Nutritional management of cats with chronic kidney disease

Introduction

Chronic kidney disease (CKD) is commonly diagnosed in cats, with a reported prevalence of more than 80% in animals over 15 years of age, and nutritional management is a crucial component of veterinary care provided to affected cats, as it has the potential to slow progression of disease and also prolong survival. Specific dietary approaches can be tailored to the individual cat based on International Renal Interest Society (IRIS) staging alongside any concurrent medical conditions, and this article focuses on what can be done in terms of nutrition to optimize patient wellbeing. 

Body composition

An animal’s body composition [body weight (BW), body condition score (BCS), and muscle condition score (MCS)] may yield clues about the impending diagnosis of CKD, and has also been shown to affect survival in dogs and cats with CKD. Loss of body weight may precede a diagnosis of CKD in cats by up to 3 years, and weight loss often increases after diagnosis (1). Cats with CKD and a BW of < 4.2 kg at diagnosis had a shorter survival than cats with CKD that had a BW ≥ 4.2 kg (1).

Muscle loss seen in CKD patients is likely multifactorial, related to sarcopenia (i.e., age-related loss of muscle), cachexia (i.e., muscle loss affected by inflammatory cytokines, and/or reduced protein and amino acid (AA) intake (whether due to specific dietary management and/or reduced caloric intake). Protein-energy wasting (PEW), a cachectic state characterized by nutritional and metabolic derangements, is commonly identified in people with CKD, and it contributes to decreased quality of life and increased morbidity and mortality (Figure 1). Maintaining adequate caloric intake is therefore imperative to maintaining BW, BCS, and MCS. Some cats will maintain weight when eating their resting energy requirement (RER) (Box 1); however, others will require multiplication of a maintenance energy requirement (MER) factor. If an animal is losing weight despite eating more than 2 x RER, it should be evaluated for other diseases that can contribute to increased energy needs (e.g., hyperthyroidism), maldigestion (e.g., exocrine pancreatic insufficiency), or malabsorption (e.g., inflammatory bowel disease).

 

Box 1. What is RER (resting energy requirements)?

Appetite dysregulation and assisted enteral nutrition

Animals with CKD are often hyporexic or anorexic, being reported in up to 92% of affected cats (1). It can be helpful to offer a variety of both dry and canned diet options to increase food intake, and medications to ameliorate nausea may be useful (e.g., maropitant, ondansetron); however, bioavailability and efficacy of these drugs vary across species. Acid-reducing agents are not generally recommended, as cats rarely develop uremic gastropathy. The exception to this would be if there is evidence of gastrointestinal bleeding, which is more common in advanced CKD. Appetite stimulants can also be useful; mirtazapine can be effective in both oral and transdermal forms to aid in weight gain, reduce vomiting and improve appetite in cats with CKD (Figure 2). 

When a cat will not eat enough to maintain its bodyweight, placement of a feeding tube may be a viable option to provide enteral nutritional support, and offers a good route for additional water and medications (Figure 3). The feeding tube will likely be in place for the remainder of the animal’s life, thus placement of either an esophagostomy (E) or gastrostomy (G) tube is appropriate. With proper maintenance, these tubes can be used for months to years. Canned veterinary therapeutic renal diets can be blended with water (or a liquid enteral diet designed for kidney disease) to achieve appropriate consistency to be fed via the tube (Box 2).

 

Box 2. Equation to determine caloric density of blended canned diet.

 

Nutritional modification

Phosphorus

There is strong evidence for dietary modification in cats with CKD, as feeding a veterinary therapeutic renal diet can prolong survival and reduce the risks of uremic crises. The primary nutrient of concern for CKD is dietary phosphorus; hyperphosphatemia is related to reduced survival in cats with CKD. In one study, for every 1 mg/dL (0.32 mmol/L) increase in serum phosphorus, there was an 11.8% increased risk of death (2). Plasma phosphate concentration is a potent stimulator of fibroblast growth factor-23 (FGF-23), a phosphatonin that affects the development of a complex condition known as CKD-mineral and bone disorder (CKD-MBD). Feeding a reduced phosphorus diet has been shown to decrease plasma phosphate and FGF-23 in cats with CKD (3). 

The 2023 IRIS treatment guidelines suggest maintaining plasma (or serum) phosphate concentrations in dogs and cats with CKD between 2.7-4.6 mg/dL (0.87-1.49 mmol/L), although a target of < 5.0 mg/dL (1.62 mmol/L) for patients with stage 3 CKD, and < 6.0 mg/dL (1.94 mmol/L) for patients with stage 4 CKD, is deemed more realistic (4). Controlling circulating phosphate levels are first addressed by reducing dietary phosphorus intake, then adding oral phosphate binders with food, if needed.

Not only the amount of phosphorus, but also the form of dietary phosphorus, as well as the dietary calcium:phosphorus (Ca:P) ratio, may influence renal health. Phosphorus from organic sources (e.g., meat, bone meal, grains) has less bioavailability than phosphorus from certain inorganic sources (e.g., sodium or potassium phosphate salts). Feeding these highly available phosphate salts, especially in a diet with too little calcium, has been shown to result in renal damage in previously healthy cats. Some of this damage is alleviated by maintaining a dietary Ca:P intake ≥ 1.0 (5).

Protein

It is controversial if and/or when protein should be restricted in cats with CKD, as dietary protein intake has been shown to influence lean body mass (LBM). Protein requirements have conventionally been determined based on maintenance of nitrogen balance; this differs from using maintenance of LBM as a marker of protein adequacy. One study in 20 healthy cats reported that to maintain nitrogen balance, 1.5 g protein per kg (2.1 g/kg (BW)^0.75) was needed, but in order to maintain LBM, 5.2 g protein per kg (7.8 g/kg (BW)^0.75) was required (6). Another consideration is that dietary amino acid profiles can differ between diets, even if crude protein is similar. Diets enhanced with essential AAs may be better able to maintain LBM. There are diets available that provide lower phosphorus concentrations (i.e., < 1.00-1.35 g/Mcal; < 135 mg/100 kcal) and higher protein concentrations, which may be preferable for some cats (7). 

More recently, there has been attention paid to uremic toxins (e.g., indoxyl sulfate, p-cresol sulfate); these are waste products of amino acid catabolism from colonic fermentation. One study noted that indoxyl sulfate concentrations increased in cats with CKD relative to healthy cats (8). Strategies to address this gut-kidney dysbiosis include reducing excessive protein intake, increasing prebiotic fiber intake, and giving intestinal adsorbents to increase fecal loss of uremic toxins.

Potassium

Serum potassium concentrations may be abnormal due to underlying kidney disease, dietary intake, acid-base abnormalities, gastrointestinal complications, and medications. Hypokalemia may result in muscle weakness, polyuria and polydipsia, and constipation. Currently available veterinary renal diets have a wide range of potassium content (1.7-5.6 g/Mcal; 166-560 mg/100 kcal), so if hypokalemia is present, it may be helpful to offer a higher potassium-containing diet or oral supplementation with either potassium gluconate or potassium citrate. 

Sodium

The role of dietary sodium restriction for cats with CKD is controversial. In one study that included 6 cats with renal insufficiency, feeding a high sodium diet (2.9 g/Mcal; 290 mg/100 kcal) increased serum concentrations of creatinine, urea nitrogen and phosphorus, and there was no effect noted on blood pressure (9). Given these findings, it has generally been recommended to avoid high sodium intake in dogs and cats with CKD. Conversely, in other larger long-term studies, there have been no adverse effects on renal function noted in healthy cats fed high sodium diets (2.9-3.3 g/Mcal; 290-330 mg/100 kcal) (10). One study in cats with experimentally induced CKD demonstrated that feeding a low sodium veterinary therapeutic renal diet for one week caused activation of the renin-angiotensin-aldosterone system and subsequent kaliuresis (11). An inverse relationship between hypokalemia and systemic hypertension has been documented in cats, and consideration is given to the prevalence of a relative or absolute hyperaldosteronism contributing to both.

One of the biggest issues with regards to recommendations for dietary sodium intake is the lack of standardization for what is considered a “high,” “moderate,” or “low” sodium intake. Diets that are typically promoted as “reduced” in sodium can provide up to 2 x AAFCO (Association of American Feed Control Officials) minimum for adult cat maintenance. The author does not currently specifically aim to feed a reduced sodium diet to animals with CKD; however, this is often a moot point, as all veterinary therapeutic renal diets are relatively similar in their sodium concentrations, providing about 5-10 g/Mcal (50-100 mg/100 kcal).

Metabolic acidosis

Metabolic acidosis is a common complication observed with CKD. In cats, overt metabolic acidosis may not be recognized until late-stage disease, and there is minimal data to specifically suggest that metabolic acidosis precedes worsening renal function. It is however likely that the blood pH remains normal in many animals with CKD at the expense of bone health, as increased dietary acid loads cause bone to resorb calcium (i.e., releasing calcium into the circulation). In cats with CKD, bone quality is affected, likely due to a complex relationship between metabolic acidosis and other hormonal derangements observed with CKD-MBD (e.g., hyperparathyroidism, increased FGF-23). Veterinary therapeutic renal diets are typically fortified with alkalinizing agents (e.g., potassium citrate), but for animals that develop metabolic acidosis, treatment with additional potassium citrate or sodium bicarbonate may be considered.

Vitamin D

Derangements in vitamin D metabolism have been identified in cats with CKD. Interestingly, cats with early or well-compensated CKD have been demonstrated to have higher vitamin D metabolites [25-hydroxyvitamin D, 1,25-dihydroxyvitamin D (calcitriol), and 24-25-dihydroxyvitamin D] than healthy cats. Calcitriol concentrations are lower in cats with more advanced or end-stage CKD (12,13). Calcitriol treatment has been recommended for several decades to reduce parathyroid hormone (PTH) concentrations and improve quality of life in cats with CKD, but the cost, monitoring, and potential for toxicity (e.g., hypercalcemia) are sometimes limiting factors for pet owners. The most recent IRIS guidelines have removed the recommendation for prophylactic calcitriol to cats, given the paucity of data to support this treatment (4). Additional research is needed to determine the manner in which supplementation with various forms of vitamin D influences vitamin D repletion, PTH and FGF-23 concentrations, quality of life, preservation of renal function, and survival.

Calcium

Cats with CKD may demonstrate derangements in calcium homeostasis, with ionized hypercalcemia reported to occur in around 25% of affected animals. Cats with CKD have also been reported to develop hypercalcemia after transition to a lower-phosphate renal diet, and feeding a higher phosphate diet may subsequently resolve the hypercalcemia. It has recently been reported in cats (n=10) with CKD and cats with idiopathic hypercalcemia (IHC) that feeding diets with controlled calcium concentrations (i.e., < 2.0 g/Mcal; < 200 mg/100 kcal) and a calcium:phosphate (Ca:P) ratio < 1.4:1 can resolve hypercalcemia (14). Another nutritional intervention that can alleviate hypercalcemia includes the addition of chia seeds (1-2 grams per day per cat) (15); it seems likely that the higher fiber, low calcium and low Ca:P qualities of the seeds affect calcium metabolism. 

Magnesium

Magnesium has recently received additional attention in the context of feline CKD. Cats with IRIS stage 4 CKD demonstrate higher total serum magnesium concentrations than those with earlier stages (16). Diagnosis of either hypermagnesemia or hypomagnesemia has been associated with a lower survival in cats with CKD than those with normomagnesemia (16,17). Serum concentrations of ionized calcium are negatively correlated with magnesium concentrations, while serum phosphate concentrations are positively correlated with magnesium, consistent with the derangements in CKD-MBD.

The impact of feeding a magnesium-enriched diet (0.62 g/Mcal; 62 mg/100 kcal) was recently evaluated in cats with CKD, as compared to a control diet that provided 0.13-0.18 g/Mcal (13-18 mg/100 kcal). The study demonstrated that cats eating the higher magnesium diet trended toward decreasing ionized calcium concentrations, while the cats on the control diet trended toward increasing ionized calcium concentrations. Additionally, cats eating the magnesium-enriched diet had a slower rate of progression in log-transformed FGF-23 concentrations compared to the cats eating the latter diet (18).

Omega-3 fatty acids & supplement use

Many pet owners wish to provide additional dietary supplements and nutraceuticals to their pets with CKD. In one study, 38% of owners administered vitamins, minerals or other supplements to their cats with CKD (Figure 4) (19). A plethora of supplements marketed for patients with kidney disease make careful selection of type, dose and brand necessary to avoid toxicities or lack of efficacy. This entails consideration of the specific brand (e.g., reputable, tested by an independent company), potential benefits (research-driven vs. hypothetical), risks (known or hypothetical), and interaction with other medications and supplements. Some supplements provide unwanted calories and added nutrients that may be nominal or, alternatively, toxic. Additionally, for an animal that is already wary of taking its necessary medication(s), forcing it to take unnecessary (or even potentially harmful) supplements may add undue stress. 

However, omega-3 fatty acid supplementation with eicosopentaenoic acid (EPA) and docosahexaenoic acid (DHA) may be considered for anti-inflammatory properties. Although an optimal dose of EPA/DHA for cats with kidney disease has not determined, it is fair to provide up to a total of 500-600 mg EPA/DHA per cat per day. Many veterinary therapeutic renal diets already contain these supplements, so the total amount the cat is receiving from food should be determined based on its caloric intake (i.e., mg EPA/DHA per 100 kcal ingested daily). It can then be decided whether or not to add to that amount. 

Other diet options

If an animal will not eat (or the owner is unwilling to feed) any available veterinary therapeutic renal diet, there may be some other diets (either veterinary therapeutic diets marketed for other diseases, or over-the-counter commercial diets) that still provide acceptable nutrient profiles. The author typically considers phosphorus as the “primary” nutrient of concern for CKD, and subsequently aims to provide < 1.5 g phosphorus per Mcal (150 mg/100 kcal) to cats with CKD. Not all senior diets are appropriate options for cats with CKD, and careful attention must be paid to specific nutrient profiles. One study demonstrated that 31 senior cat foods provided a median (range) of 3.2 (1.5-4.4) g/Mcal phosphorus [310 (150-440) mg/100 kcal], which did not differ significantly from the adult maintenance diets analyzed (20). 

Comorbid patients & home-cooked diets

Choosing an appropriate diet for cats with comorbid conditions can be challenging, as each patient’s needs are unique (Figure 5). Nutritional management goals must be identified and prioritized to achieve the results most favorable to the patient’s overall health and quality of life. For example, in a cat with concurrent CKD and inflammatory bowel disease, feeding a low to moderate phosphorus-limited ingredient, hydrolyzed, or fiber-enriched diet would be recommended. Even when appropriate commercial diet options are available, owners may elect to feed home-prepared diets to their pets. However, most recipes an owner will find online or in books, including those designed for pets with CKD, do not provide complete and balanced nutrition. Thus, for owners who prefer to feed a home-prepared diet, or if a suitable diet cannot be identified, a board-certified veterinary nutritionist^® should be consulted. It is imperative that owners are given precise directions in order to avoid contributing to nutritional deficiencies or toxicities, and many owners have trouble following explicit instructions over time, so monitoring is important.

Conclusion

It is best practice when determining a nutritional plan for any cat with CKD to consider that animal as an individual. The cat’s energy needs and specific nutrients of concern should be determined first. Using that information, appropriate diet options can be chosen and offered; maintaining adequate energy intake is of utmost importance in CKD patients. Concurrent medical management may be required in many cases, and assisted enteral nutritional support can offer sustenance for hyporexic patients.

References

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