The dietary therapy is often considered the core of the treatment of small animals with renal diseases. However the level of evidence of most dietary interventions remains low and is typically based on pathophysiological justifications and on extrapolation from other species. The dietary therapy is rarely designed individually with clear treatment goals and monitoring tools for re-evaluation. The oversimplification of the concept of "renal diet for renal disease" should therefore be reviewed and take in consideration the various types of renal diseases and their degree of affection.
Chronic Kidney Disease (CKD)
The essential role of the diet in CKD is exemplified by the fact that the first commercially available prescription diet has been elaborated to decrease the uremic complications of advanced renal failure. Lower dietary protein decreases generation of urea and of other metabolic waste products associated with the clinical manifestations of uremia. The exact nature of these uremic toxins and their mechanisms of toxicity remain elusive, but uremia seems to correlate with the serum urea concentration, a surrogate marker for other protein-derived uremic toxins. Although protein restriction is considered essential in advanced renal disease, the level of restriction and the stage of CKD at which it is indicated are still debated. Protein restriction is not the only characteristic of modified protein (renal) diets and their efficacy to combat uremia cannot be attributed solely to their lower protein content. An important goal in early disease is not a decrease of the uremic manifestations (since these animals are not truly uremic) but the slowing down of the natural progression of CKD towards endstage disease. Dietary manipulations have been shown to reach this goal by decreasing glomerular hypertension, hyperfiltration, hypertrophy, and proteinuria and by improving renal hemodynamics. The administration of a renal diet to animals with CKD stages 2–3 markedly prolonged their renal and overall survival, it decreased the rate of decline of renal function, and it delayed the onset of uremic crises. These findings, although they don't answer the central question of the mechanism of protection, show the value of early dietary intervention in animals with CKD. In a study evaluating the metabolism of urea in dogs with CKD, we showed that dogs with more advanced CKD displayed a marked increase in their extrarenal (GI) excretion of urea and a marked increase in their endogenous urea generation (catabolism). However a practical approach to quantify under clinical conditions the effect of protein restriction on metabolism is still lacking and the clinicians are usually limited to evaluate indirect evidence such as rate of progression, serum albumin concentration, proteinuria, and body condition score.
In summary, we have evidence supporting the use of modified protein (renal) diet in dogs and cats with CKD stages 2–3, but we do not know: 1) whether intervention in stage 1 would be more beneficial; 2) whether all renal diets are equal in efficacy; and 3) what in the renal diet is truly beneficial.
The design of homemade diets individually tailored to fit the taste of animals with CKD can be tempting but it is particularly difficult since we do not know the optimal composition of such a diet. Next to protein modification, phosphorus restriction, alkalinizing properties, addition of antioxidants, and inclusion of n-3 fatty acids are likely to be critical for slowing disease progression. In advanced CKD, dietary changes are more difficult and affected animals are less likely to accept diets to which they have not been used. Feeding these animals necessitates either a compromise with more palatable (and less optimal) diets or the use of assisted feeding strategies. The acceptance of feeding tubes is certainly viewed by some owners as artificial life support. However, esophagostomy tubes or PEG tubes can markedly improve the quality of life of small animals with advanced CKD. Administration of additional water to help maintaining optimal hydration, ease and reliability of administration of medications, and administration of the qualitatively ideal food in sufficient quantity are major benefits of tube feeding. The use of this type of nutritional support is the only way to push the limits of the medical management without compromising the animal's quality of life. The personal and time involvement of the owner for the tube feeding should however not be underestimated and clearly explained.
Acute Kidney Injury (AKI)
Dogs and cats with AKI have very different nutritional requirements and goals. Provision of adequate nutrition has been linked to better recovery rates in humans with AKI and it is likely to be similar in small animals. Prospective studies are however difficult to design with sufficient statistical power considering the lack of uniformity in the underlying etiology, the variable degree of function loss, and the paucity of clinical material. Recommendations are therefore mostly based on anecdotal observations and indirect evidence. A catabolic condition is unlikely to be suited for adequate tissue repair and renal recovery. Dogs with severe AKI are however commonly observed to lose 5–10% of their dry body weight during the first week of therapy despite active support, suggesting significant catabolism. Since appetite is rarely the first body function to recover in AKI, aggressive nutritional support is indicated from the first day of the disease using an enteral and/or parenteral approach to overcome the marked gastrointestinal disturbances. Renal replacement therapies improve appetite within a few days, but they also cause additional nutrient losses as filtered amino acids that should be compensated with early nutritional support. Temporary feeding tubes are typically used in these dogs, including E-tubes or the more recently described esophago-jejunostomy tubes.
The qualitative nutritional requirements are even more poorly characterized in dogs and cats with AKI. A high quality, highly digestible, and fat-restricted diet may help to accelerate gastric emptying and decrease nausea. These diets are commonly less calorie dense, but they could be a reasonable start for the first days of therapy. Renal diets with high energy density may prove useful in a second phase to better cover the animal's caloric needs. Recommendations concerning the ideal protein content vary widely from reduced (to decrease uremic signs) to increased (to improve renal recovery) and clearly lack consensus, although evidence is slowly accumulating against protein restriction. Energetically dense recovery diets can be used occasionally in animals with AKI but caution should be observed because of their high fat content.
In summary, the design of a nutritional plan for an animal with AKI should be based on individual parameters including the degree of GI disturbances, the degree of metabolic derangements, the degree of renal impairment, the type of therapy provided, and the degree of water, electrolyte, mineral, and acid-base disturbances. Daily reassessment of nutritional adequacy is mandatory since regular corrections and adaptations are the rule.
Urinary protein losses lead to protein malnutrition and weight loss and account for the main manifestations of these diseases. Dietary intervention is therefore essential for the management of affected animals. Previous recommendations with increased dietary protein to compensate for their loss tend to increase the proteinuria and the resulting protein balance is even more negative. Current recommendations of the IRIS canine GN study group include a seemingly paradoxical moderate (high-quality) protein restriction and the resulting decrease in proteinuria tends to improve the animal's nutritional status and to create a more positive protein balance. The decreased proteinuria also has a renoprotective effect, diminishing the secondary tubulo-interstitial damage and the progression to azotemia and end-stage renal disease. Since the individual protein requirement is difficult to evaluate for clinical patients, regular assessment of the animal's clinical and laboratory status, haircoat, and lean body mass is essential. N-3 polyunsaturated fatty acids have many features beneficial for animals with glomerular diseases: they are antiinflammatory; they decrease proteinuria; they are antihypertensive; and they are beneficial for restoring normal renal hemodynamics. Since most renal diets have increased n-3/n-6 ratios, it is unclear what benefit additional administration can potentially bring. Additionally, the study group recommends feeding diets with reduced salt content in affected dogs.
In conclusion, dietary interventions are central for the therapy of most renal diseases. A clear understanding of the metabolic derangements resulting from the disease and of the potential benefits of the dietary changes is essential for appropriate interventions. Similarly to most other forms of therapy, setting clear and realistic nutritional goals for the treatment and for its monitoring is necessary for an optimal support.
1. Steinbach S, et al. Quantitative assessment of urea generation and elimination in healthy dogs and in dogs with chronic kidney disease. J Vet Intern Med. 2010;24(6):1283–1289.
2. Hinden S, et al. Evaluation of an esophago-jejunal feeding technique in dogs with severe acute kidney injury. In: Proceedings from the ACVIM. 2013. Abstract.
3. Brown S, et al. Consensus recommendations for standard therapy of glomerular disease in dogs. J Vet Intern Med. 2013;27:S27–S43.