David J. Polzin, DVM, PhD Dip ACVIM
Jessica Quimby, DVM, PhD Dip ACVIM
Sheri Ross, DVM, PhD Dip ACVIM
(Original article authored by David J Polzin 2016)
Dietary management of feline chronic kidney disease (CKD) 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 renal diets be considered for cats with IRIS CKD Stage 2 and recommend feeding renal diets to cats with IRIS CKD Stages 3 and 4. As of yet, it is unclear what the recommendation should be in patients with IRIS Stage 1 disease.
Veterinarians typically use therapeutic diets in much the same way as they use pharmaceuticals to manage medical conditions. When they prescribe feeding a "kidney diet" for cats with CKD, they expect the diet to achieve four specific goals: 1) ameliorate or prevent clinical consequences of CKD including signs of uremia; 2) slow progression of CKD and prolong survival; 3) minimize derangements of electrolyte, calcium and phosphorus, and acid-base balance; and 4) maintain adequate nutrition. To achieve these multifaceted goals, renal diets are typically formulated to have reduced phosphorus content, modified amounts of high-quality protein, increased caloric density, added B vitamins, increased omega-3 polyunsaturated fatty acid and antioxidant content, supplemented in potassium, and to have a neutral effect on acid–base balance. Recently, early-stage renal diets that are phosphorus restricted but less protein restricted have also become available for cats (Parker 2021). Clinical trials have supported clinical benefits of "kidney diets" formulated similar to these dietary modifications.
Several studies address the effectiveness of feline kidney diets compared to typical feline maintenance diets in mitigating uremic crises and extending survival. The consistent findings in these studies using different diets and methodologies and performed in different countries by independent groups of researchers strongly support the conclusion that kidney diets favor better clinical outcomes (longer survival and fewer uremic crises).
The first study was a randomized and masked clinical trial with 22 cats fed a kidney diet and 23 cats fed a feline adult maintenance diet (Ross et al, 2006). The principal dietary modifications in the kidney diet included reduced protein, phosphorus and sodium, and supplementation with polyunsaturated fatty acids. While there were no uremic crises or renal deaths over the two-year study among the 22 cats fed the kidney diet, 6 cats fed the maintenance diet developed clinical and biochemical evidence of uremia and 5 cats fed the maintenance diet died of consequences of kidney disease.
The second study compared a manufactured protein- and phosphorus-restricted kidney diet to continuing to feed the cats' regular (non-renal) diets (Elliott et al, 2000). This study was neither randomized nor masked; cats that chose not to eat the kidney diet continued on their usual diet. Cats that consumed the kidney diet survived significantly longer (n=29; median survival time = 633 days) than cats that continued to consume their regular diet (n=21; median survival time = 264 days).
The third study was a retrospective study performed in 31 first-opinion veterinary practices in The Netherlands and compared survival times for cats fed one or more of 7 commercial feline kidney diets to those not fed a kidney diet. (Plantinga et al., 2005) Median survival time for cats fed a kidney diet was 16 months compared to 7 months for cats fed their usual (non-renal) diet.
Additionally, studies have been performed that support the benefit of renal diets based on biomarkers of CKD-MBD such as FGF-23. FGF-23 is increased in cats with CKD and is associated with a poorer prognosis. One retrospective study that compared FGF-23 concentrations in 33 cats that ate a renal diet to concentrations in 11 cats eating a non-renal diet determined that feeding a renal diet was associated with reductions in FGF-23 in both hyperphosphatemic and normophosphatemic cats (Geddes et al 2013).
In order to compensate for the decline in phosphorus excretion with advancing CKD, dietary intake of phosphorus must be reduced. Most maintenance diets contain substantial quantities of phosphorus, with protein typically contributing significantly to the phosphorus content. It is perhaps a common misconception that the purpose of renal diets is protein restriction. There is little consensus on the appropriate amount of protein in renal diets (see below), but there is a significant amount of evidence regarding the importance of phosphorus restriction (Geddes et al 2013b; Parker 2021).
Recent evidence also suggests that not only is the amount of phosphorus important, but the form of phosphorus may affect phosphorus balance. (Parker 2021) Phosphorus from inorganic sources (e.g., sodium or potassium phosphate salts) is more bioavailable that phosphorus from organic sources (e.g., meat, bone meal, grains). Additionally, the dietary calcium:phosphorus ratio is important as feeding highly bioavailable phosphorous salts in combination with too little calcium (leading to a calcium to phosphorus ratio of <1) has been documented to result in renal 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 discernible effect on phosphorus; in cats with CKD, full dietary effect was apparent after 28 to 49 days (Barber et al 1999). Thus, serum phosphorus concentrations should be rechecked 4-6 weeks after initiating the renal diet. If in the IRIS target range, the diet should be continued, and the serum phosphorus reassessed every 3 to 4 months (every 4-6 months may be adequate for IRIS CKD stage 2). Control of phosphorus is more likely achieved with renal diet alone in patients with Stage 2 and 3 CKD. If a renal diet alone fails to achieve the serum phosphorus target after 4-6 weeks, adding an intestinal binding agent is recommended.
While the amount of dietary phosphorus can be mitigated by administration of intestinal phosphorus binders, particularly in combination with a kidney diet, the ability of intestinal phosphorus binders to limit phosphorus uptake from diets containing high levels of phosphorus is finite. This limitation combined with the fact that many cats resist administration of medications increases owner frustration and reduces quality of life for cats having to receive unpalatable medications with every meal. This lowers compliance and makes the strategy of supplementing high protein foods with phosphorus binders of questionable efficacy. Administering phosphorus binders at dosages above the recommended dose range can also lead to adverse drug effects, toxic effects due to absorption of cations associated with the binders (e.g., aluminum, calcium etc.).
Hypercalcaemia is sometimes seen in cats with CKD (see IRIS Education article: Hypercalcaemia in CKD). The risk factors for its occurrence, including its association with restricted phosphate intake (accomplished by formulated diets or phosphate binding agents) remains to be determined. Increasing phosphate intake leads to normalization of serum calcium concentration in some cases of hypercalcaemia diagnosed after institution of diets (Geddes et al 2021). Further research is warranted to facilitate identification of cats with CKD at risk of hypercalcaemia and to understand how treatment can be better tailored to meet their specific physiological needs.
Recently, use of kidney diets in treating cats with CKD has become controversial, weighing the potential benefits of these diets in mitigating the clinical consequences of CKD versus the purported risk of protein malnutrition. Much of this debate has been focused specifically on cats, as they are considered to be obligate carnivores and thus have increased protein requirements compared to dogs and humans (Zoran 2002; Zoran 2011). As a result, some veterinarians have recommended feeding diets containing high levels of dietary protein instead of feeding the currently available kidney diets specifically designed for cats with CKD. These high protein diets do not include the other dietary modifications found in kidney diets and problematically may be high in phosphorus. This divergence in therapeutic opinion has likely evolved from recent studies suggesting that senior cats may require more protein than younger cats (Laflamme & Hannah 2013) and the observation that in many cats with CKD, body weight, body condition score and/or muscle mass may decline over time.
Additionally, less dichotomous debates exist such as when and to what degree modification of protein levels is necessary. In the past, the emphasis has been on reducing the protein content of the diets. The rationale behind the modification of protein ingestion in patients with CKD is based on the observations 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 metabolites contribute significantly to many of the metabolic derangements found in patients with kidney disease (Mitch 1991). Some veterinarians argue that initiating protein moderation should be delayed until the cat begins to display clinical signs of uremia, typically during later IRIS CKD Stage 3 or IRIS CKD Stage 4. Others argue that dietary protein moderation should begin early in IRIS CKD Stages 2 or 3 because it may slow progression of CKD, delay onset of uremic signs and facilitate better acceptance of diet change. In addition, delaying diet therapy until the owner recognizes that the cat is manifesting clinical signs of uremia increases the risk of developing a uremic crisis before diet treatment can be started. One possible concern regarding kidney diets in some cats with IRIS CKD Stage 2 is that initiating protein moderation with a calorically dense food may contribute to body fat gain and loss of lean body mass if protein requirements are not met with the kidney diet.
Another important point is that although the commercially available feline kidney diets have historically been described as being low protein, they actually meet, and in most cases far exceed, the AAFCO recommendations for minimum crude protein content. In addition to the amount of protein in a specific diet, the quality of that protein must be considered. Protein quality is not related to the source of the protein but is measured based on the bioavailability of the amino acids consumed, and more importantly, the composition of the protein. A high-quality protein, for an individual species, contains all of the amino acids required by that species. Required amino acids or essential amino acids are those that cannot be made by the animal through normal metabolic processes. In commercially available kidney diets, the protein used is highly bioavailable and care is taken to ensure that the required amino acids are present in more than sufficient amounts. For example, in one commonly used commercial kidney diet for cats all the essential amino acids are present in at least 150% of the recommended daily amount (Hills 2021).
Unfortunately, there are very limited data evaluating protein as the only dietary intervention in patients with CKD. One study in cats with surgically-induced disease showed significantly more morphologic kidney changes in the cats fed a high protein diet (52%) versus those fed a lower protein diet (Adams et al 1994). However, it is important to remember that surgically induced-kidney disease does not have the same biologic behaviour as the naturally occurring disease. A subsequent study did find that it was caloric intake, not protein intake, that seemed to affect the renal morphology (Finco et al., 1998). The effect of CKD on protein requirements in cats has also not been determined. Additionally published evidence that kidney diets cause loss of lean body and protein malnutrition when caloric intake is adequate is lacking. Studies on the effect of different levels of dietary protein intake in cats eating appropriate calories are needed to establish the optimal protein content for the feline kidney diet. Clinical trials using kidney diets in cats with CKD have shown that cats with CKD fed kidney diets may have stable body weight and body condition scores; however, most of these studies did not measure lean body mass, a better indicator of protein malnutrition. One recent study (Hall et al 2019) demonstrated that cats with IRIS Stage 1 and 2 CKD that were fed a kidney diet with increased caloric density and enhanced concentrations of carnitine and essential amino acids maintained lean body mass as measured by dual-energy x-ray absorptiometry over a 6 month feeding trial. Cats consuming a control food did not eat as many calories and subsequently lost weight.
The subject of protein content continues to be an evolving discussion. Other diet modifications (i.e., phosphorus restriction) are likely significantly more important in managing patients with kidney disease. As such, feline renal diets are now available with different quantities of protein so that diets can be individualized to the patient based on their needs and response to therapy.
It should be remembered that in many patients, the iconic image of the "skinny CKD cat" is not necessarily a result of decrease protein intake, but rather an overall decrease in caloric intake. This often occurs before the diagnosis of CKD and initiation of a kidney diet, thus suggesting that CKD itself promotes these changes, no doubt exacerbated by dysrexia. As CKD advances, dysrexia causes a chronic and insidious decline in caloric intake and overall body condition and muscle mass. In desperation, many owners will offer high protein foods to their pets in an effort to increase their food intake. Although the commonly heard phrase "they have to eat something" is certainly true, the quality and quantity of a patient's life will be prolonged if they eat adequate amounts of a diet formulated for kidney disease (Ross et al 2006, Plantinga et al., 2005). Therefore a key part of management is targeting nutritional adequacy in the CKD patient.
Serial evaluations of nutritional status are a key part of CKD patient management, and a nutritional plan should be performed for every patient including a specific recommendation for caloric intake. A nutritional assessment should include body weight, body condition score, muscle mass score, adequacy of caloric intake (including open ended questions about how the pet is eating), and a complete dietary history (including pet food, treats, supplements and items used to give medications). Assessment of muscle mass is particularly important in CKD patients as it can have a profound effect on serum creatinine and affect the interpretation of the severity of disease, as well as have notable implications for the nutritional status of the patient. Specific recommendations for caloric intake and close monitoring of caloric intake are key to success with dietary management of CKD. If caloric intake is not being met, dysrexia needs to be addressed and/or the nutritional plan needs to change to compensate (appetite stimulants, feeding tube).
The way in which a therapeutic food is introduced to the patient, and more importantly to the owner, has a profound effect on patient acceptance. While some patients easily transition from one diet to another, many cats are very selective and may require more coaxing to encourage diet change. In general, it is probably best to recommend that diet changes be made very slowly rather than abruptly. Most patients can be transitioned onto a new diet in 2-3 weeks by gradually mixing the new diet into the old diet. In our experience, cats are more likely to accept a new diet if transitioned over 3 weeks.
It is important to consider metabolic causes for anorexia before assuming that poor appetite is diet related. If the patient was not eating their usual diet prior to presentation, they are unlikely to accept a new diet. Often it is a general inappetence, not dislike of the kidney diets that make transition difficult. Therefore, in some patients it may be prudent to address as many factors that may be suppressing appetite as possible before attempting a diet transition. A variety of metabolic causes may be associated with poor appetite in cats with kidney disease including: 1) anemia, 2) intestinal disease, nausea 3) dehydration, 4) metabolic acidosis, and 5) hypokalemia. Most of these conditions can be managed with appropriate therapy.
Clinical trials of feeding kidney diets to cats with spontaneous CKD have shown them to be effective in improving survival, reducing uremic crises, and improve blood urea nitrogen and phosphorus concentrations. It has also been shown that when food intake is adequate, kidney diets can maintain body weight and body condition scores for up to two years. While some have questioned whether kidney diets provide adequate protein and have advocated feeding higher protein diets to cats with CKD, no convincing clinical trial evidence has been provided to support this proposal. Best current evidence supports the recommendation to feed cats with CKD kidney diets. The current IRIS clinical guidelines support feeding kidney diets to cats with IRIS CKD Stages 2, 3 and 4 in conjunction with close nutritional monitoring to ensure adequate caloric intake
The guidelines also recommend monitoring response to treatment, recognizing that there are individual cats at each stage which will need adjustments to their dietary therapy (modifying protein content based on nutritional need, increasing phosphorus restriction if serum phosphorus fails to meet the target level through the addition of phosphate binders, or reducing phosphorus restriction in cases where serum calcium increases, and hypercalcemia is a concern). The concept is that dietary therapy, like any other kind of therapy needs to be tailored to the individual cat.
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