In considering the various forms of disease of the kidneys it is proper to consider their influence on the functions of these organs. There are two principal pathological changes in function which merit more particular consideration, namely, diminution in the amount of urea and albuminuria.

(A) Diminution In Urea And Other Excreta

The secretion of urea (and other excretory products of less known composition) is chiefly, as-already mentioned, a function of the renal epithelium. It has also been indicated that the secretion of water is effected in the glomeruli, so that these two functions are exercised in different situations and may be variously altered without relation to each other. The amount of water may be greatly in excess, whilst the percentage of urea in the urine may be so small as that the total daily amount is greatly under the normal. It may be said that relaxation of the renal arteries or increase in the general blood-pressure by increasing the amount of blood passing through the kidneys, will directly increase the amount of water separated in the glomeruli, and will also stimulate the separation of urea should there be an excess of the latter in the blood. But, if the renal epithelium be lost or paralyzed, then there may be a great diminution in the urea excreted, even though the water is greatly increased. Loss of the epithelium tends in another way to produce a watery condition of the urine, as the function of the epithelium in concentrating the urine will be diminished. It may thus be inferred that while interference with the circulation of the kidneys by stagnation of the blood or otherwise, is likely to diminish both the water and urea, interference with the epithelium diminishes the amount of urea whilst not diminishing the secretion of water.

(B) Uraemia

The subject has already been referred to in the general part of this work. This term is applied to a group of symptoms, the principal of which are vomiting, sleeplessness, headache, convulsions and coma, which are liable to occur when the excretion of the essential urinary constituents is seriously diminished. These constituents retained in the blood act as poisons, but it has not been found possible to discriminate amongst the various symptoms as to how they are related to the different constituents of the urine, the chief of which are urea, creatine, and creatinine. Urea, at least, is not a vigorous poison, and it seems to be only when in great excess and acting for a considerable period that ursemic symptoms are produced.

There are two different ways in which the urinary constituents may be caused to accumulate in the blood. The excretory apparatus in the kidneys may be diseased in the manner referred to above; in particular the secreting epithelium may be interfered with. But the outflow of urine may be hindered by obstruction to the urinary passages. In this latter case there is to some extent a re-absorption of the urinary constituents, but as the ureters and pelves get distended by the accumulating urine the secretion in the kidneys gradually ceases (see under Hydronephrosis), so that the constituents are retained in the blood. It will be understood that whilst uraemic symptoms most readily develop when the urine is diminished or suppressed either by disease of the kitlneys or by obstruction to the outflow, yet its occurrence is not inconsistent with even an excess of watery urine.

Considerable doubt was at one time thrown on the view that the symptoms of urftmia were due to poisoning by the urinary constituents. The injection of urea or urine into the blood of animals, or the ingestion of urea with the food, failed to produce the symptoms, leading only to an excessive secretion of urine. Two theories were devised to account for these apparent discrepancies. The theory of Traube, that the symptoms are due to (edema of the brain, is not now accepted. Nor is that of Frerichs, according to which it is not the urinary constituents themselves, but the products of their decomposition, chiefly carbonate of ammonia, which act as poisons. Chemical investigation shows that there is no excess of carbonate of ammonia in the blood in uramiia, and experiment indicates that carbonate of ammonia when introduced into the blood produces symptoms different from those of uraemia.

It is the accumulation of the constituents in the blood whicli produces, after a time, an intolerance of them. If, besides injecting urine into the blood in animals, the ureters be ligatured, then the symptoms of ura-mia rapidly manifest themselves.

(C) Albuminuria

By this term is meant the escape of the serum-albumen along with the water of the blood, which no doubt occurs at the glomerulus. The albumen probably undergoes some changes after or during its passage (Kirk). Albumen is found in small quantities in the urine of some persons apparently healthy, so that a condition of so called Physiological albuminuria has been distinguished. There are, however, in such cases, only slight traces, and the presumption is that some disturbance actually exists in the kidneys in all cases of albuminuria. It is clear from the variety of conditions which may lead to it that it may be induced by a comparatively slight derangement.

The water of the urine is eliminated, as already mentioned, mainly at the glomeruli by a process which has been compared to filtration. If it were a simple filtration, albumen would be present, and some observers have supposed that albumen does pass through, to be reabsorbed by the epithelium of the uriniferous tubules. It is generally acknowledged that water is reabsorbed in the tubules, and that the urine is thus concentrated, but the reabsorption of albumen is much more problematical. Such a hypothesis would imply that the appearance of albumen in tho urine was due to the failure of the epithelium to absorb, and we should expect it to be associated with an excess of water.

Precisely the opposite is in general the case, and albumen is more frequent in concentrated than in dilute urine.

The truth seems to be that the process in the glomeruli is not a simple nitration, but a transudation through a living membrane of complicated structure. Wherever such transudations occur in the living body there is some selection of the constituents which are allowed to pass, and although the transudation-fluids are albuminous they are so in very varying degrees. Thus the percentage of albumen in cerebrospinal transudations is about 1'5 per cent., whereas in the peritoneal and pleural cavities it may be five or ten times as great (see p. 122). The glomerulus is more like a secreting or glandular organ than a simple filter. The water in passing out has to penetrate the walls of the vessels and then a layer of epithelium. The capillary vessels themselves are highly cellular, being very abundantly nucleated, and the epithelium clothes the tuft completely (Heidenhain). These structures exercise a selection in allowing the passage of the constituents of the blood, giving transit especially to water and salts. It is a very interesting fact, and one entirely confirmatory of this view, that while serum-albumen is retained, egg-albumen when injected into the blood of animals is passed into the urine. (Stokvis and others.) Any derangement of the delicate glomerulus is likely to allow of the passage of albumen, and it will be found that diseases which specially affect this delicate organ, such as acute inflammation and amyloid disease, are specially characterized by albuminuria.

It is not improbable that albumen may reach the urine from other sources than the glomeruli. The arteriae rectae of the pyramids occupy a somewhat similar position in the vascular system to that of the glomeruli. They come off to a large extent directly from the larger arteries, and the blood after leaving them also passes into capillaries. It is noticeable also that they and the glomeruli are the structures first and chiefly affected by amyloid disease. It is not improbable that in inflammations and in amyloid disease there may be considerable transudation of serous fluid from these vessels, which may find its way into the uriniferous tubules.

Literature

See full account in Heidenhain, in Hermann's Phys., v., 1880; Pantyuski, Virch. Arch., lxxix., 1880. Urcemia - Traube, Ges. Afchandl., 1871; Frerichs, Die Brightsche Krankh., 1851; Cohnheim, Gen. Path., Syd. Soc. transl., iii., 1890. Albuminuria - Stokvis, Eecherches exper. sur l'albuminurie, Journ. de Soc. Boy. de Bruxelles, 1867; Kirk, Glasg. Med. Jour., xv., 1881; Heidenhain, I.e.; Senator, Die Albuminuric, 1882; Discussion on Albuminuria in Path. Soc. of Glasg. (by Boberts, Hamilton, Gairdner, Greenfield, Newman, Coats, etc.), Glasg. Med. Jour., 1884.