Diets for Cats with Chronic Kidney Disease (CKD)

David J. Polzin, DVM, PhD Dip ACVIM

Feline "renal diets" are specifically formulated for the purpose of clinical management of cats with chronic kidney disease (CKD). These diets include commercial products and diets specifically designed for cats with CKD formulated by boarded veterinary nutritionists. "Renal diets" have been considered the "gold standard" therapy for managing cats with CKD for many decades. 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.

Veterinarians typically use therapeutic diets in much the same way as they use pharmaceuticals to manage medical conditions. When they prescribe feeding a "renal diet" for cats with CKD, they expect the diet to achieve four specific goals: 1) to ameliorate or prevent clinical consequences of CKD including signs of uremia; 2) to slow progression of CKD and prolong survival; 3) to minimize derangements of electrolyte, calcium and phosphorus, and acid-base balance; and 4) to maintain adequate nutrition. To achieve these multifaceted goals, modifications beyond just reduced protein content are incorporated when formulating renal diets, including: reduced content of phosphate and sodium; increased content of omega-3-polyunsaturated fatty acids, antioxidants, fiber, vitamin D and potassium; and a neutralizing effect on systemic pH. Clinical trials have supported clinical benefits of "renal diets" formulated similar to these dietary modifications.

Recently, use of "renal diets" in treating cats with CKD has become controversial, weighing the potential benefits of these diets mitigating the clinical consequences of CKD versus the purported potential risk of protein malnutrition consequent to the high protein requirements of cats. As a result, some veterinarians have recommended feeding diets containing high levels of dietary protein instead of "renal diets". This divergence in therapeutic opinion has evolved from recent studies suggesting that senior cats may require more protein than younger cats and the observation that at least in some cats with CKD, body weight, body condition score and/or muscle mass may decline over time. Further, substantial loss of lean mass has been shown to be associated with increased mortality in cats with CKD. The specific point of disagreement between these two schools of thought is focused on how much protein should be fed to cats with CKD. More specifically, those advocating feeding higher protein diets to cats with CKD have generally recommended feeding commercial or non-renal therapeutic diets containing more protein instead of feeding the currently available "renal diets" specifically designed for cats with CKD. These high protein diets do not include the other dietary modifications found in "renal diets".

What is the Rational for Limiting Dietary Protein in Renal Diets?

It has been known for over a century that reducing protein intake reduces clinical signs of uremia. Most uremic signs are caused, at least in part, by accumulation of protein metabolites which are excreted by the kidneys. While reducing protein intake to ameliorate clinical signs of uremia has been standard practice for decades, the decision as to when protein restriction should be initiated remains controversial. Some veterinarians argue that initiating protein restriction 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 restriction 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 risks development of a uremic crisis before diet treatment can be started. One possible concern regarding "renal diets" in some cats with IRIS CKD Stage 2 is that initiating protein restriction with a calorically dense food may contribute to body fat gain with lean mass loss if protein requirements are not met with the "renal diet".

Evidence Supporting Effectiveness of Renal Diets in Cats with CKD

Three studies address the effectiveness of feline "renal diets" compared to typical feline maintenance diets in mitigating uremic crises and extending survival. The consistent findings in these three studies using different diets and methodologies and performed in different countries by independent groups of researchers strongly support the conclusion that "renal diets" favor better clinical outcomes (longer survival and fewer uremic crises).

The first study compared a manufactured protein- and phosphorus-restricted "renal 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 "renal diet" continued on their usual diet. Cats that consumed the "renal 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 second study was a randomized and masked clinical trial with 22 cats fed a "renal diet" and 23 cats fed a feline adult maintenance diet (Ross et al, 2006). The principal dietary modifications in the "renal 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 "renal 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 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 "renal diets" to those not fed a "renal diet". (Plantinga, 2005) Median survival time for cats fed a "renal diet" was 16 months compared to 7 months for cats fed their usual (non-renal) diet.

Phosphorus and Renal Diets

"Renal diets" are formulated to be low in phosphorus content in part because excessive dietary intake of phosphorus has been linked to progression of CKD in cats and other species. Although dietary phosphorus content is not directly linked to protein content in pet foods, protein is a significant source of phosphorus in foods. Thus, limiting dietary protein is a strategy for limiting dietary phosphorus intake. The goal of limiting dietary phosphorus intake may influence the maximum amount of protein that can be fed. While the amount of dietary phosphorus can be mitigated somewhat by administration of intestinal phosphorus binders, 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 adherence 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, lanthanum, etc.). Hypercalcaemia is sometimes seen in cats with 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. Anecdotally, increasing phosphate intake leads to normalization of serum calcium concentration in some cases of hypercalcaemia diagnosed after institution of diets or binders. Further research is warranted to facilitate identification of the minority of cats with CKD at risk of hypercalcaemia and to understand how treatment can be better tailored to meet their specific physiological needs.

Is the Protein Content of Renal Diets Optimal for Cats with CKD?

The effect of CKD on protein requirements in cats has not been determined. Studies on the effectiveness of "renal diets" in cats with CKD were performed using "renal diets" as commercially produced. Evidence that these "renal diets" cause loss of lean body and protein malnutrition is lacking. Many cats with CKD lose weight and become underweight. However, this often occurs before the diagnosis of CKD and initiation of a "renal diet", thus suggesting that CKD itself promotes weight loss. Clinical trials on "renal diets" in cats with CKD have shown that cats with CKD fed "renal diets" may have stable body weight and body condition scores; however, these studies did not measure lean body mass, a better indicator of protein malnutrition. Studies on the effects of different levels of dietary protein intakes will be needed to establish whether or not "renal diets" should be formulated with higher protein content.

Conclusion and Recommendation

Clinical trials of feeding "renal 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, "renal diets" can maintain body weight and body condition scores for up to two years. While some have questioned whether "renal 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 "renal diets". The current IRIS clinical guidelines support feeding renal diets to cats with IRIS CKD Stages 2, 3 and 4. 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 (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.

Recommended Reading

Roudebush P, Polzin DJ, Ross SJ, et al. Therapies for feline chronic kidney disease. What is the evidence? J Feline Med Surg 2009; 11:195-210.

Elliott J, Rawlings JM, Markwell PJ, et al. Survival of cats with naturally occurring chronic renal failure: effect of dietary management. J Small Anim Pract 2000; 41:235-242.

Ross SJ, Osborne CA, Kirk CA, et al. Clinical evaluation of dietary modification for treatment of spontaneous chronic kidney disease in cats. J Am Vet Med Assoc 2006; 229:949-957.

Plantinga EA, Everts H, Kastelein AMC, Beynen AC: Retrospective study of the survival of cats with acquired chronic renal insufficiency offered different commercial diets. Vet Rec 2005; 157:185-7.

Geddes RF, Elliott J, Syme HM. The effects of feeding a renal diet on plasma fibroblast growth factor 23 concentrations in cats with stable azotemic chronic kidney disease. J Vet Intern Med 2013z; 27:1354-1361.

Geddes RF, Finch NC, Syme HM, et al. The role of phosphorus in the pathology of chronic kidney disease. J Vet Emerg Crit Care 2013; 23:122-133.

Finch NC, Geddes RF, Syme HM. Fibroblast growth factor 23 (FGF-23) concentrations in cats with early nonazotemic chronic kidney disease (CKD) and in healthy geriatric cats. J Vet Intern Med 2013; 27:227-233.