Nutrition in kidney disease

Summary

Chronic kidney disease (CKD) is one of the major challenges in companion animal care, affecting both animal welfare and quality of life. Appropriately planned nutritional strategies play a key role in alleviating clinical signs, supporting kidney function and improving patient comfort. This article reviews current dietary approaches to CKD management, with particular emphasis on interdisciplinary collaboration between the Animal Nutritionist and the vet. Topics discussed include protein and phosphorus restriction, omega-3 fatty acids, gastrointestinal support and the role of supplementation. The aim is to provide practical guidance for optimising nutritional plans to maximise the well-being and comfort of patients with CKD.


Nutrition in chronic kidney disease in dogs and cats

Chronic kidney disease (CKD) is one of the most commonly diagnosed conditions in older animals, and appropriate nutrition plays a key role in slowing its progression and improving patients’ quality of life.

A properly balanced diet should provide an adequate amount of energy, promote comfort, maintain appropriate body condition, body weight and muscle mass, alleviate signs of uraemia, and help stabilise fluid, electrolyte and acid–base balance.

Managing this condition requires ongoing collaboration between the vet and the owner, and often an Animal Nutritionist as well, as simply introducing a renal diet may not be sufficient. The nutritional requirements of a patient with CKD change not only as the disease progresses, but also according to the patient’s clinical condition and any concurrent diseases.


Nutritional challenges in CKD

Nutrition for animals with CKD is not simply about controlling dietary protein and phosphorus. It should take into account the specific requirements of the individual renal patient.

The main factors that both the attending vet and collaborating Animal Nutritionist should consider include:

  • restricting dietary phosphorus,
  • controlling dietary protein,
  • providing an appropriate dose of omega-3 fatty acids (EPA and DHA),
  • using antioxidants,
  • individually tailored supplementation,
  • taking concurrent diseases into account.

Diagnosing CKD

Early diagnosis of chronic kidney disease allows appropriate treatment and patient management, including nutritional intervention, which can contribute to longer survival and improved overall comfort.

Diagnosis of CKD is based on the assessment of blood biochemical parameters, including creatinine, SDMA and urea concentrations, urinalysis including urine specific gravity and proteinuria, diagnostic imaging and blood pressure measurement.

In clinical practice, most vets use the guidelines developed by the International Renal Interest Society (IRIS), which allow the disease to be staged and appropriate treatment to be selected.

In addition to blood and urine testing, diagnostic imaging, particularly ultrasonography, is an important part of the diagnostic process.

Once chronic kidney disease has been diagnosed, adjusting the diet to the animal’s current condition is an obvious step for most vets. It is important to establish both a treatment plan and a strategy for monitoring the patient’s condition and nutritional management.

An informed owner and collaboration with an Animal Nutritionist can undoubtedly help maintain the patient in better condition.


Phosphorus and its importance in the nutrition of animals with chronic kidney disease

Because CKD is so common, virtually every vet encounters renal patients in clinical practice.

In the past, the standard dietary recommendation immediately following a diagnosis of kidney disease was to introduce a renal diet. The requirements for such diets are regulated by Commission Regulation (EU) 2020/354 of 4 March 2020. They are characterised by reduced protein and phosphorus levels.

Historically, dietary protein – particularly high protein intake – was considered one of the main contributors to renal problems in dogs and cats. Today, phosphorus is recognised as one of the key nutrients requiring careful control.

Appropriate phosphorus regulation is crucial in the management of chronic kidney disease because excess phosphorus contributes to mineral disturbances and accelerates disease progression.

In CKD, the kidneys progressively lose their ability to excrete phosphorus effectively, resulting in increased levels of fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH). Initially, these hormonal changes help maintain normal blood phosphorus concentrations. In later stages of the disease, however, hyperphosphataemia and secondary hyperparathyroidism may develop.

Studies indicate that restricting dietary phosphorus slows CKD progression and reduces the risk of mineralisation of soft tissues, including the kidneys.

The source of phosphorus is also important. Organic phosphorus, for example from meat, is better tolerated than inorganic phosphates, which have high bioavailability and can cause a more rapid increase in serum phosphorus and place a greater burden on the kidneys.

Phosphorus intake should be controlled from the early stages of kidney disease. If dietary phosphorus restriction alone is insufficient, phosphate binders may be required.


The role of calcium in kidney disease

Calcium plays an important role in regulating mineral balance, but its metabolism is altered in CKD.

Hypercalcaemia is frequently observed in cats with CKD and may result from reduced glomerular filtration, increased renal calcium reabsorption and increased release of calcium from bone.

High serum calcium concentrations increase the risk of calcium deposition in the kidneys and other soft tissues and may also contribute to cardiovascular abnormalities.

Some studies suggest that excessive dietary phosphorus restriction in renal diets may contribute to increased calcium concentrations. In one study, switching to a diet with less restrictive phosphorus levels resulted in normalisation of serum calcium concentrations in most cats.

This suggests that maintaining an appropriate calcium-to-phosphorus ratio is important rather than focusing solely on restricting either mineral individually.

It is also important not to use phosphate binders automatically without first assessing the patient’s mineral status. Many phosphate binders contain calcium compounds. When combined with a diet containing very low phosphorus levels and a calcium-to-phosphorus ratio of approximately 1.2–1.3:1, they may contribute to hypercalcaemia.


Sodium and potassium – why should these nutrients be monitored in renal diets?

Sodium and potassium play key roles in maintaining electrolyte balance and blood pressure.

High dietary sodium intake may contribute to hypertension, which commonly occurs alongside CKD. However, studies in cats indicate that increased sodium intake does not significantly increase arterial blood pressure and may even improve glomerular filtration rate.

At the same time, low-sodium diets have been associated with a greater risk of hypokalaemia and increased potassium excretion, negatively affecting patients with CKD. Nevertheless, high sodium intake may increase phosphorus digestibility, particularly that of inorganic phosphorus.

Hypokalaemia is more common in cats than in dogs and may accelerate disease progression. It can cause muscle weakness, reduce appetite and impair the kidneys’ ability to concentrate urine.

Renal diets for cats are recommended to contain approximately 0.7–1.2% potassium on a dry matter basis.

In dogs, hyperkalaemia is more common and may contribute to cardiac abnormalities and nausea. Dogs receiving renal diets should generally have dietary potassium levels maintained within the range of 0.4–0.8%.

Serum potassium should be monitored regularly in both canine and feline renal patients, with supplementation or dietary restriction adjusted according to the animal’s current condition.


The importance of magnesium in renal diets

Magnesium is not always associated with nutritional management of renal patients, yet it plays an important role in mineral balance and kidney function.

Magnesium deficiency may contribute to metabolic disturbances, vascular calcification and an increased risk of cardiovascular events.

Studies in cats have shown that appropriate magnesium intake may support phosphorus and calcium homeostasis and reduce the risk of hypercalcaemia.


Protein and its importance in the diet of dogs and cats with chronic kidney disease

One of the main challenges for vets and owners caring for animals with CKD is maintaining appropriate body weight.

Studies investigating weight loss in cats with CKD indicate that this process may begin several years before diagnosis. The mean weight loss during the three years following diagnosis was 1.76 kg, with a significant impact on quality of life and survival.

Being underweight, and particularly losing muscle mass, is associated with an increased risk of earlier death in renal patients.

Numerous cases involving cats fed diets tailored to their stage of disease rather than conventional renal diets indicate that diets with reduced phosphorus but standard protein levels may help preserve muscle mass during the early stages of CKD. In more advanced stages, progressive muscle loss may occur.

Selecting appropriate nutrition for every stage of disease is therefore essential. At present, routinely recommending a renal diet during the earliest stages of CKD is not always considered appropriate, primarily because of restricted protein intake and high fat content.


Is protein restriction necessary?

Historically, high dietary protein intake was thought to accelerate the progression of chronic kidney disease by increasing proteinuria and glomerular damage.

However, studies in dogs and cats with varying degrees of kidney impairment have not demonstrated a clear correlation between protein intake and disease progression.

Protein quality and digestibility are therefore particularly important. Low-quality or plant-based proteins may result in greater production of uraemic toxins such as indoxyl sulphate and p-cresyl sulphate, which can contribute to renal fibrosis and deterioration of kidney function.

A diet based on highly digestible animal protein may help reduce the production of these compounds and support the animal’s overall condition.

As the disease progresses and proteinuria and glomerular damage develop, reducing dietary protein intake may become necessary. However, this should always follow appropriate diagnostic assessment and evaluation of the patient’s clinical condition rather than being introduced prophylactically simply to “protect” the kidneys.

Regardless of whether a renal patient receives a commercial or home-prepared diet, wet food is particularly recommended for cats.


Low-protein diets and muscle mass

One of the greatest challenges in the nutritional management of CKD is preserving muscle mass.

Restricting dietary protein too early may lead to rapid muscle loss while body fat increases. This may be particularly pronounced in older patients, in whom age-related changes already make maintaining muscle mass more difficult.

During the early stages of disease, a diet containing controlled but not excessively restricted amounts of protein is therefore recommended, preferably from highly digestible animal sources.

Further protein restriction may become necessary only during later stages of disease, particularly in patients with significant proteinuria.


Additional supplementation in CKD – is it necessary?

A properly balanced renal diet will often provide essential nutrients in appropriate proportions. However, additional supplementation may be indicated in certain cases.

Every intervention should be tailored to the individual patient and based on laboratory findings.


Vitamin D – when should it be supplemented and when should it be avoided?

Chronic kidney disease disrupts vitamin D metabolism, affecting calcium and phosphorus homeostasis.

There is a negative correlation between phosphorus concentrations and active vitamin D metabolites, meaning that vitamin D deficiency may become more pronounced as the disease progresses.

However, vitamin D supplementation should only be considered once phosphorus levels are adequately controlled.

When blood phosphorus concentrations exceed 1.9 mmol/l (6.0 mg/dl), additional vitamin D intake increases the risk of tissue mineralisation, including mineralisation of the kidneys, potentially accelerating renal damage.

Regular monitoring of blood phosphorus and calcium concentrations is therefore essential before supplementation is introduced.


Omega-3 fatty acids – anti-inflammatory and renoprotective support

Omega-3 fatty acids, particularly EPA and DHA, have strong anti-inflammatory and antioxidant properties.

Studies in dogs and cats have demonstrated beneficial effects on kidney function, including reductions in proteinuria, improvements in glomerular filtration and reduced interstitial fibrosis.

One study involving dogs with renal insufficiency found that a diet enriched with omega-3 fatty acids reduced proteinuria and blood creatinine concentrations while also limiting degenerative changes within the kidneys.


Vitamin E – is supplementation beneficial?

Oxidative stress plays an important role in the progression of chronic kidney disease, and vitamin E is a potent antioxidant that may help protect renal cells against damage.

However, studies in cats with CKD suggest that additional vitamin E supplementation may not provide significant clinical benefits.


Chronic kidney disease, the microbiome and dysbiosis – the impact of diet on gut and kidney health

A growing body of research indicates an important relationship between the gut microbiome and kidney function.

The gut–kidney axis involves interactions between the intestinal microbiota, intestinal barrier and microbial metabolism, all of which can directly influence renal health.

Patients with chronic kidney disease develop intestinal dysbiosis, which can lead to increased production of uraemic toxins, increased inflammation and impaired intestinal barrier function.

Studies in cats with CKD have demonstrated a significant reduction in faecal microbiome diversity compared with healthy animals. At the same time, cats with CKD had increased blood concentrations of indoxyl sulphate (IS), one of the major uraemic toxins. Similar associations have been reported in dogs.

Dysbiosis impairs intestinal barrier function, allowing urea and bacterial toxins to enter the circulation, exacerbating systemic inflammation and accelerating CKD progression.

There is evidence that dietary interventions can beneficially modulate the gut microbiome and reduce the adverse effects of dysbiosis.


Probiotics and prebiotics in animals with CKD

Animal studies indicate that certain probiotic bacterial strains, including Lactobacillus acidophilus, may have renoprotective effects.

In a study involving rats with experimentally induced renal failure, administration of Lactobacillus acidophilus for 12 weeks reduced blood urea concentrations and urinary protein loss. Concentrations of uraemic toxins, including indoxyl sulphate and p-cresyl sulphate, were also reduced.

In uraemic conditions, the intestinal microbiota undergoes unfavourable changes and intestinal barrier function becomes impaired, resulting in increased circulating endotoxin concentrations and greater inflammation.

This systemic inflammation is one of the factors contributing to the progression of renal failure.

Probiotics, particularly strains belonging to the genus Lactobacillus, may help restore a healthier intestinal microbiota, reduce the production of uraemic toxins and improve intestinal barrier integrity.

The diet of patients with CKD should also take prebiotics into account, including fermentable fibre, which promotes the growth of beneficial intestinal bacteria and increases the production of short-chain fatty acids (SCFAs).

An appropriate amount of dietary fibre may help reduce dysbiosis, improve intestinal function and decrease systemic inflammation.

Chronic kidney disease affects not only the urinary system but also the gastrointestinal tract, resulting in impaired digestion and absorption as well as changes in defecation frequency.

Potential causes of reduced defecation frequency in cats with CKD include dehydration, which directly contributes to harder stools, hypokalaemia impairing intestinal motility, reduced physical activity, intestinal dysbiosis and medications used to manage CKD, including opioids, phosphate binders and antihypertensive drugs.

In some cases, constipation in cats with CKD requires veterinary intervention, including laxatives or enemas.

Dietary adjustments, monitoring electrolyte concentrations and an individualised approach to symptomatic treatment can help improve the quality of life of patients with CKD.


Dietary management

When a dog or cat is diagnosed with chronic kidney disease, it is important not only to establish a treatment plan but also to review the current diet and adapt it to the patient’s current requirements.

CKD has several stages and does not progress in the same way in every animal. Nutrition plays an important role in preserving kidney function and maintaining the patient’s quality of life.

There is no single universal solution. The diet should reflect not only the principles of nutrition for renal patients but also the animal’s other individual requirements.

Most animals affected by kidney disease are older, and CKD is often not their only health problem. A well-designed diet should therefore provide renoprotective support without exacerbating other conditions.

Determining an appropriate portion size, daily calorie requirement and feeding frequency is equally important. Selecting the right diet alone may not be sufficient, as loss of appetite, vomiting and digestive problems commonly occur in affected animals.

Much also depends on the owner’s knowledge, commitment and practical circumstances.

A range of dietary approaches is available and should be adjusted according to the patient’s current condition. Supplementation should likewise be selected for the individual case and the animal’s clinical status.

In the past, switching to a renal diet immediately after diagnosis was routinely recommended. Today, the vet, either independently or in consultation with an Animal Nutritionist, may select an appropriate complete maintenance diet, whether commercial or home-prepared, with suitable levels of protein, fat, phosphorus and calcium.

This approach can help preserve muscle mass for longer and prevent or delay the development of additional health problems.

As the disease progresses, transitioning to a renal diet may become appropriate. However, this should not simply be any product labelled “renal”. The analytical composition is important, but so are the sources of individual nutrients, particularly protein and fat.

In cats especially, it is extremely important that protein is of high quality and primarily of animal origin.

Collaboration between vets or owners and Animal Nutritionists is becoming increasingly common. Based on diagnostic results and the vet’s recommendations, the Animal Nutritionist can continually adjust the diet to the patient’s changing condition.

Although chronic kidney disease cannot be cured, it can be appropriately treated and managed. A well-selected diet can help both canine and feline patients maintain a good quality of life for many years.


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