• NAVC Brands
Nutrition, Nutrition Notes

Nutritional Management for Chronic Kidney Disease Versus Acute Kidney Injury

Dietary management is a valuable, and sometimes overlooked, aspect of managing patients dogs and cats with CKD or AKI.

April E. Blong DVM, DACVECC

Dr. Blong is an assistant professor of Small Animal Emergency and Critical Care at the Iowa State University Lloyd Veterinary Medical Center. She completed her residency at Cornell University Hospital for Animals and in 2014 became a Diplomate of the American College of Veterinary Emergency & Critical Care. Her professional interests include acute kidney injury, mechanical ventilation, nutrition, and sepsis.

Nutritional Management for Chronic Kidney Disease Versus Acute Kidney Injury

Over the past 3 decades, attention has been drawn to the differences between chronic kidney disease (CKD) and acute kidney injury (AKI). These conditions differ not only in pathophysiology, diagnosis, and treatment but also in nutritional management. This article focuses on the nutritional management of veterinary patients with each condition (Table 1).

CKD is a well-recognized entity in veterinary medicine; feeding strategies to slow its progression have been known for almost a century. The International Renal Interest Society (IRIS) estimates that CKD affects 0.5% to 1% of all dogs and 1% to 3% of all cats; however, prevalence increases with age.1 With appropriate management, including dietary modification, animals with CKD can survive years with elevated serum creatinine levels.2

AKI is a growing area of concern in both human and veterinary medicine. IRIS guidelines define AKI as being present when a patient’s creatinine level increases by as little as 0.3 mg/dL, even if still within the reference range.3 Although the true incidence of AKI remains unknown, it has now been established that AKI is probably underrecognized and, regardless of recognition, substantially affects morbidity and mortality rates.4


Effective dietary strategies for patients with CKD include protein restriction, phosphorus restriction, modest salt restriction, and provision of omega-3 fatty acids. Although some supplements have been marketed to improve outcome in patients with CKD, there is little clinical evidence supporting their efficacy.


The quality of life for CKD patients is significantly affected by uremia. Uremia occurs secondary to the accumulation of waste products associated with protein catabolism and results in clinical and metabolic disturbances.5 A strong level of evidence for human patients and some evidence for veterinary patients indicates that reducing dietary protein intake slows the progression of kidney disease.6 Protein restriction has become a mainstay in the treatment of CKD in dogs and cats and is recommended for patients with IRIS stage 2 CKD and above.7,8 Restricted dietary protein intake reduces clinical signs associated with uremia, especially as CKD progresses. Protein restriction has also been shown to reduce proteinuria in animals with glomerular disease, probably associated with the effects of protein on intraglomerular pressure.5 Because proteinuria causes progressive renal injury, limiting proteinuria is beneficial.5 Although protein restriction is helpful, it should not be too extreme or the patient will begin catabolizing lean body mass to meet protein requirements. The minimum protein levels recommend by the Association of American Feed Control Officials (aafco.org) are 18% dry matter for healthy dogs and 26% for healthy cats. However, most popular brands of pet food far exceed these levels. TABLE 2 lists the recommended levels of protein and other nutrients for animals with CKD.


Another nutritional management component for patients with CKD is phosphorus restriction. Limiting phosphorus intake helps limit hyperphosphatemia and renal secondary hyperparathyroidism and slows CKD progression,5 although the reason for delayed progression of CKD is not entirely clear. If dietary management alone is not sufficient to maintain phosphorus at normal levels, then oral phosphate binders should be administered to try and maintain acceptable plasma levels, per IRIS guidelines.7,8

Sodium and Chloride

Although not proven, reducing sodium and chloride intake may be beneficial for CKD patients. As glomerular filtration rate decreases, the kidneys are not as readily able to alter sodium excretion, potentially leading to sodium and water retention and resultant hypertension. Systemic hypertension has many deleterious effects, including on the kidney itself. Chloride, especially at high levels, may also have negative effects on renal blood flow.5

Fatty Acids

Omega-3 fatty acids have a variety of potential benefits for kidney function. They can decrease platelet aggregation, increase renal blood flow, decrease blood pressure, have antioxidant effects, and decrease the proliferation of glomerular mesangial cells. Adequate levels of the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid compete with the omega-6 fatty acid arachidonic acid for use by cyclooxygenase, which results in production of different eicosanoids. This altered eicosanoid profile is considered to be renoprotective.5 However, the ideal dosage for omega-3 fatty acids and ideal ratio of omega-6 to omega-3 fatty acids have not yet been determined.

Fortunately, a variety of diets that address the dietary needs of dogs and cats with CKD are commercially available. Apart from palatability for individual patients, one veterinary prescription diet is not recommended over another. However, as CKD progresses and becomes more severe, a diet with more protein restriction to further control the clinical signs of uremia may be useful.5


Recommendations surrounding the dietary management of patients with AKI are still evolving, but early provision of calories—especially via the enteral route—and adequate amounts of protein are strongly recommended.

AKI differs somewhat from CKD in that not only does kidney function decline, but it occurs in the presence of critical and/or systemic illness as well. There is not necessarily a correlation between the degree of creatinine elevation and the level of illness. For example, a dog with leptospirosis whose baseline creatinine increased from 0.7 mg/dL to 2 mg/dL may be at as much risk for disease progression as a dog with the same pathologic changes and a creatinine of 6 mg/dL. Both conditions warrant aggressive treatment and monitoring to try and preserve remaining renal function and allow the kidney to repair itself over time. During disease states, metabolism undergoes significant alterations that cause rapid and substantial catabolism of lean body mass. Furthermore, there is already a large and continually growing body of evidence that outcomes for critically ill patients are better when enteral nutrition is provided.9,10

Some patients with AKI from prerenal causes only (e.g., dehydration) or postrenal causes (e.g., urethral obstruction) may be in a noncatabolic state. For these patients, AKI typically resolves rapidly after rehydration or alleviation of the obstruction. The prognosis for these patients—from the standpoint of azotemia resolution—is good, and hospitalization duration is typically short. For this subset of patients, specific dietary considerations are probably not necessary. Each patient should be evaluated individually for degree of systemic illness, which should be addressed accordingly.


Patients with AKI are substantially more likely than CKD patients to be critically ill, especially if they have intrarenal injury; as such, they tend to use more protein and are typically in a catabolic state.6 Because protein/calorie malnutrition is an independent risk factor for death in patients with AKI,9 waiting for voluntary intake to be adequate is often unacceptable. Even if a patient with AKI is eating voluntarily, the amount ingested should be quantitated to ensure that it is meeting resting energy requirements (RER) for that patient (TABLE 3). Patients who do not voluntarily consume their RER for more than 48 hours should immediately receive assisted feeding via tube feeding. Remember that most patients are inappetent or anorexic before presentation, and this time should count toward that 48-hour window. Appetite stimulants are reasonable to try but should not delay the implementation of assisted feeding. Although enteral nutrition can be started gradually, the goal should be to get to full RER as quickly as possible. Aggressive management of gastrointestinal intolerance (high gastric residual volumes, vomiting, regurgitation) by using antiemetic and/or promotility agents may be necessary. Enteral nutrition is always preferred to parenteral nutrition if at all feasible.6,11


Protein restriction is not recommended for patients with AKI, especially because some of these patients will be in a hypercatabolic state.9 Although the ideal protein requirement of AKI patients is unknown, recommendations for humans are to feed at least what a healthy person requires for maintenance. For veterinary patients, the volume of feeding should be accounted for as part of fluid intake, and careful attention to fluid balance is necessary to avoid overhydration, which is associated with worse outcomes in patients with AKI.12,13


Although attention to electrolyte levels is important and efforts should be made to maintain reference levels, it is more important that the patient receives adequate calories than the most balanced or appropriate diet for their condition.11 If the patient is hyperphosphatemic after they are otherwise stable, it is reasonable to start oral phosphate binders rather than a phosphate-restricted diet. Although phosphate contributes to acidemia, it has not been proven that controlling phosphate levels is beneficial for patients with AKI.13 Certainly, if oral phosphate binders are resulting in food aversion or reduced willingness to eat, then they should be withheld. If a feeding tube is in place, medications, including phosphate binders, can be given via the tube when possible to limit aversion to eating.

Commercial and Home-Cooked Diets

No single diet can be recommended for AKI patients, but prescription diets intended for the management of CKD are not recommended. If the patient is eating voluntarily, then whatever the patient will eat is probably reasonable. For short-term use, temporary home-cooked diets that combine a lean protein source (e.g., hamburger, fish, egg) and a carbohydrate source (e.g., pasta, rice, potato) in equal portions may be used. Part of diet choice will be dictated by the limitations of whatever assisted feeding device is used (i.e., a liquid diet for nasogastric feeding tubes versus a canned food slurry for larger esophagostomy or gastrostomy tubes).


Outcomes for AKI patients are many, including return to baseline or preinjury creatinine levels, partial resolution with or without ongoing CKD (persistently elevated creatinine level), or death. One question that is often posed revolves around protein for patients who survive AKI but have resultant CKD. If we should not restrict protein for AKI patients but we should restrict protein for CKD patients, when does that crossover occur? Although for some patients serum creatinine (i.e., kidney function) improvements have been documented for several months after an AKI event, guidelines typically define azotemia persisting beyond
3 months from an AKI event as ongoing CKD.13 Therefore, it is reasonable to consider transitioning an animal that survives AKI but has resultant CKD to a renal diet 3 to 4 months after the AKI event.


Although beyond the scope of this article to cover in depth, one often overlooked intervention is assisted feeding. Numerous studies of acutely ill patients have demonstrated that early enteral nutrition generally decreases the manifestation of infections and other complications, reduces the risk for disease state worsening, and may decrease hospitalization times and mortality rates. In the hospital, nasogastric feeding tubes are quick and easy to place but should be used only for the short term (i.e., for AKI patients). For intermediate to long-term needs, esophageal and gastrostomy tubes can be used in the hospital or at home (for AKI and CKD patients). For patients who do not tolerate prepyloric feeding during acute illness, esophageal or gastric tubes with a jejunostomy tube inserted through them can be useful.

For patients with CKD, feeding tubes should also be considered for medication administration and fluid support in the form of enteral water supplementation (as opposed to subcutaneous fluid administration). For patients with AKI, assisted feeding should be implemented to limit catabolism of lean body mass if intake has been inadequate for more than 48 hours. One of the limitations to discharging a patient with AKI from the hospital is the need to gradually taper fluid therapy. Having a long-term feeding tube in place for AKI patients is helpful because it enables clients to provide water enterally at home. The ability to potentially give relatively large volumes of fluid enterally can allow some patients to be discharged sooner because the patient does not need to be fully tapered from fluid support before going home. Feeding tubes can give clients a “no fuss” and consistent way to administer medications, feedings, and enteral fluids to their pets, which can reduce stress on both the patient and the client and help preserve the human–animal bond.


Nutrition is a valuable, and sometimes overlooked, aspect of managing AKI and CDK patients. Although a variety of commercial diets are available for CKD patients, no specific diets are designed for AKI patients. Fortunately, many maintenance or recovery diets are probably adequate for AKI patients. The most important consideration for patients with AKI is to ensure adequate provision of calories, ideally via the enteral route, early during hospitalization, even if that means using some type of feeding tube.


1. Roura X. Risk factors in dogs and cats for the development of chronic kidney disease, updated 2019. International Renal Interest Society. iris-kidney.com/education/risk_factors.html. Accessed April 2020.

2. Boyd LM, Langston C, Thompson K, et al. Survival in cats with naturally occurring chronic kidney disease (2000-2002). J Vet Intern Med 2008;22(5):1111–1117.

3. Cowgill L. Grading of acute kidney injury. International Renal Interest Society. iris-kidney.com/pdf/4_ldc-revised-grading-of-acute-kidney-injury.pdf. Accessed April 2020.

4. Harison E, Langston C, Palma D, Lamb K. Acute azotemia as a predictor of mortality in dogs and cats. J Vet Intern Med 2012;26(5):1093-1098.

5. Forrester SD, Adams LG, Allen TA. Chronic kidney disease. In: Hand MS, ed. Small Animal Clinical Nutrition, 5th ed. Topeka, KS: Mark Morris Institute; 2010:765–810.

6. Kalantar-Zadeh K, Moore LW. Why the nutritional management of acute versus chronic kidney disease should differ. J Ren Nutr

7. International Renal Interest Society. Treatment recommendations for CKD in dogs. iris-kidney.com/pdf/IRIS-DOG-Treatment_Recommendations_2019.pdf. Accessed April 2020.

8. International Renal Interest Society. Treatment recommendations for CKD in cats (2019). iris-kidney.com/pdf/IRIS_CAT_Treatment_Recommendations_2019.pdf. Accessed April 2020.

9. Kellum JA, Lameire Nl. KDIGO clinical practice guideline for acute kidney injury. kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf. Accessed June 2020.

10. Pan LL, Li J, Shamoon M, et al. Recent advances on nutrition in treatment of acute pancreatitis. Front Immunol 2017;8:762.

11. Nutritional considerations in adult patients with acute kidney injury. Think Kidneys. thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/
. Accessed April 2020.

12. Labib M, Khalid R, Khan A, Khan S. Volume management in the critically ill patient with acute kidney injury. Crit Care Res Pract 2013;2013:792830.

13. Langston C, Eatroff A. Acute kidney injury. In: Little SE, ed. August’s Consultations in Feline Internal Medicine, Vol. 7. St. Louis, MO: Elsevier; 2016:483-498.