Chronic kidney disease is defined as persistent azotaemia for 3 or more months, with or without a decrease in glomerular filtration rate (GFR) or more than a 50% reduction in GFR for at least 3 months (Forrester et al, 2010). The first ability that is lost with the failing kidney is often the ability to concentrate urine. In a cat, the urine becomes both dilute and excessive when 66% of the kidney function has been lost.
This change will precede the rise of metabolic waste in the blood (urea-creatinine) which occurs only when approximately 75% of the kidney function is lost. Chronic kidney disease involves a loss of functional kidney tissue due to a progressive process that is irreversible (Chew et al, 2011).
Therapeutic kidney nutrition is the cornerstone for managing cats with CKD. Cats have cyclical appetites that wax and wane as their disease progresses. It is important that cats with CKD eat enough. Nurses should advocate for their patients by helping owners with the successful transition to a kidney therapeutic food and can be instrumental in helping with the management of the condition (Figure 1).
Cachexia and sarcopenia
Cachexia and/or sarcopenia are often seen in cats with CKD. This needs to be considered in the diet recommendation. Cachexia is the loss of lean body mass due to diseases such as CKD or cardiac disease.
Sarcopenia is the age-related loss of lean body mass in the absence of disease. It is related to cachexia, but uniquely different. Like cachexia, its cause is multifactorial. When cats have acute or chronic diseases, they lack the metabolic adaptations needed to switch to burning fat for energy, which means amino acids are used as an energy source, resulting in muscle and lean body mass being catabolised. The classic sign of cachexia is loss of lean body mass. More research needs to be done, but it is thought that decreased nutrient absorption may contribute to cachexia and sarcopenia. Cats with cachexia have decreased appetite resulting in lower calorie intake (Freeman, 2012). For this reason, just increasing protein intake has not been shown to lessen this muscle loss.
Symmetric dimethylarginine (SDMA)
It is generally accepted that creatinine does not increase above the reference interval, until up to 75% of kidney function is lost. Clearly, there has been a need for a more sensitive test of kidney function in order to detect kidney disease earlier (Figure 2); SDMA has been shown in cats to increase when there is as little as 25% kidney function loss and on average when there is 40% loss of kidney function (Braff et al, 2014; Hall et al, 2014).
The SDMA test is more specific for kidney function than other traditional test; creatinine, blood urea nitrogen (BUN) and specific gravity of the urine. SDMA is a methylated form of arginine, an amino acid. Arginine is released into the circulation during protein degradation and is excreted by the kidneys. SDMA has three key attributes: it is a biomarker for kidney function; it increases earlier than creatinine in cats with CKD; it is specific for kidney function. SDMA is not impacted by lean muscle mass, like creatinine, making it a more reliable test than creatinine for detecting CKD. SDMA should be considered complementary to creatinine, therefore SDMA and creatinine both should be evaluated when assessing kidney function in cats. A SDMA persistent value above 14 µg/dl suggests reduced kidney function. In a study, SDMA identified CKD 17 months on average earlier than creatinine increased above the reference range (Hall et al, 2014; Hall et al, 2016).
International Renal Interest Society (IRIS)
Staging of CKD through the International Renal Interest Society (IRIS) is used to facilitate the management of feline patients with CKD. Staging is based initially on two tests on a stable fasting cat. Then sub-staging is used to further identify which stage the cat is in (IRIS, 2017). IRIS splits kidney disease into four basic stages according to creatinine and SDMA levels (see Table 1). Following these four stages, there are sub-stages of each with respect to proteinuria and the presence of hypertension. IRIS recommends a urine protein: creatinine ratio (see Table 2) and a blood pressure measurement (see Table 3) to evaluate the cat for sub-staging. According to IRIS, starting a kidney therapeutic food should be considered even in stage I if there is proteinuria or hypertension.
| Kidney function remaining | |||||
|---|---|---|---|---|---|
| Stage I — <100% | Stage II — <33% | Stage III — <25% | Stage IV — <10% | ||
| Azotaemia | None | Mild renal | Moderate renal | Severe renal | |
| Plasma creatinine (mg/dl) | <1.6 | 1.6–2.8 | 2.9–5.0 | >5.0 | |
| SDMA (µg/dl)a | >14 | >14 | Moderately increased | Markedly increased | |
| SDMA (µg/dl)a consider understaged based on creatinine | >25 go to stage III | >45 go to stage IV | |||
aLevels apply to average size cats measured when patient is well hydrated; SDMA, symmetric dimethylarginine
| UP/C value | Sub stage |
|---|---|
| <0.2 | Non proteinuric |
| 0.2 to 0.4 | Borderline proteinuric |
| >0.4 | Proteinuric |
UP/C, urine protein: creatinine ratio
| Systolic blood pressure mmHg | Blood pressure sub stage | Stage IV — <10% |
|---|---|---|
| <150 | Normotensive | Minimal |
| 150–159 | Borderline hypertensive | Low |
| 160–179 | Hypertensive | Moderate |
| >180 | Severely hypertensive | High |
In 2016 IRIS updated its guidelines to include SDMA. Using SDMA it has identified stages II and III to be earlier than previously thought. If there is a persistent SDMA >25 µg/dl in stage II, this may indicate more advanced degree of renal dysfunction than previously thought, especially if the cat has a low body condition; these cats should be considered stage III and treated as a stage III cat. A cat in stage III with a SDMA of >45 µg/dl should be considered a stage IV cat and treated accordingly (IRIS, 2017). With these new guidelines cats may need to start a kidney therapeutic food sooner than some have suggested in the past.
Nutritional management of CKD
When addressing CKD the goals of dietary management are to maximise the quality and quantity of life of the cat by ensuring adequate intake of energy, limiting the extent of uraemia, and slowing the rate of progression of the disease (Polzin, 2007; Forrester et al, 2010). Research has shown cats with naturally occurring CKD when fed a kidney therapeutic food (Figure 3) had increased quality and length of life (Ross et al, 2006).
It is typically recommended to start a kidney therapeutic food when the cat has stage II CKD, earlier if proteinuria and hypertension are present, per IRIS staging recommendations. Some would suggest starting earlier, even when there is no proteinuria or hypertension, before symptoms are present to make it easier to switch the cat to a kidney therapeutic food. Taste can be affected by CKD, starting a kidney therapeutic food before the advancements of the disease may facilitate easier transition to an appropriate kidney therapeutic food.
Phosphorus and sodium
Kidney therapeutic foods are controlled and enhanced with certain nutrients. Kidney therapeutic foods are formulated to avoid excessive phosphorus and sodium. Decreasing the intake of dietary phosphorus in cats with CKD has been shown to be beneficial in limiting phosphorus retention, hyperphosphataemia, and secondary renal hyperparathyroidism. In addition, limiting dietary phosphorus intake was shown to significantly prolong survival times compared with patients that were fed a higher phosphorus maintenance food (Elliott et al, 2000; Ross et al, 2006).
Controlled amounts of sodium and chloride help control clinical signs associated with sodium and fluid retention (ascites/oedema) and minimise systemic and kidney hypertension (primary) (Forester et al, 2010).
Protein
Kidney therapeutic foods have reduced levels of protein that help meet nutritional needs while reducing kidney workload. Limiting protein also benefits a cat with proteinuria. Additionally, the protein should be highly digestible and of high biologic value. It is very important that a kidney therapeutic food has enough of all of the amino acids needed for muscle protein synthesis provided in amounts that will be adequate, even if the patient does not always eat 100% of the recommended daily food dose. Just adding more protein will not help preserve muscle mass if all of the essential amino acids are not present in the proper quantities (Forrester, 2010). Cats with CKD may benefit from foods high in L-carnitine. L-carnitine allows cells to spare muscle from being broken down into amino acids to be used for energy by preferentially using fatty acids (Center, 2012). Cats synthesised carnitine from lysine and methionine found in meat and dairy proteins. Carnitine is synthesised in the kidneys. Iron and several vitamins B are required for synthesis of carnitine, therefore it may be limited in sick or anorectic cats (Zoran, 2002).
Antioxidants and omega fatty acids
Antioxidants defend cells from free radical oxidation and promote a healthy immune system. Oxidative damage can contribute to the progression of CKD. Renal oxidative stress has been associated with proteinuria as possible tubulointerstitial damage and advancement of CKD. A study showed cats with CKD supplemented with vitamin E, C and β-carotene had reduced markers of oxidative injury compared with a control food (Forrester, 2010).
Dietary omega-3 fatty acid, e.g. docosahexaenoic acid and eicosapentaenoic acid, supplementation combined with antioxidants can further reduce kidney oxidant injury and is considered renoprotective. In a study using dogs, supplemented with omega-3 fatty acid, there was reduced proteinuria and glomerular hypertension and lower production of proinflammatory eicosanoids. A similar study in cats has not been done, but the author hypothesised that the result would be similar (Forrester, 2010). Supplemental omega-3 fatty acids from fish oil have also shown promise in management of cachexia and sarcopenia (Whitehouse, 2001).
Alkalinisers and buffers
The kidneys excrete dietary acids and play a role in regenerating bicarbonate. Alkalinisers and buffers help to counteract the CKD patient's predisposition to metabolic acidosis, a common complication of CKD. They also help decrease muscle wasting associated with acidosis. Cats with CKD develop metabolic acidosis because of impaired ability of the failing kidneys to excrete the daily net acid load. Plasma bicarbonate, venous blood pH and total CO2 are commonly decreased in cats with uraemia or end stage CKD. Kidney therapeutic foods have ingredients that work to alkalinise the urine and blood, decreasing the dietary acid load (Forrester, 2010).
Potassium
Hypokalaemia is frequently a complication of CKD. Inadequate potassium intake, acidifying diets, or increased urinary losses are all potential reasons for hypokalaemia in CKD patients, as are vomiting and inappetence. The proper maintenance of potassium in the body also helps maintain the quality of life. Loss of potassium leads to functional changes in the kidneys, which includes reduced glomerular filtration rate and urine concentrating ability (Forrester, 2010).
B vitamins
B vitamins help compensate for urinary losses due to CKD. Cats with CKD are at risk of deficiency; B vitamin deficiency can be caused by decreased appetite, vomiting, diarrhoea and polyuria. Anorexia associated with CKD may be exacerbated by thiamin and niacin deficiency. It is important not to over supplement this vitamin. Therapeutic CKD foods should provide adequate amounts; there is no need to supplement if the cat is eating enough. Veterinarians may consider supplementing if there is a need, for example, if the cat is anorexic (Forrester, 2010).
The nurse's role
Nurses work with the veterinarian to reinforce, implement and follow up the food recommended for the cat. They accomplish this by working with the cat owner; calculating the feeding amount of the new food, explaining what and why the food is being recommended and answering any questions the owner may have. It is important to recommend a slow transition to a new diet for a cat with kidney disease. Taste can be affected when a cat has kidney disease. Transition should be slow: give increasing amounts of the new food while decreasing the original food, this could take 1 or even 2 months to complete. Cats can have a texture issue, so it is especially important to recommend a transition when offering a texture the cat has not previously been exposed to, for example a cat that has only eaten dry food and is offered canned food may be unwilling to eat it (Roudebush, 2010) It is important for a nurse to follow up with the cat owner to ensure compliance, but more importantly to be a support for the owner and the cat. Cat owners need to know someone is there for them to help with questions or concerns even after the initial visit.
Conclusions
Nutritional management is the single-most effective treatment for CKD in cats (Figure 4). A new test SDMA will help with earlier detection and intervention. Using IRIS staging, treatment may start earlier than previously thought necessary. Early nutritional intervention can drastically alter the course of CKD. This gives cats the opportunity to live longer and with a better quality of life (Roudebush, 2010). Cats with CKD should be on a food that is controlled in phosphorous, sodium, protein, with added L-carnitine, antioxidants, omega-3 fatty acids, alkalinisers, buffers, potassium and B vitamins. Cat owners need to understand the importance of a kidney therapeutic food, how to transition and the treatment recommendations the veterinarian has advised. A nurse's role is to help owners understand what the veterinarian is recommending and help them with questions and support. A cat with CKD can survive a long time, feeding a kidney therapeutic food can help extend quality and length of life (Ross 2006).
