Nutritional Management of Chronic Renal Disease
Nutritional Management of Chronic Renal Disease - Andrea J. Fascetti and Sean J. Delaney
Chronic renal (kidney) failure is an irreversible loss of all of the kidney's functions. Although commonly considered an illness of older dogs and cats, it can occur in animals of all ages. Chronic renal failure is not reversible and may have been present in your pet for months to years before the time of diagnosis. Although there is no cure for this disease, it can be successfully managed, and nutritional therapy is an important part of that treatment. Recent studies in dogs and cats have shown both a reduction in the complications associated with renal failure, and an increase in life expectancy by feeding diets designed to manage renal disease. The goals of nutritional management are to meet the patient's nutrient and energy requirements, as well as to alleviate the clinical signs and to slow the progression of the disease. Specific recommendations regarding dietary therapy will vary from patient to patient and need to be based on clinical and laboratory findings. Chronic renal disease is progressive and therefore repeated assessment and subsequent changes in your pet's care and diet may be necessary to successfully manage this process.
In a majority of cases, your veterinarian will recommend a dietary change once your pet has been diagnosed with renal disease. Recommending a diet with moderate to severe protein restriction is one of the most common approaches to managing kidney failure. Restriction of dietary protein has been demonstrated to slow the rate of progression of renal damage in rats and people. However the effect of protein restriction on the progression of renal damage in dogs and cats remains controversial and no definitive study exists on this matter. Many of the clinical signs that you see in your animal such as vomiting, lethargy, anorexia, diarrhea, oral ulcerations and the foul ammonia odor to their breath can be partially or completely alleviated by reducing the protein concentration in your animal's diet. These clinical signs, that are often referred to as uremia, can be caused by an accumulation of the breakdown products of protein metabolism (sometimes referred to as nitrogenous waste products). This protein comes from both the protein in your animal's diet, as well as mobilization and degradation of their own body's protein stores. Consumption of protein in amounts greater than what your animal needs to maintain normal bodily functions can exacerbate these clinical signs. However, not enough protein in the diet can be equally detrimental and protein malnutrition in patients with renal failure can facilitate the occurrence of other complications or lead to an early death.
The consumption of diets containing reduced protein levels decrease the amount of nitrogenous waste delivered to the kidneys for excretion in the urine. This may help reduce the excessive drinking (polydipsia) and urination (polyuria) in your animal. A reduction in dietary protein may also help reduce the degree of anemia in some patients. Anemia enhances the weakness and reluctance to eat in animals with renal failure. Anemia can occur for several reasons with renal disease, but one factor that is believed to make it worse is excessive dietary protein. Nitrogenous waste products are believed to contribute to anemia by reducing the life span of red blood cells. The waste products may also enhance blood loss by leading to the formation of gastrointestinal ulcers and a reduction in blood clotting ability.
Close attention must be paid to the mineral balance in patients with chronic renal disease. Phosphorus, calcium, sodium and potassium are of particular concern. The latter two are often referred to as electrolytes. All of these can be easily measured using blood tests and are part of a routine screen in patients with chronic renal disease. Most diets designed to manage renal disease also contain alterations in these minerals to meet the special needs of these patients.
One of the first alterations in mineral status that occurs with renal disease is phosphorus retention by the kidneys and this is manifested as elevated phosphorus concentrations in the blood (referred to as hyperphosphatemia). This increase in body phosphorus concentration can lead to numerous deleterious consequences such as vitamin D deficiency, in addition to alterations in the actions of other hormones that regulate calcium metabolism and subsequent calcification of bodily tissues. In dogs, dietary phosphorus restriction has been shown to slow the progression of renal failure. One goal in the management of renal disease is to normalize blood phosphorus concentrations. By reducing hyperphosphatemia, these changes can be minimized or prevented. This can be achieved by reducing the amount of phosphorus contained in the diet or by reducing the intestinal absorption of dietary phosphorus. Dietary protein sources contain high levels of phosphorus. This is another reason that foods designed for the management and treatment of renal failure contain reduced amounts of dietary protein. Unfortunately as renal disease progresses, restriction of dietary protein alone is often not sufficient to control blood phosphorus levels. Further control of phosphorus can be achieved by the addition of intestinal phosphate binders. These binders help to reduce the absorption of phosphorus through the gastrointestinal tract. The point when one begins to institute the use of phosphate binders in the management of chronic renal failure will vary from animal to animal.
Secondary to alterations in phosphorus concentrations, calcium may also be altered in patients with chronic renal failure. While phosphorus most commonly increases, calcium concentrations may increase, decrease or remain normal. Your veterinarian will monitor calcium concentrations using blood analysis and manage changes accordingly.
Restriction of dietary sodium is a common feature in diets designed to help manage chronic renal disease. Sodium restriction is instituted to help control high blood pressure (hypertension) that is associated with the diseased kidney's inability to excrete sodium normally. Hypertension is also theorized to contribute to the progression of renal disease. It is important to note however, that severe sodium restriction is also not prudent. Severe restriction can result in volume depletion and dehydration, exacerbating clinical signs and the disease. Gradual sodium restriction is also recommended, as the kidney's ability to adjust to different sodium loads diminishes with this disease.
Potassium is another mineral that can either increase or decrease with chronic renal failure. The most common scenario is potassium depletion. Potassium depletion occurs with chronic renal disease due to a reduction in dietary potassium intake in animals that are not eating well, as well as an increase in loss through the urine. However, there is a population of animals that may have elevated potassium concentrations. Your veterinarian will monitor potassium concentrations in the blood and will adjust intake accordingly. Some animals require the addition of extra potassium to their diets to maintain normal blood concentrations.
Animals with renal failure have an increase in their urine volume, and therefore an enhanced excretion of water soluble vitamins (B Vitamins and Vitamin C). Loss of these vitamins may contribute to the anorexia associated with renal disease. Diets designed for the management of renal disease are supplemented with increased amounts of water soluble vitamins, and further vitamin supplementation is rarely necessary. Humans with renal failure have a reduced capacity to excrete vitamin A, and although no similar information exists in dogs and cats, the feeding of supplements containing vitamin A is not recommended.
Acid-base abnormalities are commonly seen in dogs and cats with renal failure because it is the kidney's job to excrete hydrogen ions and retain bicarbonate ions in order to maintain blood pH within the normal range. When the kidneys begin to fail, hydrogen ions are retained and bicarbonate ions are not reabsorbed, leading to a state called metabolic acidosis. Metabolic acidosis affects the entire body and enhances the clinical signs of renal disease, making your animal feel ill. In an effort to counter this disturbance, the body will mobilize its own resources from muscle and bone. This initially palliates the problem, but over the long-term can lead to the further decline in your animal's health. Dietary protein restriction reduces the production of protein-derived acid precursors which helps to some extent. In addition, renal failure diets have increased amounts of alkalinizing agents such as potassium citrate, sodium bicarbonate or calcium carbonate to further combat this problem.
As previously mentioned, diets designed for renal disease have reduced amounts of protein compared to normal maintenance diets. In order to compensate for this protein reduction, the concentration of fat is usually increased. An increase in dietary fat can be beneficial in several ways. On a weight basis, fat has almost twice as many calories as protein or carbohydrates. This increases the energy density (number of calories per cup or can) of the diet and therefore allows an animal to consume less food to meet its energy needs. Fat also enhances the palatability of the diet and makes it more appealing to an animal that might be reluctant to eat. However, in some animals extra dietary fat can cause problems. Signs that your animal may not tolerate the higher fat concentrations in these diets may include a reluctance to eat or a reduction in food intake, lethargy, nausea, vomiting, diarrhea or abdominal pain. Should any of these signs occur, you should contact your veterinarian immediately. Some of these clinical signs can also be caused by the kidney disease itself and your veterinarian may have to do some diagnostics tests to determine the cause of the problem.
Nutritional Management at Home
Your pet needs to consume sufficient calories to supply essential nutrients, as well as to prevent the breakdown of their body's protein stores that will cause malnutrition and exacerbate the clinical signs of uremia. If you notice that you animal is not eating well, or has stopped eating entirely, contact your veterinarian immediately. Do not attempt to force-feed the reduced protein diet to your animal. This may result in the animal associating feeling ill with the consumption of the therapeutic diet (also known as a learned aversion). Once they feel better, they will not want to resume eating the diet. It can then be very difficult to get them to consume any diet designed to address their special needs. In some cases, dogs and cats that are reluctant to eat will require the placement of an enteral feeding tube (a tube that allows the delivery of food directly into the gastrointestinal tract) to provide some, or all of their daily energy needs.
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