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SPECIFIC diets for kidney disease                         

SPECIFIC offers a complete range of diets for the management of chronic kidney disease in dogs and cats, including high digestible and highly palatable hydrolysed kidney diets. We have both dry and wet diets for both dogs and cats and our new hydrolysed kidney diets are state of the art nutrition for renal care in dogs and cats. the most important features are:

 

  • Highly digestible diets and diets with hydrolysed protein - reduces production of unremic toxins in the gut
  • Uniquely high levels of omega-3 fatty acids EPA and DHA from fish - helping reduce inflammation and glomerular hypertension
  • Support for a healthy gut microbiome and gut barrier integrity
  • High palatability - support appetite maintanance of lean body mass
  • Restricted protein, phosphorous and sodium level

SPECIFIC Derma and Allergy diet Range

Chronic Kidney Disease (CKD) in cats and dogs

The kidneys are responsible for filtering metabolic waste, regulating fluid and electrolyte balance, secretion and metabolism of compounds (Bartges J.W. (2012)). Chronic kidney disease (CKD) is a progressive and irreversible disease that affects the kidneys' ability to filter waste products and maintain electrolyte and fluid balance. 

Nutrition is an important part of the management of CKD in dogs and cats to help to slow down the progression of the kidney failure, improve quality of life, and prevent secondary complications in dogs and cats. 

What are the nutritional needs of cats and dogs with kidney disease  

The goals of the nutrition intervention in CKD patients are: 

  • To prevent or improve the clinical signs 
  • To reduce progression rate of the disease and extension of the survival time 
  • To reduce electrolyte (calcium and phosphorus) and acid-base imbalances 
  • To provide adequate nutrition 

There is existing legislation that states what characteristics are mandatory in a diet that claims to reduce the progression of kidney failure. It relates to the levels of phosphorus and protein (Commission Regulation (EU) (2020)). But there are also additional nutritional adjustments that according to science can benefit CKD patients, especially in the area of supporting gut dysbiosis. 

 

Hyperphosphatemia is a well-known complication of CKD and in humans with renal disease it has been associated with progression of the disease, in cats it has been associated with shorter survival time (Elliot, J. et al. (2000)) and a reduction of the dietary phosphorus level resulted in prolonged lifespan (Ross, S.J. et al. (2006), Barber, P.J.,Elliot, J. (1998)). 

Hyperphosphatemia is the result of declined renal function depending on decreased excretion of phosphorous. To get back to normal serum concentrations of phosphorus a decreased intake is necessary. Because of this phosphorous restriction is one of the main characteristics of renal diets. Renal diets are also most often protein restricted, partly because protein is a main source of phosphorus. (Grelová S. (2022))  

An old study by Ross LA et al. (1982) showed an association between a high dietary phosphorus intake in cats (1.56% phosphorus in dry matter) for 65 to 343 days and kidney mineralization, fibrosis and mononuclear cell infiltration, lower phosphorus intake (0.42% phosphorus in dry matter) did not show this association. 

In general, therapeutic diets for cats and dogs with CKD are formulated with a reduced amount of phosphorus. The legislation states ≤ 5 g/kg for dogs and ≤ 6,5 g/kg for cats in a complete diet with 12% moist (Commission Regulation (EU) (2020)).  

If plasma concentrations remain too high only on a phosphorous restricted diet phosphorus binders can be used to limit intestinal absorption (http://www.iris-kidney.com/pdf/IRIS_CAT_Treatment_Recommendations_2023.pdf). They can be given as supplements or be included in the diet. Example of phosphorus binder are lanthanum carbonate that is used in CatneyOne from Dechra. 

Restricted dietary protein level for dogs and cats with CKD can help to decrease accumulation of end products from protein metabolism, such as urea, creatinine, and other uremic toxins in the blood stream and in the gut, this will decrease uraemia and can help to slow down the progression of CKD (Ephraim, E. & Jewell D.E., (2021), Adams, L.G. et al. (1994)). The legislation states protein levels to ≤220 g/kg for dogs and ≤320 g/kg for cats in a complete diet with 12% moist (Commission Regulation (EU) (2020)).  

To meet the animal’s need of amino acids for tissue repair and muscle maintenance, with a restricted amount of protein, the protein source needs to have a high biological value (optimal proportion of all essential amino acids) and be highly digestible. This will secure a high absorption in the gut and reduce the production of waste products and reduce the load on the kidneys (Finco, D.R. et al. (1998)). Sources with these characteristics are typically hydrolysed proteins, egg, lean meat, and fish proteins.   

The CKD patient will need to be fed these lower protein diets for the rest of their life, so it is important that they meet the animal’s nutritional needs even with the restrictions. 

High-digestible diets are essential for dogs and cats with CKD and refer to the proportion of dietary nutrients that are absorbed. It reduces the production of metabolic waste and helps manage electrolytes and acid-base balance.  

Since animals with CKD often are anorexic and may be malnourished, it is also essential that the diets are highly palatable and high in calories to secure their intake even with reduced consumption. This can also help to prevent weight loss, cachexia and muscle breakdown and maintain optimal nutritional and body condition (Hanna et al., (2020). Laflamme DP, (2005)). Adjustment of the texture and flavour can help to increase consumption in anorexic patients.  

Cats and dogs with CKD may be at risk for hypokalaemia (especially cats) or hyperkalaemia (especially dogs on certain treatments). Diets should be carefully balanced in potassium and depending on IRIS stage the level of potassium varies, especially in cats (Dow, S.W. et al (1990)). High digestibility allows for more controlled and efficient absorption of electrolytes.  

Metabolic acidosis is a complication of CKD that can worsen the breakdown of muscle proteins and contribute to osteodystrophy (Dow, S.W. et al (1990)). It comes from an inability of the kidneys to excrete hydrogen ions (H⁺) and regenerate bicarbonate (HCO₃⁻). Alkalizing agents, such as potassium citrate in the diet can help to maintain acid-base balance and prevent acidosis (reference?). 

Vitamins C, E and Selenium are effective antioxidants that can help to reduce systemic oxidative stress that exacerbates kidney damage (Brown, S.A. (2008), Yu, S. & Paetau-Robinson, I., 2006)). 

Diets enriched with high levels of omega-3 fatty acids EPA and DHA, can help modulate systemic and renal inflammation (Brown SA et al. (1998)). These fatty acids are highly digestible and have beneficial effects on cardiovascular and kidney health, reducing the risk of secondary complications and studies have shown that high levels can help to prolong the lifespan of the animal (Plantinga EA et al. (2005)).  

Gastrointestinal disorders, such as dysbiosis, uremic ulcers and gastritis, are common in CKD animals. Highly digestible diets, preferably with hydrolysed proteins are gentler on the gastrointestinal tract, reducing the incidence of these problems and improving the animal's comfort and quality of life. 

Maintaining optimal hydration is essential to support kidney function. Wet food or diets specifically formulated for pets with CKD can help. 

Regular monitoring of biochemical parameters  

Electrolyte levels, biochemical parameters (such as urea, creatinine and bile acids) and body condition should be regularly monitored to adjust diets accordingly. High digestibility allows for more precise and efficient adjustments, meeting the dynamic needs of CKD patients. 

What is the gut kidney axis 

Here we need an illustration and an animation for the website 

Recently there has been a growing interest and focus on the effect of the gut microbiome – not only its effect on gut health but also regarding the effect of the gut microbiome on other organs, including renal health. 

There is a close relationship between the gut microbiome and renal health, the so-called gut-kidney axis. This refers to the bisectional relationship between the gut and the kidney – where kidney disease triggers gut dysbiosis which in turn exacerbates the progress of kidney disease (Vaziri, N. D. et al. (2013), Kim, S.M. & Song I.H. (2020)). 

The gut-kidney axis is bidirectional, and the microbiome can also affect kidney health in a number of ways which all together can develop a self-perpetuating process of inflammation, intestinal permeability and dysbiosis.  

The intestinal barrier – the microbiome, dysbiosis and intestinal permeability “leaky gut” 

There is a close interplay between the intestinal barrier, intestinal microbiota, and the immune response. A disruption in the interaction can lead to intestinal but also systemic diseases.  

The microbiome in the gut consists of approximately 1010 to 1014 microorganisms (bacteria, viruses, fungi and protozoa), interacting with each other and with the host. Almost all microorganisms in the microbiome found in the intestinal tract of healthy cats and dogs belong to the phyla Firmicutes, Bacteroidetes, Proteobacteria, Fusobacteria and Actinobacteria (Suchodolski, (2011)). A balanced microbiome contributes to the hosts health by metabolites produced by the microorganisms, this also prevents against pathogenic microbes (Wu, H.J., Wu, E., (2012)). 

Dysbiosis is when the equilibrium between microbiota, epithelial barrier, and immune response is disturbed, and the microbiome gets unbalanced. The diversity of the microbiome is reduced, with a decrease in beneficial saccharolytic bacteria and an increase in pathogens.

A change in microbiota can be induced by several factors such as a change in available substrate (e.g. more undigested food in the gut, a change in dietary composition), increase amount of uremic toxins, use of antibiotics, loss of colonization resistance, change in environmental conditions, invasion of pathogenic bacteria or altered immune response. Changes in the type or number of bacteria and their metabolites can have a direct effect on the integrity of the intestinal barrier and the intestinal immune response (Vaziri, N. D. et al. (2013)). 

Increased intestinal permeability, often referred to as "leaky gut", due to dysbiosis and increased amounts of uremic toxins and precursors in the gut is a condition where the gut barrier becomes compromised, allowing potentially harmful substances to pass into the bloodstream.

When the gut barrier becomes compromised the function of the tight junctions, the link between the epithelial cells in the intestinal barrier, are altered. Normally it is the tight junctions that regulate the passage of substances from the gut to the blood stream. But in a leaky gut there are possible spaces between the mucosal cells where harmful molecules can pass.

Factors that can cause the alteration of the junctions are chronic inflammation, dysbiosis, infections, certain medications (such as antibiotics and NSAIDs), stress, and certain dietary components. In dysbiosis the imbalanced microbiota produces less metabolites, mainly SCFAs, that plays a key role in the maintenance of the tight junctions (Suchodolski et al. (2012), Suzuki, (2020)). 

What are the implications of gut dysbiosis and intestinal permeability in cats and dogs with CKD 

CKD in dogs and cats is often associated with the presence of dysbiosis and impaired intestinal permeability (Chen Y. et al., (2019)). In humans it is shown that dysbiosis can lead to dysregulation of metabolic processes, cardiovascular disease, impaired intestinal barrier, systemic inflammation, and increased systemic uremic toxins which all can worsen renal failure (Staropoulou et al., (2020)). 

Similar disruptions in the gut-kidney axis have been shown in dogs and cats, also specific microbials has been associated with impaired metabolism in cats with CKD (Summers et.al., (2019), Kim et.al (2023), Winston, (2024)). Disruption of the gut microbiota can have profound implications for overall health and CKD progression in these animals and there are several reasons behind the dysbiosis (Vaziri et al., (2012)). 

Studies have shown that renal patients have more uremic toxins, like indoxyl-sulfate and P-cresyl sulfate in their blood, originating from decreased excretion depending on compromised kidney function (Hall, et. Al., (2020), Ephraim & Jewell., (2020)). Uremic toxins can affect the composition of the gut microbiome and cause dysbiosis, impair the gut barrier integrity, and the metabolic products produced by the microbiome, such as beneficial short chain fatty acids (SCFA) (Vaziri, N. D. et al. (2013). Undigested protein in the gut, can be metabolised by microbiota, resulting in the production of uremic toxin precursors indole and p-cresol. Increased amount of uremic toxins or precursors in the gut can in turn favour the abundance of more uremic toxin producing bacteria (Van Vliet et al., (2018)). All this leads to increased levels of systemic indoxyl sulfate and p-cresyl sulfate in the blood stream.  

Normally these toxins are eliminated by the kidneys, in CKD patients they accumulate and contribute to the progression of CKD in different ways and systemic symptoms like anorexia, lethargy, etc. Uremic metabolites may also have direct nephrotoxic effects, accelerating the decline of renal function and have deleterious effects on the cardiovascular system, increasing the risk of heart disease in animals with CKD (reference). 

 

(For this section we need visuals, animations for website) 

Leaky gut is of particular concern in patients with CKD because endotoxins, like bacterial lipopolysaccharides (LPS) and uremic toxin precursors entering the systemic circulation and stimulates the production of pro-inflammatory cytokines (such as TNF-α, IL-6), which will increase systemic inflammation and progression of the kidney failure (Ghoshal et al., (2012)). Systemic inflammation also increases oxidative stress, which can further damage kidney tissue (Vaziri, N. D. et al. (2013)). A study by Sabatino et al., (2015) has shown a correlation between increased intestinal permeability and CKD severity. Markers in serum of intestinal permeability, like elevated levels of zonulin and LPS are often seen in CKD patients, indicating increased intestinal permeability. In mouse models of CKD, administration of uremic toxins led to increased intestinal permeability and systemic inflammation, confirming the role of uremic toxins in this process (Anders et al., (2013)). 

It is often difficult to say if leaky gut is a cause or a result of CKD because dysbiosis, often seen in CKD patients, is a common cause behind the condition, but on the other hand uremic toxins, that increases in the blood stream in CKD patients, can induce an inflammatory response that can damage the epithelial cells of the intestine, increasing intestinal permeability and compromise the function of the intestinal barrier (Vaziri et al., (2012)).  

Animals with gut dysbiosis and CKD can have a variety of gastrointestinal disorders, such as diarrhoea, constipation, and vomiting. These symptoms can affect digestion and nutrient absorption leading to malnutrition and nutritional deficiencies, decreased appetite and weight loss, worsening the pet's overall condition and a common symptom is renal cachexia (Hanna et al., (2020)). Gut dysbiosis can affect immune function, making animals more vulnerable to infections (Kim, S.M. & Song I.H. (2020)). 

Nutritional interventions to improve gut health, such as the administration of pre- and probiotics, have shown beneficial effects in reducing intestinal permeability and systemic inflammation (Vaziri, N. D. et al. (2013), Kim, S.M. & Song I.H. (2020)) and can be an important part of the treatment of CKD (Chen Y. et al., (2019). 

The Dechra academy provides a range of on-line learning including this course related to kidney disease

The Role of Nutrition in Managing Kidner Disease

This training addresses the role of diet as part of a multimodal approach to the management of chronic kidney disease in dogs and cats, in particular the value of a high digestibility and hydrolysed protein diet and the importance of high levels of anti-inflammatory omega-3 and -6 fatty acids.

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Dechra Academy The Role of Nutrition in Managing Allergies and Atopic Dermatitis

HOW CAN NUTRITION SUPPORT THE GUT KIDNEY AXIS

Nutritional management of CKD in dogs and cats and support of gut dysbiosis and leaky gut 

Nutrition plays an important role in the processes related to the gut-kidney axis and to decrease the risk of gut dysbiosis and leaky gut. The goal is to reduce the level of systemic uremic toxins and inflammatory mediators to slow down the progression of kidney failure. 

Effective nutritional adjustments can include 

  • High-quality protein, hydrolysed protein, and reduced protein levels 
  • High digestible diets 
  • Hypoallergenic diets to identify and avoid potential allergens 
  • Use of the amino acid glutamine to support repair of the intestinal mucosa 
  • Anti-inflammatory omega-3 fatty acids (EPA/DHA) to reduce systemic and local inflammation in the intestine 
  • High fibre content with prebiotic fibres to help nourish a healthy microbiota, and fibres to prevent constipation 
  • Probiotics to support the microbiota 
  • Other components for support of the intestinal barrier like antioxidants, zeolite and natural polyphenols 

THE IMPORTANCE OF HIGHLY DIGESTIBLE DIETS AND HYDROLYSED PROTEINS 

For dogs and cats with CKD the digestibility of the diet is of paramount importance and refers to the proportion of dietary nutrients that are absorbed and used by the body and plays a key role in managing and optimizing the health of these animals.

High digestible diets reduce the production of metabolic waste and allows for more controlled and efficient absorption of electrolytes (reference), helping to maintain proper blood levels of potassium with less risk of hypo- or hyperkalaemia and regulation of the acid-base balance (reference).

They also allow for maximum absorption of essential nutrients (proteins, fats, carbohydrates, vitamins and minerals) and calories even with reduced consumption. This helps prevent anorexia, malnutrition, weight loss and muscle breakdown which is common in patients with CKD (Hanna et al., 2020)) and maintain optimal nutritional status and quality of life. 

Another way nutrition can interfere with the gut-kidney axis is through the protein level and quality of protein in the diet. Plasma levels of urea and other uremic toxins are all derived from protein catabolism. By reducing the protein level in the diet, less protein waste will be produced from protein catabolism. Studies in cats and dogs with CKD show that a reduction in dietary protein level is associated with a reduction in the blood urea level, but also with a reduction in plasma level of uremic toxins (Summers et al., (2023), Ephraim & Jewell, (2021), Ephraim et al., (2020)). 

It is not just the protein levels that matter but also the digestibility of the protein. Protein which is not digested and absorbed will end up in the colon, where proteolytic bacteria can ferment it and produce uremic toxins precursors, transported to the liver where they are reformed to uremic toxins ((Vaziri, N. D. et al. (2013), Kim, S.M. & Song I.H. (2020)). The higher the digestibility of dietary protein, the lower the amount of undigested protein in the colon, the lower the microbial production of uremic toxin precursors (Ephraim & Jewell, (2021), Ephraim et al., (2020)).   

Moderate, but high-quality protein with high biological value and digestibility, covering the need for essential amino acids, are recommended to reduce the production of uremic toxins and minimize the metabolic weight on the kidneys (Ephraim & Jewell, (2021)). Hydrolysed proteins are highly digestible and a good source to CKD patients that can help to reduce inflammatory reactions in the gut, helping to maintain a healthy intestinal barrier (reference).  

Not only the protein level or the digestibility are essential also sufficient amount of essential amino acids in the diet is something that has shown to be important to maintain muscle mass and decrease malnutrition because of CKD. Cats fed a renal diet fortified with essential amino acids it maintained their lean body mass better than cats on a regular renal diet (Hall et al., (2019)). 

Hydrolysed proteins are intact proteins that have undergone an enzymatic process, which has cut the big intact proteins into smaller peptides and single amino acids, makes them pre-digested. This increases their specific surface area and facilitates their interaction with digestive enzymes, which speeds up their digestion and the absorption of single amino acids. The metabolism of these peptides will also be more complete in the small intestine of animals, with less undigested protein in the colon. This will decrease the risk for dysbiosis and lower the microbial production of uremic toxin precursors. The increased absorption of amino acids can help support recovery, growth, and tissue repair in sick or convalescent (Reference). 

Hydrolysis of proteins also reduce their allergenic potential by degrading allergenic epitopes into non-immunogenic peptides. In animals with food sensitivities, compromised intestinal barrier or allergic reactions, the use of hydrolysed protein may be beneficial in minimizing adverse reactions due to molecules that pass the tight junctions into the blood stream causing systemic reactions (reference). Hydrolysed proteins are often used in therapeutic diets for pets with gastrointestinal disorders, such as inflammatory bowel disease or gastritis due to their increased digestibility. They can reduce the work for the gastrointestinal tract and alleviate symptoms associated with these conditions, such as diarrhoea, vomiting, and abdominal pain. Since patients with CKD often suffer from these problems hydrolysed proteins can be a big benefit in kidney diets.  

The CKD patient will need to be fed lower protein diets for the rest of their life so a high quality, highly digestible diet is required to ensure an adequate supply of amino acids in the longer perspective. 

Nutritional management to reduce intestinal permeability – fibre, pre- and probiotics and other components 

Increased intake of prebiotics (fibre that promotes the growth of beneficial bacteria), probiotics (beneficial bacteria) or postbiotics (beneficial metabolites like SCFAs) can help restore a balanced and healthy microbiota, strengthen the intestinal barrier, and change their production of metabolic uremic toxins. 

Prebiotics are fermentable fibres such as fructo-oligosaccharides (FOS) and beet pulp. They have long been known to affect the composition of the gut microbiota (Bindels et al. (2015)) They promote the growth of beneficial saccharolytic bacteria like Lactobacillus, Bifidobacterium and Firmicutes, that can ferment these fibres and increase production of SCFA such as butyrate (Mondo et al. (2019), Pilla & Suchodolski (2021)). This in turn will nourish cells in the intestinal mucosa with increased protective effects on the gut barrier integrity and thereby reduce inflammation and improve gut health.  

Uremic toxin accumulation can be decreased by increasing the dietary intake of soluble fibre either by increased levels in the diet or by supplementation (Chen et al., 2022, Liu et al., 2022, Yang et al., 2021). Other studies have shown that plasma concentrations of uremic toxins decreased when feeding dogs and cats with CKD with a renal diet with high soluble fibre content compared to feeding a renal diet with lower fibre content (Ephraim and Jewell, 2020, Hall et al., 2022). 

Probiotics are living microorganisms that can give the host a beneficial effect in terms of restoring a healthy microbial balance in the gut and reduce inflammation and strengthen the tight junctions between epithelial cells. They often consist of Bifidobacteria species, Lactobacilli and Streptococci. In human studies it is shown that probiotics can help to support the intestinal barrier function (Bron et al. (2017), Makielski et al. (2018)), in animals there is so far no sufficient proof of beneficial effects in clinical studies.  

Postbiotics are a fermented product consisting of residual dead microorganisms like bacteria and yeast cells, cell wall fragments, fermentation metabolites, SCFAs and media used during fermentation, which can provide important nutrients for the intestinal mucosa and microbiota helping to decrease intestinal permeability and support a balanced micro flora (reference).

Postbiotics can exert effect by modulation of microbiota, enhancement of epithelial barrier function modulation of local or systemic immune response, metabolic response, or systemic signalling via the nervous system (Salminen et al. 2021). Since composition of various postbiotics can vary a lot, depending on the type of microorganism which are used, formed metabolites, presence of cell fragments and inactivation process, the efficacy will vary and should be evaluated for each specific postbiotic product (reference). 

Other dietary components – natural polyphenols, zeolite and Omega-3 fatty acids (EPA/DHA) 

Other dietary components that can affect the intestinal barrier function directly or indirectly by affecting the microbiota can play a role in the gut-kidney axis and be of importance in slowing down the progression of the kidney function in animals with CKD.  

The presence of natural polyphenols in the diet (AuraGuard) can improve tight junction function through increased expression of tight junction proteins and improved assembly of these proteins in the tight junction structure and support a healthy microbiome, the production of SCFA and prevent inflammation (Suzuki, (2020)).  

Dietary zeolite can bind ammonium in the gut and thereby reducing the plasma level of uremic toxins (reference). 

Anti-inflammatory omega-3 fatty acids EPA and DHA, found in fish oil, can help reduce systemic and gut inflammation, contributing to better CKD management in dogs and cats (Hawthorne AB et al. (1992), Stenson WF et al. (1992), Brown SA et al. (1998), Plantinga EA et al. (2005)) 

Monitoring of the gut health 

Regular monitoring with checks of kidney function and gut health, including blood tests and gut flora tests, are essential to adjust nutrient intakes. Proactive management of nutrient intake, including introducing a special kidney diet based on changes in the animal's health status, is essential to slow the progression of CKD and improve quality of life. 

Conclusion 

Gut dysbiosis in cats and dogs with CKD is a significant challenge, but proper nutritional management can mitigate its harmful effects. To promote the growth of beneficial saccharolytic bacteria, to reduce the number of proteolytic bacteria that produce uremic toxins, by different nutritional supplements can be an effective nutritional strategy to reduce the microbial production of uremic toxins and toxin precursors which can prevent their adverse effects on kidney function (Kim, S.M. & Song I.H. (2020)). 

By incorporating pre-, pro- and postbiotics, high-fibre level, and adjusting protein level and quality and omega-3 fatty acids it is possible to support the gut and kidney health in animals with CKD. Regular monitoring and proactive management are crucial to tailor interventions to the specific needs of each animal. 

What is the role and benefit of omega-3 for the management of kidney disease  

Here we need an animation on how EPA and DHA work in relation to kidney health 

Omega-3 fatty acids have many characteristics that can benefit patients with CKD. Diets enriched with high digestible omega-3 fatty acids can help modulate systemic and renal inflammation, have beneficial effects on cardiovascular and kidney health and reduce the risk of secondary complications (reference). The results of studies done in humans, rats, dogs and the results of a retrospective study in cats, show that long chain omega-3 PUFA supplementation can have a beneficial role as an adjunctive treatment for CKD patients (Hu, J. et al. (2017), Zanetti, M. et al. (2017), Brown, S.A. et al. (1998), Plantinga, E.A. et al. (2005)).  

The beneficial effects of EPA and DHA are attributed to their ability to reduce inflammation and oxidative stress by interfering with the production of pro-inflammatory eicosanoids (prostaglandins (PGE2) and leukotrienes (LTB4)) (Freeman, L.M. et. al. (1998)). They also synthetize different metabolites known as resolvins and protectins. These metabolites act as potent anti-inflammatory mediators blocking the actions of eicosanoids and by helping clear the site of inflammation (Serhan, C.N. et.al. (2002)). Omega-3 fatty acids, especially EPA and DHA also increase the bioavailability of nitric oxide, a potent vasodilator that can help reduce systemic and intraglomerular blood pressure, this improves endothelial function and can help reduce blood pressure and improve blood flow, which contributes to the reduction in proteinuria (Brown S.A. et al. (1998)). They also have antiplatelet effects that reduce the risk of thrombosis (Adili R., et al. (2017)), and they can inhibit the production of pro-fibrotic growth factors such as TGF-β (transforming growth factor beta) (Endres, S. et al. (1989)), thereby reducing the progression of renal fibrosis (reference?). 

In dogs with experimentally induced CKD, high dosages of EPA and DHA were able to reduce proteinuria, prevent glomerular hypertension and decrease the production of proinflammatory eicosanoids - with reduction of histopathologic lesions (decreased mesangial matrix expansion, glomerulosclerosis, and renal interstitial cellular infiltrates) (Brown S.A. et al. (1998), Brown S.A. et al. (2000)).  

Data on the effect of EPA and DHA in cats is limited to one retrospective study where cats with CKD fed a maintenance diet were compared to the ones fed 1 of 7 renal diets. In this study, the renal diet with the highest EPA content (2g/1000kcal) was associated with the longest survival time (Plantinga, E.A. et al. (2005)). 

Omega-3 fatty acids can contribute to maintaining body weight and muscle mass due to decreased cachexia, which is important for prolonged survival time for dogs and cats with CKD (Freeman, L.M. (1998)).  

In summary, there is evidence that higher intake of EPA and DHA improves kidney function and potentially slows down the progression of renal disease and can contribute to prolonging the lifespan of the animal (Plantinga, E.A. et al. (2005)). 

EPA & DHA dosage for renal patients 

Although EPA and DHA are omega-3 fatty acids, not all sources of omega-3s have the same effects. α‐Linolenic acid (18:3n‐3, ALA) is an omega- 3 fatty acid found in many vegetable oils and, although it could be a precursor of eicosapentaenoic acid (20:5n‐3, EPA), cats and dogs have very limited capacity to synthesize EPA and DHA from α‐linolenic acid and so they must be obtained pre‐formed from the diet (reference). 

Dosage of EPA and DHA to renal patients

The minimum amount of total EPA + DHA that showed a reduction in glomerular hypertension and proinflammatory eicosanoids in dogs was 0.41% on a dry matter basis together with a total omega-6: total omega-3 ratio of 5:1. This would be equivalent to a dose of approximately 130 to 140 mg of EPA and DHA /kg 0.75 body weight for a dog (reference?). 

From the retrospective study in cats with CKD, the minimum effective beneficial dosage of EPA in cats with CKD cannot be defined. However, the EPA content of the renal diet which was associated with increased survival time compared to the other renal diets would be equivalent to a dosage of approximately 95 to 127 mg EPA per kg body weight (based on a 4-kg cat eating 75 to 100 kcal/kg0.67). As the ratio of EPA:DHA in fish oil is roughly 1:1, this would mean that the dosage of combined EPA and DHA in the cats fed the diet associated with the longest survival time was around 190 to 254 mg/kg body weight (Plantinga, E.A. et al. (2005)).   

The omega-3 / omega-6 ratio is also important to consider, due to their metabolic competitive behavior. Higher dosages might give an extra benefit, but the NRC (2006) safe upper limit for dogs is 760 mg of EPA and DHA/kg0.75 body weight, since high dosages might be responsible for secondary side effects, for instance: gastrointestinal upset, decreased wound healing, decreased platelet function, and altered immune function (Lenox, C.E., Bauer, J.E., (2013)). It should be noted that the FEDIAF’s Nutritional Guidelines do not indicate a nutritional maximum for EPA and DHA. Any risk of gastrointestinal upset can be reduced by a slow transition to higher EPA + DHA in the diet and these fatty acids should always be accompanied by a fat-soluble antioxidant like vitamin E. 

Omega-3 in renal diets 

Therapeutic kidney diets are often supplemented with high concentrations of the omega-3 fatty acids, which include EPA, DHA, and ALA. Although ALA is considered an essential fatty acid (as already mentioned), its conversion to EPA and DHA is residual in these species. Therefore, information on the specific concentration of EPA and DHA in the diet is important for the clinician. If this information is not readily available in the food package or support information, it is possible to obtain it by contacting the manufacturer or the distributor. 

Table with omega 3 in SPECIFIC and competitor diets 

Uremic Toxins and kidney disease 

Uraemic toxin precursors are produced in the gut when the amino acids tryptophan, phenylalanine, and tyrosine are digested by the bacteria in the intestinal microbiome. The uraemic precursors are then absorbed and transported to the liver where they are metabolised into the uraemic toxins indoxyl sulfate and para-cresyl sulfate. In healthy cats and dogs these toxins are excreted continuously by the kidneys via active tubular secretion. In patients with CKD the ability to excrete is decreased and these toxins are accumulated in the bloodstream and will contribute to progression of kidney failure (Hall, et. Al., (2020), Ephraim & Jewell., (2020)). 

Indoxyl sulfate is a uremic toxin produced from the breakdown of tryptophan by the gut microbiota. It plays a key role in the progression of CKD due to its detrimental effects on various body systems, including the gut and kidneys (reference). 

Indoxyl sulfate formation starts in the intestine when the essential amino acid tryptophan is metabolized by intestinal bacteria to indole. The indole is then absorbed into the systemic circulation and transported to the liver where it is hydroxylated to indoxyl. Indoxyl is then sulfoconjugated by sulfotransferase enzymes to form indoxyl sulfate. 

In CKD patients, with decreased ability to excrete, indoxyl sulfate accumulates in the blood where it stimulates the production of pro-fibrotic mediators such as TGF-β (transforming growth factor-beta), contributing to renal fibrosis and CKD progression (Reference). 

It also increases the production of ROS (reactive oxygen species) and activates inflammatory pathways (via NF-κB), inducing oxidative stress that damages kidney cells and increasing the production of pro-inflammatory cytokines (Reference). 

Indoxyl sulfate can also disrupt the tight junctions between intestinal epithelial cells, increasing intestinal permeability and cause local inflammation in the intestine, exacerbating dysbiosis and increasing permeability (Vaziri, N. D. et al. (2013), (Van Vliet et al., (2018)). 

Indoxyl sulfate has been associated with endothelial dysfunction, contributing to cardiovascular complications common in CKD patients. It can also interfere with mineral metabolism, contributing to bone disorders in CKD patients (Reference). 

Nutrition management approaches to decrease the level of indoxyl sulfate are as described earlier, 

  • use of pre-, pro- and postbiotics, high digestible protein and diets that help to decrease the risk of dysbiosis  
  • reduced protein level, especially animal protein, which contains about two times more tryptophan, to decrease the amount of tryptophan available 
  • use diets rich in antioxidants to counteract oxidative stress  
  • use phosphate binders like lanthanum carbonate (Catney One from Dechra), these agents can also bind certain uremic toxins in the gut (reference) 
  • activated Charcoal can be used to adsorb uremic toxins in the gut and reduce their systemic absorption, Porus One from Dechra (reference) 

Understanding and treating the effects of indoxyl sulfate may improve quality of life and slow the progression of kidney failure in patients with CKD. 

 

P-cresyl sulfate (pCS) is a uremic toxin derived from the metabolism of tyrosine-containing proteins, primarily produced by gut bacteria. It accumulates in the blood of patients with CKD due to the decreased ability of the kidneys to excrete it.  

P-cresyl sulfate is synthesized in the body, mainly in the liver, from the amino acid phenylalanine. Phenylalanine is converted into tyrosine, catalyzed by the enzyme phenylalanine hydroxylase. It adds a hydroxyl group (-OH) to phenylalanine to form tyrosine. Tyrosine is then fermented by bacteria in the intestine to P-cresol, which are sulphoconjugated in the liver to P-cresyl sulfate.  

It contributes to systemic inflammation, increases oxidative stress in various tissues, are associated with cardiovascular complications in patients with CKD and may affect the function of endothelial cells and other cell types (Reference). 

P-cresyl sulfate levels can be used as an indicator of kidney function. Reducing pCS levels is a goal in the treatment of CKD to decrease associated complications.  

Pro-, pre and postbiotics may help alter gut flora and reduce p-cresol production together with restricted protein levels (Reference). 

Substances that can bind to p-cresol in the gut to reduce its absorption and conversion to pCS are activated charcoal (Porus One from Dechra), soluble dietary fibre, pro- and prebiotics, cholestyramine, etc. 

P-cresyl sulfate is an important toxin to monitor in patients with CKD due to its adverse effects on overall health and associated complications. 

SPECIFIC Kidney Support diets

SPECIFIC Heart & Kidney Support CKD/CKW

SPECIFIC Kidney Support FKD/FKW/FKW-P

SPECIFIC Heart & Kidney Support CKD-HY/CKW-HY

SPECIFIC Kidney Support FKD-HY/FKW-HY/FKW-P-HY

SPECIFIC Kidney Diets - FAQ

Födoämnesallergi kan endast diagnostiseras med hjälp av eliminationstest, det finns inga andra tillförlitliga tester. För att kunna ställa rätt diagnos är det därför viktigt att utföra ett elimineringstest med efterföljande provokation med djurets tidigare foder och sedan enskilda proteinkällor. Om djurägaren inte villig eller kapabel att utföra ett eliminationstest kan man göra ett foderbyte till en hypoallergen diet och helt enkelt utvärdera hur djuret svarar på detta. Då får man dock inte reda på vilket födoämne som djuret faktiskt är allergisk emot, eller om det underliggande problemet faktiskt var en födoämnesallergi eller inte. Djuret kan ha blivit bättre av någon annan orsak under tiden som den stått på det hypoallergena fodret.

Ja, det är möjligt att uppvisa en reaktion mot källor till omega-3- och omega-6-fettsyror (t.ex. fetter och oljor). Allergeniciteten hos ätliga oljor och fetter är relaterad till förekomsten av restprotein i produkten. Det finns uppgifter på att proteininnehållet i "råa" livsmedelsklassade oljor är i storleksordningen 0,1–0,3 mg/ml. I raffinerade oljor reduceras denna nivå cirka 100-faldigt. Studier har visat att just den "råa" oljorna kan framkalla allergiska reaktioner hos känsliga allergiska individer. Det antas att raffinerade oljor inte utgör en risk för att framkalla allergiska reaktioner hos majoriteten av allergiska individer.

De typer av fett som används i hypoallergena dieter bör vara testade för eventuella proteinrester och man bör ta med i beräkningen att även en raffinerad olja kan innehålla spår av potentiella allergener i form av proteinrester.

Det fläskfett som används i SPECIFICs hypoallergena foder har kontrollerats med PCR-test som visat att det är fritt från fläskprotein och därför inte ska framkalla någon allergisk reaktion hundar eller katter med allergi mot fläskprotein.

Även fiskoljan som används i de hypoallergena SPECIFIC-dieterna har testats med PCR-analys och är fria från fiskprotein, och därmed säkra att utfodra till individer med allergi mot fisk.

Hundar och katter med födoämnesallergi, som är utan kliniska symtom på en viss hypoallergen diet och byts till en annan hypoallergen diet, kan uppvisa ett återfall av kliniska symtom inom en period på några timmar upp till 2–3 veckor. Det beror på vilken typ av reaktion de får av allergenet.

Hos individer som för närvarande lider av symtom på födoämnesallergi i form av magtarm problem så ser man ofta en förbättring på dagar upp till 2-3 veckor, medan det vid hudsymtom kan ta upp till 6–10 veckor innan en tydlig förbättring ses när man byter till en hypoallergen kost som djuret tolererar. Ett eliminationstest, vid hudrelaterade symtom, bör därför utföras under ca 8 veckor för att man ska få en tillräcklig förbättring av hudens kondition (Olivry et al 2015). Nya forskningsrön visar också att man kan göra eliminationstestet under en kortare period (3-4 veckor) om man kombinerar en hypoallergen diet med ett antiinflammatoriskt läkemedel som påskyndar förbättringen av hudsymtomen.

For further information including answers to questions about SPECIFIC:

Visit SPECIFIC FAQ page

References

SPECIFIC diets for management of Kidney Disease

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