Introduction

The kidney is a homeostatic organ that has three basic functions: the regulatory one in charge of the maintenance or control of the extracellular fluids, the volemia, regulates the balance of a variety of electrolytes; the excretory in charged of the excretion of nitrogenous products; and the biosynthetic responsible for the production of some hormones or autacoids in charged of the stimulation of the erythropoiesis like the erythropoietin, the calcitriol for the regulation of the balance calcium phosphorus and the prostaglandins in charged of the regulation of the arterial local pressure.

When we have indications of an alteration of the basic functions we have before us a patient with renal insufficiency (RI) which depending on the type of presentation it could be acute or chronic being the latter the one that we will approach in this article.

Differentiating our patients

The chronic renal insufficiency (IRC) is a progressive disease that we can divide it in four phases:

 Phase I: Loss of the renal reserve

 Phase II: Not azotemic RI

 Phase III: Azotemic RI

 Phase IV: Uremic RI

The phases I and the II in general does not demonstrate clinical signs, nevertheless in the phase II some patients can present polyuria-polydipsia that in the majority of the cases happens unnoticed for the owner and alone under a strict hospitable monitoring it could be detected; in some occasions we can observe small elevations of the creatinine serum levels without presentations of urinary densities above of 1.030, as well as trends to anemia; as suggestion of the author, for the cases of geriatric patients and not azotemic patients with competing diseases, always it is good bear in mind that these patients can be inside the phase II and to take the suitable precautions when these patients are submitted to procedures that could generate an hypotension effect as the anesthesia and the surgical ones or as consequence of clinical complications as vomit, diarrhea, cardiac insufficiency, etc., as well as the utilization of medicaments that could have nephrotoxic effects or alter the blood flow towards the kidney as in case of the non steroidal analgesics. In case of the phase III on having evaluated the rate of glomerular filtration by means of the determination of the blood values of urea, creatinine and phosphorus we find that these values are higher than normal values resulting in an azotemic patient, in this phase the patient could only present sings as dehydration, polyuria-polydipsia, lethargy; and in some cases finding the azotemia only in patients who are submitted to routing studies for some concurrent disease.

The phase IV is a renal insufficiency that shows a great variety of clinical signs related with uremic syndrome, as: vomit, diarrhea, hematemesis, melaena, clotting alterations, dyspnea, stupor, etc... depending on the gravity of the clinic frame.

In any of these studies patients with proteinuria can be found due to glomerulonephritis or glomerular hyperfiltration (See chapter article of proteinuria of Dr. David Senior).

The Renal Insufficient and the Diet

In every phase a frame of chronic RI is presented but within different degrees, which require different therapeutic supports therefore a specific nutritional support and that's the reason why we can not offer to these three patients the same type of diet with the same characteristics.

The diet represents the "key point" of the Chronic RI therapy because it shows the four primarily objectives of the treatment of this disease:

 Promoting an optimum nutrition.

 Minimizing the differences and the fluid excesses, electrolytes, minerals and acid-basics.

 Decreasing the uremic signs.

 Making slower the illness progression.

Protein

The diet for patients with IRC traditionally has consisted of reducing the content of protein; provided that in the patients with symptomatology attributable to the biochemical disturbances of Chronic RI, the dietetic modification can muffle the clinical manifestations. In uremic patients, the restriction of the protein is recommended as routine to reduce the generation of a variety of toxins derived from the metabolism of the proteins. The restriction of the dietetic protein can limit the generation of nitrogenous products and like that, diminish the scope of the uremic complications of the Chronic RI, as the lethargy and the vomit. The decision to limit the ingestion of protein has only taking if it is possible to support the caloric suitable consumption. Though strict guidelines do not exist to restrict the dietetic protein in the uremic control, there is the general principle of which the protein restriction should be considered providing that the concentration of ureic nitrogen blood level should overcome 27 mmol/L; to major signs attributed to Chronic RI a major degree of protein restriction is necessary to control the uremic phase.

On the base of the current indications, a diet with moderate protein (15-25 % of protein content on dry matter contributes near 2.5-4 g / kg / day) is good for the dogs with moderated azotemia even by plasmatic levels of urea <25 mmol/L that do not present uremic signs as those of the phases I, II and III. The diets with major protein content can be tolerated by the dogs with a minor degree of azotemia. The additional restriction of the protein (9-18 % of protein content on dry matter that contributes near 1.3-2.5 g / kg / day) only justifies himself if signs of uremia exist or the plasmatic levels of urea are near of 27 mmol/L in patients in phases III and IV with a major level of serum urea.

The restriction of proteins can minimize the renal progressive damage (glomerulosclerosis) and spontaneously in patients with Chronic RI by the modification of the renal hemodynamic or of the compensatory hypertrophy. The restriction of phosphorus in the diet reduces the speed of development of glomerulosclerosis, as well as the improvement and prevention of the nutritional secondary hyperparathyroidism. The severity of the polyuria-polydipsia sign and the anaemia in general they control themselves when the patients with RI receive diets with moderate restrictions of protein. Due to the fact that the hydrogen ions are an intermediary product of the catabolism of proteins, the restriction of these can reduce the metabolic acidosis.

In patients with Chronic RI with presence of proteinuria of renal origin (glomerulonephritis) opposite to what is thought, is advisable to handle a diet with protein restriction with the purpose of limiting the proteinuria, the glomerular hyperfiltration and hypertension and supporting the plasmatic concentrations of albumen. They must begin receiving a diet formulated for patients with RI and to realize controls for intervals from 2 to 4 weeks that allow determining the ideal quantity of the diet. The diet has to of being kept if the proteinuria diminishes, without association of a serious signs of caloric protein malnutrition. Before the first signs of malnutrition the protein ingestion have to increase gradually meanwhile the patient is controlled.

Phosphorus

In the recent years the concepts have changed, rolling over principally towards the phosphorus as the important one component to reducing in the diet, owed that the decrease in the rate of glomerular filtration originates an increase in the levels of plasmatic phosphorus generating an alteration in the relation calcium/phosphorus, which results in the activation of the liberation of the PTH that acts as an uremic toxin and originates the renal secondary hyperparathyroidism responsible for some signs of uremia previously seen.

The studies documented a relation between the ingestion of dietetic phosphorus and mortality in dogs and cats with induced Chronic RI. Though it can only for establishing the exact mechanism of the nephrotoxicity of the phosphorus, its restriction in the diet has been associated with the maintenance of the renal function, decrease of the presentation of the interstitial tube damage and reduction of the hyperphosphatemia, hyperparathyroidism and hyperlipidemia degree. There is not known the goal most adapted for the restriction of the dietetic phosphorus, but the efficiency can be supervised with the measurement of the plasmatic concentrations of the phosphorus. The simplest objective of alertness is to support the normophosphatemia.

The restriction of the phosphorus must be proportional to the degree of renal disease. Of general form, initially are indicated the diets that contain less than 0,5 % of phosphorus on dry weight. It is probable that in some affected animals they need severer restrictions of phosphorus to reach the normophosphatemia. A variety of factors besides the restriction can reduce the intestinal absorption of the phosphorus. From the theoretical point of view, the restriction of the phosphorus that takes to the increase of the proportion calcium / phosphorus would be of benefit to increase the relative union of both in the intestine. Nevertheless the hypercalcemia might be the result in an animal that consumes a diet with a proportion calcium / phosphorus excessively high. Based on the fact that binders of intestinal phosphorus reduce the absorption of the ingested phosphorus, they must be incorporated in the animals that are kept hyperphosphatemic in spite of the restriction of the dietetic phosphorus. These agents must manage with food and be dosed up to effect. The agents who contain calcium or aluminium are acceptable. The medicaments with binders of phosphorus that contain calcium can induce hypercalcemia and must not be used in hypercalcemic patients or together with the vitamin D (calcitriol).

In some animals with dietetic managing promotes the normophosphatemia by itself, but the attributable manifestations persist to secondarily renal hyperparathyroidism, as the renal osteodystrophy. In such cases, the administration of oral calcitriol (initial dose of 2-6 ng / kg / day) can take advantage as co-alternative therapy. Frequent adjustments of the dose of calcitriol can be needed, based on the plasmatic concentrations of the parathyroid hormone and calcium. The therapy with calcitriol does not reduce the plasmatic concentrations of parathyroid hormone in all the animals.

Other factors of the diet that can influence the development of chronic renal insufficiency include: content and composition of the lipids, consumption of sodium and potassium, total consumption of calories, acidic nature of the diet.

Composition of oily dietetic acids

The dietetic supplementation with polyunsaturated oily acids (AGPI) can modify the renal hemodynamic and anticipate or retard the renal progressive damage in dogs with induced IRC. Compared with the supplementation of Carthamus oil (AGPI omega 6), to add sebelum oil (AGPI omega 3) to the diet, the intraglomerular pressure diminishes and preserves the structure and renal functions. This dietetic modification should be considered to be a measurement to retard the progression of the azotemic IRC in dogs. Though for the present time this is a motive of controversy.

Potassium

The hypokalemia is frequent in dogs with IRC, particularly in patients with marked polyuria or tubular affections. Though the relation reason / effect was not established by clarity, there was postulated that the renal insufficiency leads the kaliuresis and hypokalemia, which reduces the renal function. This decline of the renal function favors the excretion of potassium, a vicious circle being created. For it, it is important to assure a suitable ingestion of the potassium for these patients. To achieve this goal, the diet can be supplemented with salts of potassium, if it is necessary, supporting the eupothasemia. As the acidose or acidification of the diet increase the kaliuresis, it is necessary to have the caution of valuing and supporting the acid / alkaline balance in the animals with renal disease.

Sodium

The systemic hypertension is frequent in dogs with IRC. The increase of arterial systemic pressure can induce renal hyperextensive damage. In the animals with RI, in which the measurement of the blood pressure establishes the existence of a marked systemic hypertension (systolic arterial pressure > 180 mmHg), the restriction of the dietetic sodium is an appropriate therapeutic maneuver, though of unknown efficiency.

When it is implemented, the dietetic restriction of sodium must be moderated, with an objective closer to 15-40 mg / kg / day that the therapeutic diets handle for patients with RI in comparison with the normal diets that contribute 75-150 mg / kg / day. Provided that the homeostatic mechanisms for the sodium balance can be less effective in animals with renal disease, the changes in the revenue (oral or parenteral) must proceed in gradual form, for 7-14 days. The excessive or rapid sodium restriction can cause decrease of the extracellular volume and systemic dehydration and hypotension. In the ideal situation, the efficiency of the sodium restriction should be valued measuring the arterial pressure. At least, the physical examination and measurement of serum creatinine must be realized 1-2 weeks after the ingestion of the sodium fits.

Energy

Sufficient calories must be provided to support a corporal normal and stable weight. It is possible to consider the supplementation with vitamins of the complex B for dogs and cats with IRC, particularly during the periods of limited consumption of food.

Different methods exist to determine the energetic needs of the patients. As general rule, the base caloric requirements estimated for dogs are from 40 to 60 kcal / kg / day and in cats 70 kcal / kg / day, depending on the size. The energetic needs can be determined on the basis of the basal energetic requirements (REB = kcal/24 hrs) or necessary energy to support the vital cellular functions: REB = 70 x kg ^(0.67-0.75). In the majority of the ambulatory patients it is necessary to handle the energetic metabolic requirements (REM), which are the necessary ones in order that a patient has a certain activity and could generate a good homeostasis; as a rule it is the double of the REB: REM = REB x 1.4 to 2

Remember that the previous parameters are only the beginning and they must be adjustment to fit to every patient, I suggest you to take the result as the minimum that this patient must eat and if its eats more very much better. (Never forget that it is a sick patient and needs energy for its maintenance and homeostasis.)

If the hospitalised patient, presents anorexia that cannot be brought down by an increase in the palatability of the diet and in the hospitable managing it is possible to be necessary to use pipes of enteric nutrition; providing that the vomits could be controlled, these pipes constitute an easy route to give water and food in some cases is required to use paraenteric nutrition.

Recommendations

To minimize the production and retention of products of the protein catabolism (together with uremic toxins) providing a diet with limited quantities of high quality protein seems to help to improve the clinical signs of the uremia. Nevertheless some patients can push back such, due to its minor palatability that often assumes the minor contained of sodium, phosphorus and protein of the diet. If the hyper catabolic patients with renal disease do not consume the sufficient food to satisfy its diaries requirement of nutrients, there will increase the catabolism of endogenous proteins what in turn will increase the production of products of the protein catabolism accentuating the malnutrition and the signs of uremia, which can turns favored with an excessive reduction of the protein ingestion. Since there have not been established minimal requirements of proteins and amino acids for the different phases of RI, but nonetheless, in the serious cases it is necessary to restrict gradually the protein ingestion in order to minimize the consequences of the RI. There will be used only proteins of high biological value. It is necessary to find a balance to achieve a nutritional suitable condition and to control the clinical manifestations of the uremia. In general is observed progressive improvement of the clinical signs concerning 2 to 4 weeks. To determine if it is necessary to increase or to reduce the quantity of dietetic protein it becomes indispensable to resort to repeated monitoring of the general evaluation of the patient and laboratory tests, as well the evaluation of the global clinical reaction to the diet.

Of personal form in patients with RI in phase I, which in general they are not diagnosed, only is necessary to handle commercial diets of good quality as the premium food; in phase II commercial premium diets or diets of maintenance for geriatric patients (Senior) as well as constant monitoring and to support to the patient in its ideal weight with a corporal condition 3; for patients in phase III is advisable diets for geriatric patients or therapeutic diets called medium protein and with base in the monitoring to change to diets with minor protein content; in case of the patient in phase IV is advisable to approach it with therapeutic diets designed for insufficient renal patients and to realize the necessary modifications on the basis of frequent evaluations.