The primary approach to CKD in cats is dietary management to lessen the abnormalities caused by marginal kidney function. These nutritional measures have been proven to reduce uremia and extend the lifespan of cats with this common disease.

The incidence of chronic kidney disease (CKD) in cats is shockingly high. Reported ranges of CKD in young cats (< four years) are between 13% to 37.5%, depending on the specificity of testing. In middle-aged cats (four to ten years), CKD was diagnosed at 24% to 40.9%. CKD is especially prevalent in older cats (> 15 years), at 32% to 80%. Nutrition is key to managing feline CKD, and is the focus of this article.

Before we jump into the details of diet, let’s step back a moment. The nutritional management of CKD in cats is contingent on the fact that felines are obligate carnivores with unique nutritional needs, processes, and physiology. The overall basis of a veterinary diet for an obligate carnivore must include, if not have, a foundation of animal-based protein, meat and organs.

It can be challenging to balance the needs of the carnivore and the nutrient restrictions of the renally-challenged using a whole food, species-appropriate diet, but to do so, the following areas must be focal points.


There is no question that blood phosphorus levels are a prognostic indicator, and that dietary levels of phosphorus affect the blood levels in a direct relationship. But cats are obligate carnivores, and as such, have a biological and physiological need for meat or animal-based proteins. Meat has the highest levels of phosphorus and protein, yet dietary restriction of phosphorus is necessary and effective for controlling hyperphosphatemia. However, some whole food choices reduce dietary phosphorus consumption. Beef, for example, has some of the lowest phosphorus levels of all meats, and eggs are an easily digested animal-based protein source.

Phosphorus binders, such as chitosan and calcium carbonate, even out the phosphorus load. Chitosan is the exoskeleton of a crustacean, and will bind the consumed phosphorus in the gut. This combination is then passed out of the body via stool. Calcium carbonate, the major mineral in eggshells, also acts as a phosphorus binder in the gut. For obligate carnivores, restricting dietary phosphorus in combination with appropriate phosphorus binders has been shown to manage serum phosphorus levels.


Another balancing act in the dietary needs of the obligate carnivore is protein consumption. As in all things nutritional, too much or too little can cause issues. Too much protein increases the formation of urea, the by-products of protein catabolism. Urea excretion is restricted by the marginal kidney and therefore accumulates in the blood, increases metabolic pressure on the kidneys, and leads to the clinical signs of vomiting, diarrhea, lethargy, anorexia, polyuria and polydipsia, and proteinuria.

On the other hand, cats have a physiologic need for the amino acids abundant in meat. Too little protein in a cat’s diet can contribute to catabolism of their own tissue to meet their nutritional needs, leading to muscle loss, cachexia, and malaise. Most importantly, low dietary protein levels do not slow the progression of CKD in most cats. Current research suggests that moderate levels of high quality digestible meats can meet a cat’s protein needs and avoid cachexia.


Supporting potassium levels in the cat with CKD is important due to the connection between hypokalemia and CRF. This does not seem to be the case with dogs. Hypokalemia has been shown to negatively affect the glomerular filtration rate (GFR), and supplementation with potassium can reverse this decline. Hypokalemia is also seen in cats with excessive urinary potassium loss. Potassium levels may be depleted in cats with CKD for several reasons: decreased appetite and therefore decreased food consumption; diets with low potassium levels; changes in gastrointestinal absorption or excretion; and increased kaliuresis. It is generally thought that decreased intake and increased urinary losses represent the change in potassium levels. Dietary potassium supplementation such as potassium chloride or “lite salt” will improve renal function in cats.


The percentage of CKD patients with concurrent hypertension is high — 60% of cats and 93% of dogs with CKD have hypertension. Suggested underlying mechanisms include sodium retention, activation of the renin-angiotensin system, and sympathetic nerve stimulation. The relationship between dietary sodium or salt concentration and hypertension has not been established in cats or dogs; this notion is extrapolated from human data. However, caution should be used with high levels of sodium intake in patients with renal disease, as levels above AAFCO’s dietary recommendations may have a negative effect on the kidneys independent of any effect on blood pressure. And vice versa: low sodium levels may lead to a decrease in the volume of extracellular fluids, and prerenal azotemia. And certainly, low sodium levels in food negatively affect palatability and diet acceptance.


Acid-base imbalance due to damaged kidneys not excreting hydrogen ions and retaining bicarbonate can lead to metabolic acidosis. In a study of cats with CKD, approximately 80% had metabolic acidosis. Combined with the fact that most commercial cat foods tend to be acidifying only exacerbates the pH imbalance. This is the one instance where alkalizing the diet can be beneficial. Sodium bicarbonate or potassium citrate can help alkalize the blood.


Renal oxidative stress is unquestionably a component of CKD. Oxidative stress has recently been shown to be most prevalent in the early stages of feline kidney disease. It is not associated with increasing disease progression as it is in humans.

Researchers measured urinary F2‐isoprostanes, an indicator of oxidative stress in cats with CKD. The hypothesis was that this marker of oxidative stress would increase by IRIS stage in cats as it does in humans. They found that urinary F2‐isoprostanes were highest in early (Stage 1) CKD in cats, compared to Stage 2 where they were significantly decreased with progressive IRIS stage. Interestingly, decreased indicators of oxidative stress were strongly and inversely correlated with increased serum creatinine concentration. This data suggests that adding dietary antioxidants to a feline CKD patient’s diet would be most helpful in the early stages of disease.

Dietary antioxidants can come from many superfood fruits, vegetables, and herbs. Superfoods are defined as plant-based materials that are uniquely dense in phytonutrients and antioxidants. These are particularly important in a carnivore’s diet due to the lower percentage of predigested plant material consumed in a species-appropriate diet.


Omega-3 polyunsaturated fatty acids (PUFAs) in the active forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) competitively inhibit the formation of pro-inflammatory leukotrienes and prostaglandins from Omega-6 fatty acids. High dietary levels of Omega-3 fatty acids have been shown to be reno-protective by reducing glomerular capillary pressure and proteinuria, abating the decline of GFR, and decreasing the progression of renal disease in dogs.

A retrospective study in 2005 found that cats fed a therapeutic kidney diet with a higher concentration of EPA had longer survival times compared to cats eating other therapeutic kidney diets. A dosage of 40 mg/kg body weight EPA combined with 25 mg/kg body weight DHA per day has been recommended for cats with CKD. The cleanest whole food sources of EPA/DHA are algae, krill and anchovies, then larger fish species.

Where higher concentrations of the Omega-3 fatty acids EPA and DHA have shown to be reno-protective, increased dietary Omega-6 fatty acids had a negative effect on kidney function. The differences seem to be in the process of lipid metabolism, glomerular hypertension and hypertrophy, and urinary eicosanoid metabolism, with supplementation of Omega-6 PUFAs enhancing kidney decline and supplementation of Omega-3 PUFAs having reno-protective actions.


Cats with CKD have concurrent intestinal dysbiosis. A recent study (2019) showed that the microbiome of cats with CKD was less rich and diverse as compared with healthy cats. Although there is no proven link between the gut microbiome, diet, and kidney disease in cats, there are plenty of indications of an association — for instance, the correlation between high uremia levels, increases in urease-producing bacterial growth in the gut, and an increase in uremic toxin concentrations, such as ammonia, in the gut. Urease breaks urea down into ammonia. These uremic toxins negatively change the environment within the gut, including pH levels and microbial populations. Furthermore, recent research has associated gut-derived uremic toxins with the progression of CKD, cardiovascular disease, and mortality in humans. In fact, higher numbers of urease-producing bacteria are found in subjects with end-stage renal disease. CKD affects the gut microbiome, and the disrupted gut microbiome worsens CKD.

Furthermore, several recently-published studies demonstrate that feeding diets high in fermentable fibers (prebiotics) decreased the absorption of uremic toxins and reduced the concentration of bacterial produced uremic toxins within the gut of both dogs and cats. As well, an improvement in various markers of kidney health, including creatinine and urea, were observed in cats consuming a food high in fermentable fibers versus controls.

Probiotics have also been shown to improve the levels of uremic toxins in blood. Streptococcus thermophilus, Lactobacillus acidophilus and Bifidobacterium longum Have been shown to utilize urea, uric acid, and creatinine as a food source, therefore leading to lower uremia levels. These bacteria are then passed in the stool as an “enteric dialysis”.


Veterinary diets for feline patients with CKD should be made of whole food ingredients, including moderate levels of high quality clean protein, low phosphorus, moderate sodium, moderately high potassium, and high levels of EPA/DHA. These recommendations should be paired with additional supplementation of fermentable fiber, prebiotics, and select probiotics to balance the gut-kidney axis. These nutritional measures have withstood the test of time and have been proven to reduce uremia and extend the lifespan of cats with CKD.


Please enter your comment!
Please enter your name here