturia is caused by wounds, blows upon the kidney, or falls in which the kidney receives the force of the blow, as in striking the edge of a fence in falling; from cancer of the kidney, impacted calculus, parasites, embolism, acute Bright's disease; also poisoning from carbolic acid, cantharides, and mustard. General causes of hæmaturia are malaria, purpura, scurvy, blood-dyscrasias due to continued and eruptive fevers, especially typhus fever and smallpox, septicæmia and pyæmia, and cholera. Finally, it must be admitted that there is a hemorrhagic diathesis manifested by hæmaturia and hæmoglobinuria. Primary hæmoglobinuria may be produced by any of the general causes just named, or by the prolonged inhalation of arseniuretted hydrogen and carbonic acid, and the introduction of numerous substances into the blood, as iodine, arsenic, etc.

While a rupture of the blood-vessels of the kidney may be supposed to be at the bottom of a certain proportion of cases of hæmaturia, it is by no means a necessary condition of their occurrence, as it is well known that in inflammations there may be extravasations of blood without rupture of the blood-vessels. There is implied, however, in all these conditions an alteration of the vessel-walls which permits such transudation. Indeed, Ponfick¹ goes so far as to say that even transudations of hæmoglobin through the blood-vessels of the kidney are impossible without the presence of serious diffuse nephritis. There is every reason to believe, however, that simple alterations of the blood are of themselves sufficient to cause such transudations. Take, for instance, the extravasations in purpura, which are not confined to the vessels of the kidney. It is impossible to conceive inflammatory conditions so general as would have to be presupposed in this disease.

¹ "Ueber die Gemeingefährlichkeit der essbaren Morchel," Virchow's Archiv, Bd. lxxxviii. S. 47.

Hæmaturia from Local Causes.

It is unnecessary to consider in detail the local causes of hæmaturia. It is evident how injuries and blows upon the kidney, and impacted calculus may produce hemorrhage. The history of nephritic colic or of gravel in urine, along with blood, would suggest the latter cause. Nor is it necessary to detail the phenomena of hemorrhagic infarction which succeeds embolism and is the direct cause of hemorrhage into the tubules of the kidney. Hæmaturia is by no means a constant symptom in sarcoma and cancer of the kidney. A small amount of blood in the urine is a constant symptom in acute nephritis, where it is due to a rupture of the blood-vessels of the Malpighian tuft. It is accompanied by blood-casts and other symptoms of acute Bright's disease. Carbolic acid, cantharides, oil of mustard, and similar substances produce hæmaturia by causing congestion and inflammation of the kidney.

The parasites which may cause hemorrhage in the substance of the kidney are the Bilharzia hæmatobia, the Filaria sanguinis hominis, the Strongylus gigas, and possibly common intestinal worms which may reach the kidney through fistulous openings. The first is a thread-like worm three or four lines in length, which was discovered by Bilharz, and infests the small vessels of the mucous and submucous tissue of the veins of the intestinal tract, the pelvis of the kidney, ureter, bladder, and more rarely of the kidney itself. It is very frequent in Egypt, where Griesinger found it 117 times in 363 autopsies; also in South Africa (Cape of Good Hope), where it gives rise to an endemic hæmaturia. It has been studied by Bilharz, John Harley, and William Roberts.

The Filaria sanguinis hominis is a long, narrow microscopic worm, not wider than a red blood-disc, and one seventy-fifth of an inch long, which infests the blood. Hemorrhages result from its accumulation in the vessels, causing rupture. The cases which have been studied occurred mostly in India, China, and Australia.

The Strongylus gigas is a large worm, resembling the ordinary lumbricoid, but larger, the male being from ten to twelve inches long and one-fourth of an inch wide, while the female is sometimes more than a yard in length. It infests the kidneys and urinary passages of certain lower animals (the dog, wolf, horse, ox, etc.), but rarely those of man.

Malarial Hæmaturia and Hæmoglobinuria.

SYNONYMS.—Intermittent hæmaturia; Paroxysmal hæmaturia; Malarial yellow fever; Swamp yellow fever; Paroxysmal congestive hepatic hæmaturia (Harley).

Perhaps the most important form of hæmaturia and hæmoglobinuria resulting from general causes is that due to malarial poisoning. I prefer the term malarial to intermittent or paroxysmal, not only because it more precisely indicates the cause of the condition, but also because the condition itself is by no means always intermittent, sometimes continuing without interruption until checked by appropriate treatment; and I have known it to continue uninterruptedly for a year, in spite of all treatment.

The first complete report of an undoubted instance of this affection appears to have been published by Dressler in 1854,² although incomplete and uncertain cases were reported prior to this date—one as early as 1832 by Elliotson.³ G. Troup Maxwell of Ocala, Florida, writes me, in 1883, that he first observed cases in Florida thirty years ago, and published an article on the disease in the Oglethorpe Medical Journal, Savannah, Ga., July, 1860. George Harley⁴ early contributed to our accurate knowledge of the subject in 1865, and since then numerous papers and reports of cases have appeared in English and American journals, the southern part of the United States being a fertile scene of the affection, while it is by no means rare in the Middle States.

² "Ein Fall von intermittirender Albuminurie und Chromaturie," Virchow's Archiv, Bd. vi. S. 264, 1854.

³ "Clinical Lecture on Diseases of the Heart, with Ague (and Hæmaturia)," London Lancet, 1832, p. 500.

⁴ "Intermittent Hæmaturia," Medico-Chirurg. Trans. London, 1865.

Two degrees of the disease are met with—a milder form, in which other symptoms as well as the hæmaturia are less pronounced, and of which instances occur in the Middle States as well as the South and West of the United States. Of this kind seem to be the cases studied by Harley and other English physicians. In addition to this, there is a second, more malignant, form, attended by great prostration, vomiting, and yellowness of the skin, along with copious discharges of bloody urine. Instances of the latter are numerous in the Southern States of this country, where they have recently been studied with much care; also in the East and West Indies and in tropical countries generally. In neither degree of the disease is it necessary that the red corpuscles of the blood should be present. They may be represented by their coloring matters alone, when the condition is called a hæmoglobinuria or a hæmaturia.

The Milder Form.—The subjects, in my experience of eight cases, have been, with one exception, men, and I believe the experience of others included more men than women. They are generally able to recall a history of exposure to malaria, and often of distinct attacks of malarial fever, intermittent or remittent. The hæmaturia appears suddenly, and when paroxysmal may occur daily or on alternate days or a couple of times a week, or even at longer intervals. When the attacks occur at longer intervals, say of ten days or two weeks, if the disease is left alone the interval is apt to gradually diminish until the passage of bloody urine becomes daily. The urine in the morning may be perfectly clear, and at two o'clock is evidently bloody. It continues so through one or two acts of micturition, and then becomes clear again; or it may be bloody on rising and clear up by noon. Sometimes the bloody urine is preceded or accompanied by a sense of weariness and chilly feeling, or sometimes simply by cold hands and feet or by cold knees, or by pallor and blueness of the face, or by accelerated pulse, or by no other symptoms whatever. There is sometimes a sense of fulness in the region of the kidney and sacrum. The attacks are often induced by exposure to cold.

Harley states that in one of the two cases which he reported there was a slight jaundice, and in the second a "sallowness which appeared to be due to a disturbance of the hepatic functions," but in none of the cases which I have met was this symptom present. In the more malignant form occurring in the tropics and the Southern States of America, jaundice is a constant symptom.