Albuminuria is a most important means of recognizing the presence and sometimes the variety of renal disease present, but the degree of albuminuria is not a safe guide for dietetic treatment. This is more especially so as in some of the most serious renal diseases, e.g. granular kidney and some forms of chronic nephritis, the albuminuria is slight in amount, and it is even possible for serious and fatal renal disease to be present without any albuminuria; this absence of albumin no doubt is often only temporary, but still this fact may cause very serious errors of diagnosis and of treatment. In most instances the degree of albuminuria is only roughly estimated by the amount of deposit in a given sample, and observations on the twenty-four hours' urine are but rarely undertaken. This is most misleading, as the degree of albuminuria, even in chronic renal disease, may vary within wide limits at different periods of the day, and estimation should always be based on an examination of the twenty-four hours' sample.
Many renal diseases are accompanied by secondary effects in the cardiovascular system. High tension, cardiac hypertrophy and arterial degeneration are frequent accompaniments, especially of chronic nephritis and of granular kidney. High tension may, however, exist without any notable degree of arterial degeneration, and further, the arterial degeneration when present may not be universal in its distribution, thus in some instances though the vessels of the body generally present marked changes characteristic of arterio-sclerosis the cerebral vessels may be relatively healthy. In other cases, on the other hand, they may be profoundly sclerosed.
In determining the treatment of the disease it is important to take into consideration the degree of high tension present and also the presence or absence of marked arterial lesions. Some of the most serious complications of renal disease are dependent on the presence of these lesions. Thus epileptiform seizures of great severity may be due apparently to arterial spasm associated with high tension, and such a serious lesion as cerebral haemorrhage may owe its origin to the arterial degeneration associated with renal disease.
In regulating the diet in renal disease attention must be directed to all the factors mentioned above, and although the state of the urine must be allowed due weight, the effects of the renal disease on the circulation and on the general state of nutrition must also be considered. The main objects aimed at should be : (1) To diminish the work of the kidney so far as is possible; (2) to maintain the general nutrition and to counteract, if possible, the weakness and wasting present; (3) to regulate, so far as is possible, by diet the arterial tension; (4) to be careful that the diet should not be such as to promote a condition of hydraemic plethora which may not only tend to aggravate any dropsy present, but may also seriously affect the circulation, and especially the heart, owing to the frequent presence of cardiac dilatation in nephritis.
It is clear that in different renal diseases these varying factors are of greater importance in some than in others; thus in calculous disease the main efforts must be directed to modifying the composition of the urine; in acute nephritis the great aim will be to diminish the work of the kidney; in chronic nephritis and in granular kidney attention will often have to be directed mainly to the state of nutrition, the regulation of arterial tension and the amelioration or prevention of dropsy.
It must be borne in mind in all the attempts made to diminish the work of the kidney that a considerable proportion of the nitrogenous extractives of the urine are derived from the breaking down of the tissues of the body and that no limitation in diet will affect the quantity of this portion of the nitrogenous excreta, and that therefore to diminish the diet for long periods of time owing to a deficient excretion of urea may be followed by aggravation of the patient's general weakness. Further, the low percentage of urea in the urine is not entirely dependent on imperfect elimination as a varying proportion of protein matter representing non-metabolised protein is passed out in the urine. Again these patients have often a poor appetite and may suffer from diarrhoea and vomiting and these will also tend to diminish the metabolism of protein and the excretion of nitrogen. The diminution of the protein ingesta is especially indicated in acute renal disease such as acute nephritis, and in this malady there can be no objection to reducing the protein taken to as small an amount as possible or even, in some cases, to withhold it altogether for short periods of time. In chronic nephritis, on the other hand, much care should be taken in determining accurately the significance of the scanty urea excretion that may be present, due weight being attached to the presence of such symptoms as diarrhoea and vomiting, and the degree of albuminuria present and the amount of nitrogen ingested in the form of protein. When all these factors are duly considered it will often be found that although the percentage amount of urea and other extractives is low, the total amount excreted in the twenty-four hours is not such as to imply that there is necessarily any material retention of these substances in the blood stream, since the quantity of urine is often much increased. On the other hand, in severe cases of chronic renal disease and especially in those accompanied with uraemic symptoms there may not only be very considerable retention of these normal nitrogenous extractives, but they may also be present in undue amount in the blood owing to increased production.
The regulation of diet is probably most important of all in cases of chronic disease such as granular kidney where, notwithstanding the appearance of health, the excretory activity of the kidneys may be very seriously impaired. Many of these patients have often been large meat-eaters, and owing to their passing considerable quantities of urine it is often difficult to persuade them that there is any serious renal lesion. In such cases the deficient excretion of urea is a factor of the first importance in regulating the diet since none of the conditions mentioned above, such as diarrhoea, vomiting, or marked albuminuria, are present to minimize the significance of the deficient urea secretion.
Although the proteins are the food constituents on which most stress is laid in regulating the diet of renal 'disease, the ingestion of common salt is also a matter of considerable importance. It would seem to be clearly established that the taking of large quantities of salt may play a very considerable part in the degree of development of dropsy in certain renal diseases, especially chronic nephritis. Where dropsy is present it often increases materially in amount when a diet rich in salt is given. This applies not only to the dropsy of renal disease, but also to that of cardiac affections. Further, it can be shown that in chronic parenchymatous or chronic diffuse nephritis the quantity of sodium chloride present in the urine may sometimes be small, and this is the chronic renal lesion that is most often accompanied by dropsy. On the other hand, in granular kidney the excretion of sodium chloride may be large in amount and some have attributed the increased urinary excretion to this factor. The diminution of salt in the food may lead to the most marked improvement in, or even subsidence of, dropsy in cases where it is present, and very often better results are obtained by treating such cases with a relatively dry salt-free diet than by prescribing a milk diet as is so often done in a routine fashion.
A question of considerable difficulty is that of the administration of simple fluids. There is much to be said in their favour as flushing agents, more especially in some inflammatory affections of the kidney where the tubules are blocked to a greater or less degree by detritus and products of degeneration, such as casts and blood corpuscles, etc. Water in considerable quantities is often advised as a diuretic. On the other hand, the state of the kidney may be such that the elimination even of water is carried on with great difficulty and the administration of large quantities may lead to the development of a hydraemic plethora that tends to aggravate any dropsy or any cardiac dilatation that may be present.
The importance of cardiac dilatation in acute and chronic renal disease is often under-estimated. In acute and sub-acute nephritis death may result from cardiac dilatation in cases where dropsy is not marked and where the uraemic manifestations are only slight. It is perhaps in this type of case that the most serious risks are run from aggravating the condition of plethora by the administration of excessive quantities of fluid. Cardiac dilatation running a more chronic course is also a very familiar feature in chronic renal disease associated with more or less extensive cardio-vascular degeneration. In these circumstances the regulation of the quantity of fluid ingested may also be of great importance.