Frequently Asked Questions about Dietary Therapy for Feline Chronic Kidney Disease

Question

Answer

Is chronic kidney disease a single disease entity?

No. Chronic kidney disease is a syndrome resulting from the loss of functioning kidney tissue. It is a heterogeneous syndrome. Many disease processes can result in loss of functioning nephrons (infectious, immune-mediated, degenerative, neoplastic, toxicologic, congenital, metabolic, inherited).

The response to loss of functioning kidney tissue (whatever the cause) leads to a number of adaptive responses of the remaining function nephrons (intrinsic mechanisms) and of other body systems (extrinsic mechanisms) which can lead to further nephron damage and so are termed mal-adaptive and are common therapeutic targets regardless of the initial underlying cause of the chronic kidney disease.

Why is chronic kidney disease so common in elderly cats?

This is a question, the answer to which is not well understood. The kidney of the cat is adapted to produce a highly concentrated urine enabling this animal to live in climates where water is in short supply. It is possible that the process of generating such a concentrated urine means that nephrons in the cat kidney (of which there are 200,000 per kidney to begin with) ‘wear out’ over the life-span of the cat. This coupled with other extrinsic insults to the cat’s kidneys mean that towards the end of its natural life, less than 25% of its functioning nephrons survive. Hence cats start to show clinical signs of chronic kidney disease as they age. This is certainly not the complete story and is purely a hypothesis since the definitive reason for the high prevalence of chronic kidney disease in the cat is not known.

Why is the composition of urine so variable?

The physiological role of the kidney is to balance dietary intake of substances (water, electrolytes and minerals) with non-renal losses and requirements for growth, lactation and other activities such that homeostasis is achieved. Since dietary and water intake vary from one day to the next, urine composition is highly variable so that body fluid composition remains stable and homeostasis can be achieved.

How do we identify IRIS stage I chronic kidney disease patients if they are not azotemic?

It is important to remember that the IRIS staging system is to be applied only to animals in which a diagnosis of chronic kidney disease has been made. In stage I, kidney disease is not diagnosed based on elevated plasma creatinine so some other clinical /laboratory finding indicates the presence of chronic kidney disease. This may be anatomical abnormality of the kidneys identified on physical examination or imaging confirmed by renal biopsy; a persistent inability to concentrate urine effectively with no evidence of an extra-renal problem as a cause of this renal dysfunction; persistent proteinuria with no evidence of extra-renal disease causing this finding or serial increases in plasma creatinine concentration measured sequentially over time (although these are still within stage I range).

In IRIS stage II chronic kidney disease, there are often no outward clinical signs of chronic kidney disease. Is it necessary to alter the diet at this stage?

The goals in managing the chronic kidney disease patient, if the primary underlying cause of the disease damaging the kidney can not be identified, are to improve the quality of life of the patient and to slow intrinsic progression of the disease towards end stage. There is good evidence from naturally occurring feline chronic kidney disease patients that feeding a specifically formulated renal diet increases long term survival and reduces the occurrence of uremic crises. The patients in these controlled prospective clinical trials were in stage II and early stage III chronic kidney disease according to the IRIS classification where the major benefit of feeding formulated diets is in slowing progressive renal injury.

Why are clinical diets beneficial to feline patients in stage II chronic kidney disease?

As the clinical trials that have been conducted have involved diets that differ in a number of respects to standard maintenance diets it is not possible to say for certain which dietary manipulation benefits the clinical patient most at which stage of their kidney disease. It is likely that some of the benefit observed is derived from restricting dietary phosphate intake and limiting whole body phosphate overload.

If cats will not eat specifically formulated clinical diets is there anything that can be done?

Restricting phosphate intake is an important part of managing the cat with CKD. It may be possible to achieve appropriate phosphate restriction for the stage of CKD by adding a phosphate binder to a standard maintenance cat food. This is not as desirable as feeding a specially formulated clinical renal diet. The effect of phosphate binding agents can be monitored by measuring plasma phosphate concentration. The dose of phosphate binder to be mixed with the food will depend on the stage of CKD and the phosphate content of the food and should be titrated to effect (starting at 30 to 60 mg/kg) until plasma phosphate concentration is below the target level (i.e. 1.45 mmol/L, 4.5 mg/dL, for stage II).

Should all cats with chronic kidney disease receive an oral potassium supplementation?

No – this is not necessary provided the cat is being fed a non-acidifying diet with an appropriate level of potassium for an adult cat and has a plasma potassium concentration within the laboratory reference range. About 20% of cats with CKD are hypokalemic at diagnosis and require additional potassium by the oral route to correct this. These cats will have an improved appetite and level of activity. These cats can sometimes maintain plasma [K+] within the reference range when fed clinical renal diets, in which case oral supplementation may not need to be continued. Cats with CKD with normal plasma [K+] which are given oral potassium supplementation merely excrete more potassium in their urine to maintain homeostasis.

Why do clinical kidney diets have lower protein content than standard maintenance diets?

Protein restriction was originally thought to benefit the CKD patient by lowering glomerular capillary pressure and so reducing hyperfiltration associated with the intake of food, particularly consumption of a meal high in protein. Whilst this phenomenon clearly slows progressive renal injury in rats with experimental kidney disease, extrapolation to cats and dogs has not proved appropriate. Feeding a diet restricted in protein in stage II and early stage III is usually undertaken because lowering protein enables diets that are restricted in phosphate to be formulated. Clinical benefits of restricting protein are observed in late stage III and stage IV cases where levels of nitrogenous waste products accumulate and restricting protein intake reduces the formation of nitrogenous waste products, thus reducing clinical signs. Such a benefit is not usually evident until the plasma urea concentration approaches 30 mmol/L (87 mg/dL).

What is the most reliable prognostic indicator in a cat with CKD?

CKD in cats tends to progress at very variable rates such that within a given IRIS stage the survival time from diagnosis is highly variable. The most reliable predictor of rapidly progressive CKD is the severity of proteinuria at initial diagnosis. If the UPC is persistently >0.4 (note low level proteinuria is normal for cats with CKD) this is a poor prognostic indicator and survival time is highly likely to be much shorter than cats with UPCs <0.2. Cats with UPCs >0.4 are also likely to benefit most from anti-proteinuric therapies although this remains to be documented by a randomized controlled prospective clinical trial.