Diets for Cats With Chronic Kidney Disease
Adapted from the IRIS education article by David J. Polzin, DVM, PhD, DACVIM; Jessica Quimby, DVM, PhD, DACVIM; and Sheri Ross, DVM, PhD, DACVIM. The original article was written by David J. Polzin in 2016.
Introduction
Dietary management of chronic kidney disease (CKD) in cats has been the mainstay of treatment for decades and remains the most commonly recommended therapy. Based on evidence from clinical studies, the IRIS Board suggests that kidney diets be considered for cats in IRIS CKD Stage 2 and recommends feeding kidney diets to cats in IRIS CKD Stages 3 and 4. It is not yet clear what the recommendation should be for cats with IRIS Stage 1 disease.
Veterinarians use therapeutic diets in much the same way as medicines to manage medical conditions. When they prescribe a kidney diet for a cat with CKD, they expect it to achieve four goals:
- Reduce or prevent the clinical consequences of CKD, including signs of uremia
- Slow the progression of CKD and prolong survival
- Minimize disturbances of electrolyte, calcium and phosphorus, and acid-base balance
- Maintain adequate nutrition
To achieve these goals, kidney diets are typically formulated to have reduced phosphorus, modified amounts of high-quality protein, increased calorie density, added B vitamins, increased omega-3 polyunsaturated fatty acids and antioxidants, and added potassium, and to have a neutral effect on acid-base balance. More recently, early-stage kidney diets that are phosphorus-restricted but less protein-restricted have also become available for cats (Parker, 2021). Clinical trials have supported the benefits of kidney diets formulated along these lines.
Evidence Supporting Kidney Diets in Cats With CKD
Several studies have compared feline kidney diets with typical feline maintenance diets for preventing uremic crises and extending survival. The consistent findings of these studies, which used different diets and methods and were carried out in different countries by independent groups of researchers, strongly support the conclusion that kidney diets lead to better clinical outcomes: longer survival and fewer uremic crises.
The first study was a randomized, masked clinical trial in which 22 cats were fed a kidney diet and 23 cats an adult maintenance diet (Ross et al., 2006). The main changes in the kidney diet were reduced protein, phosphorus, and sodium, and added polyunsaturated fatty acids. Over the two-year study, there were no uremic crises or kidney-related deaths among the 22 cats fed the kidney diet, whereas 6 cats fed the maintenance diet developed clinical and biochemical signs of uremia and 5 died of the consequences of kidney disease.
The second study compared a manufactured protein- and phosphorus-restricted kidney diet with continuing the cats' regular diets (Elliott et al., 2000). This study was neither randomized nor masked, and cats that would not eat the kidney diet continued on their usual food. Cats that ate the kidney diet (29 cats) survived significantly longer, with a median survival time of 633 days, than cats that continued their regular diet (21 cats), with a median survival time of 264 days.
The third study was a retrospective study in 31 first-opinion veterinary practices in the Netherlands. It compared the survival of cats fed one or more of 7 commercial feline kidney diets with that of cats not fed a kidney diet (Plantinga et al., 2005). The median survival time was 16 months for cats fed a kidney diet, compared with 7 months for cats fed their usual diet.
Other studies support the benefit of kidney diets on the basis of markers of chronic kidney disease–mineral and bone disorder (CKD-MBD), such as fibroblast growth factor 23 (FGF-23). FGF-23 is increased in cats with CKD and is associated with a poorer prognosis. A study comparing FGF-23 concentrations in 33 cats eating a kidney diet with those in 11 cats eating a non-renal diet found that feeding a kidney diet was associated with reductions in FGF-23 in both hyperphosphatemic and normophosphatemic cats (Geddes et al., 2013a).
Phosphorus and Kidney Diets
To compensate for the decline in phosphorus excretion as CKD advances, dietary phosphorus intake must be reduced. Most maintenance diets contain substantial amounts of phosphorus, much of it coming from protein. It is a common misconception that the purpose of kidney diets is protein restriction. There is little consensus on the right amount of protein in kidney diets (see below), but there is a significant body of evidence on the importance of phosphorus restriction (Geddes et al., 2013b; Parker, 2021).
Recent evidence also suggests that the form of phosphorus, not just the amount, may affect phosphorus balance (Parker, 2021). Phosphorus from inorganic sources, such as sodium or potassium phosphate salts, is more bioavailable than phosphorus from organic sources, such as meat, bone meal, and grains. The dietary calcium-to-phosphorus ratio also matters: feeding highly bioavailable phosphorus salts with too little calcium, giving a calcium-to-phosphorus ratio below 1, has been shown to cause kidney damage in previously healthy cats (Dobenecker et al., 2018a; Dobenecker et al., 2018b; Alexander et al., 2019).
Dietary therapy may take several weeks to have a noticeable effect on blood phosphorus. In cats with CKD, the full effect of the diet was seen after 28 to 49 days (Barber et al., 1999). Serum phosphorus should therefore be rechecked 4 to 6 weeks after starting the kidney diet. If it is within the IRIS target range, the diet should be continued and serum phosphorus rechecked every 3 to 4 months (every 4 to 6 months may be enough in IRIS CKD Stage 2). Phosphorus is more likely to be controlled by a kidney diet alone in cats with Stage 2 and 3 CKD. If a kidney diet alone does not achieve the serum phosphorus target after 4 to 6 weeks, adding an intestinal phosphate binder is recommended.
Intestinal phosphate binders can reduce the amount of dietary phosphorus absorbed, particularly in combination with a kidney diet, but their ability to limit phosphorus uptake from diets high in phosphorus is limited. This, combined with the fact that many cats resist taking medication, increases owners' frustration and reduces the quality of life of cats that must receive unpalatable medication with every meal. It lowers compliance and makes the strategy of feeding high-protein foods with phosphate binders of questionable effectiveness. Giving phosphate binders at doses above the recommended range can also cause adverse effects, including toxicity from absorption of the cations in the binders, such as aluminum and calcium.
Hypercalcemia is sometimes seen in cats with CKD (see our article on hypercalcemia in chronic kidney disease). Its risk factors, including any association with restricted phosphate intake through diets or phosphate binders, remain to be determined. In some cats that develop hypercalcemia after starting a kidney diet, increasing phosphate intake returns serum calcium to normal (Geddes et al., 2021). Further research is needed to identify which cats with CKD are at risk of hypercalcemia and to understand how treatment can be better tailored to their needs.
Is the Protein Content of Kidney Diets Right for Cats With CKD?
The use of kidney diets in cats with CKD has become controversial, weighing the potential benefits of these diets in reducing the clinical consequences of CKD against a suggested risk of protein malnutrition. Much of this debate has focused on cats, because they are obligate carnivores with higher protein requirements than dogs and people (Zoran, 2002; Zoran and Buffington, 2011). As a result, some veterinarians have recommended feeding diets high in protein instead of the kidney diets designed specifically for cats with CKD. These high-protein diets lack the other modifications found in kidney diets and, problematically, may be high in phosphorus. This divergence of opinion probably arose from studies suggesting that senior cats may need more protein than younger cats (Laflamme and Hannah, 2013), and from the observation that body weight, body condition score, and muscle mass decline over time in many cats with CKD.
There are also less polarized debates, such as when and how much protein intake should be modified. In the past, the emphasis was on reducing the protein content of diets. The reason for modifying protein intake in patients with CKD is the observation that reducing protein intake in animals with advanced disease significantly improves their clinical signs. Although a direct cause-and-effect relationship has not been proven in cats, it is generally believed that retained protein waste products contribute significantly to many of the metabolic disturbances of kidney disease (Mitch, 1991). Some veterinarians argue that protein moderation should be delayed until a cat begins to show clinical signs of uremia, typically in late IRIS CKD Stage 3 or in Stage 4. Others argue that it should begin early, in IRIS CKD Stage 2 or 3, because it may slow the progression of CKD, delay the onset of uremic signs, and make a diet change easier to accept. In addition, waiting until the owner notices signs of uremia increases the risk of a uremic crisis before diet therapy can start. One possible concern about kidney diets in some cats with IRIS CKD Stage 2 is that moderating protein with a calorie-dense food may contribute to fat gain and loss of lean body mass if the kidney diet does not meet the cat's protein requirements.
Another important point is that, although commercial feline kidney diets have historically been described as low in protein, they meet, and in most cases far exceed, the AAFCO minimum for crude protein. As well as the amount of protein in a diet, its quality must be considered. Protein quality is not related to the source of the protein but to the bioavailability of its amino acids and, more importantly, the composition of the protein. A high-quality protein for a particular species contains all of the amino acids that species requires. Required (essential) amino acids are those the animal cannot make through its normal metabolism. In commercial kidney diets, the protein used is highly bioavailable, and care is taken to include the required amino acids in more than sufficient amounts. For example, in one commonly used commercial kidney diet for cats, all of the essential amino acids are present at 150% or more of the recommended daily amount (Hill's, 2021).
Unfortunately, very few data are available on protein as the only dietary change in patients with CKD. One study in cats with surgically induced kidney disease found significantly more structural kidney changes in cats fed a high-protein diet (about 52% protein) than in those fed a lower-protein diet (Adams et al., 1994). However, surgically induced kidney disease does not behave in the same way as naturally occurring disease, and a later study found that calorie intake, not protein intake, seemed to affect kidney structure (Finco et al., 1998). The effect of CKD on the protein requirements of cats has not been determined either. In addition, there is no published evidence that kidney diets cause loss of lean body mass and protein malnutrition when calorie intake is adequate. Studies of different levels of dietary protein in cats eating appropriate calories are needed to establish the optimal protein content of feline kidney diets. Clinical trials of kidney diets in cats with CKD have shown that these cats may keep a stable body weight and body condition score, but most of these studies did not measure lean body mass, which is a better indicator of protein malnutrition. One study (Hall et al., 2019) showed that cats with IRIS Stage 1 and 2 CKD fed a kidney diet with increased calorie density and higher levels of carnitine and essential amino acids maintained their lean body mass, measured by dual-energy X-ray absorptiometry, over a 6-month feeding trial. Cats eating a control food ate fewer calories and lost weight.
The subject of protein content continues to evolve. Other dietary changes, particularly phosphorus restriction, are probably much more important in managing kidney disease. Feline kidney diets are now available with different amounts of protein, so that the diet can be tailored to each cat's needs and response to treatment.
It is worth remembering that, in many patients, the familiar image of the "skinny CKD cat" is not a result of reduced protein intake but of an overall reduction in calorie intake. This often begins before CKD is diagnosed and before a kidney diet is started, which suggests that CKD itself promotes these changes, no doubt made worse by a poor or altered appetite (dysrexia). As CKD advances, dysrexia causes a slow, insidious decline in calorie intake, body condition, and muscle mass. In desperation, many owners offer high-protein foods to get their cats to eat more. The familiar saying "they have to eat something" is certainly true, but a cat's quality and length of life will be improved if it eats enough of a diet formulated for kidney disease (Ross et al., 2006; Plantinga et al., 2005). A key part of management is therefore making sure the cat's nutrition is adequate.
The Importance of Nutritional Assessment
Regular assessment of nutritional status is a key part of managing CKD, and every patient should have a nutritional plan that includes a specific target for daily calorie intake. A nutritional assessment should include body weight, body condition score, muscle condition score, whether calorie intake is adequate (including open-ended questions about how the cat is eating), and a complete diet history covering pet food, treats, supplements, and any foods used to give medications. Assessing muscle mass is particularly important in CKD, because it can have a profound effect on serum creatinine, and therefore on how the severity of the disease is interpreted, as well as on the cat's nutritional status. Specific calorie targets and close monitoring of intake are key to successful dietary management of CKD. If the cat is not eating enough, the poor appetite must be addressed, or the nutritional plan changed to compensate, for example with appetite stimulants or a feeding tube.
Starting Dietary Therapy
The way a therapeutic food is introduced to the cat, and even more importantly to the owner, has a profound effect on whether the cat accepts it. Some cats move easily from one diet to another, but many are very selective and need more encouragement. In general, diet changes should be made very slowly rather than abruptly. Most cats can be moved onto a new diet over 2 to 3 weeks by gradually mixing the new food into the old one, and in the authors' experience, cats are more likely to accept a new diet if the change is made over 3 weeks.
It is important to consider medical causes of a poor appetite before assuming that it is related to the diet. A cat that was not eating its usual food before presentation is unlikely to accept a new one. Often it is a general lack of appetite, not a dislike of the kidney diet, that makes the transition difficult. In some cats, it may therefore be wise to address as many of the factors suppressing appetite as possible before attempting a diet change. Medical causes of poor appetite in cats with kidney disease include anemia, intestinal disease, nausea, dehydration, metabolic acidosis, and low blood potassium (hypokalemia). Most of these can be managed with appropriate treatment.
Tips to Help Cats Accept Kidney Diets
The most important factor in a successful diet change is educating the owner. Owners who understand that the kidney diet is a medical treatment, not just a food, are more likely to follow the instructions. Many owners offer the new food once and, if the cat refuses it, assume the cat will never eat a kidney diet. Owners who understand its importance will put in the time and effort to make the transition properly.
Move the cat from its original food to the kidney diet over at least 3 weeks. A typical protocol is:
- Week 1: 25% kidney diet mixed with 75% of the original food
- Week 2: 50% kidney diet and 50% of the original food
- Week 3: 75% kidney diet and 25% of the original food
- Week 4 onward: 100% kidney diet
Other tips that help:
- To minimize confusion and improve compliance, ask the owner to bring in the cat's previous food and make up pre-mixed bags labeled with the correct week. Seeing the clinic's commitment to the transition and to kidney diets can also encourage owners to follow through.
- Follow-up phone calls, at least weekly, during the transition check on the owner's and cat's progress, improve compliance, and reinforce the importance of dietary management.
- Offer small, frequent meals, and make the food as appealing as possible. Warm canned food to just above room temperature before serving. Offer all meals in a secure, familiar place with few distractions, and accompany meals with petting and praise.
- Do not mix medications into food. Many medications taste unpleasant and will reduce food intake or cause a food aversion. The one possible exception is aluminum hydroxide. Ideally, phosphate binders should be mixed with food, but only aluminum hydroxide is available as an odorless and tasteless powder. Flavored and liquid formulations should not be mixed into food, because they are unpleasant and will reduce intake.
- Do not introduce a kidney diet while a cat is hospitalized. The cat will associate the new food with the stressful surroundings, and a food aversion is likely. Wait until the cat is stable and home before introducing the kidney diet.
- "Toppers" of a senior diet, making up less than 10% of daily calorie intake, can be used to stimulate interest in the kidney diet.
- If a complete change to the kidney diet is not successful, feeding a proportion of kidney diet combined with a maintenance diet may help meet the cat's calorie needs.
- In cats that cannot meet their nutritional needs on their own, assisted feeding through an esophagostomy or gastrostomy tube may be an option.
Conclusion
Clinical trials of kidney diets in cats with naturally occurring CKD have shown that they improve survival, reduce uremic crises, and improve blood urea nitrogen and phosphorus concentrations. When food intake is adequate, kidney diets have also been shown to maintain body weight and body condition score for up to two years. Some have questioned whether kidney diets provide enough protein and have advocated feeding higher-protein diets to cats with CKD, but no convincing clinical trial evidence supports this. The best current evidence supports feeding kidney diets to cats with CKD. The current IRIS guidelines support feeding kidney diets to cats in IRIS CKD Stages 2, 3, and 4, together with close nutritional monitoring to ensure adequate calorie intake.
The guidelines also recommend monitoring the response to treatment, recognizing that individual cats at every stage will need adjustments to their diet: modifying the protein content according to nutritional need, increasing phosphorus restriction by adding phosphate binders if serum phosphorus does not reach its target, or relaxing phosphorus restriction when serum calcium increases and hypercalcemia is a concern. Dietary therapy, like any other therapy, needs to be tailored to the individual cat.
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