Dietary management is very important in the management of renal disease in older animals due to the effect that diet has on:
- · calorie intake
- · renal blood flow
- · uraemia
- · nephrocalcinosis
- · urine pH.
All animals have a requirement for energy which has to be met by dietary intake. The energy requirements of animals during their life cycle stages have been reasonably well established (NRC 1986) but the energy requirements of animals with renal disease have yet to be accurately determined.
Assessing the body weight of an animal is important in estimating the calorie requirements of an individual. A reduction in calorie intake should be considered for animals that are obese, and calorie intake should be increased for animals that are underweight. Cats and dogs with renal disease frequently present in a catabolic state and they need a high calorie intake to maintain body functions and to restore normal body weight. This may not be easy to achieve, as animals in a debilitated state or with azotaemia are frequently anorectic.
Uraemic animals may vomit any food that is eaten, and in the presence of concomitant gastrointestinal or hepatic dysfunction, ingestion may not guarantee adequate utilisation of the food. The diet for such cases should therefore be high in energy density and digestibility to minimise the amount of food that the animal has to digest and absorb. Feeding small volumes of food frequently (3-4 times daily) may improve utilisation.
Hand feeding, warming the food and sometimes the administration of diazepine drugs (e.g. diazepam at a dose rate of 2-14 mg/kg orally (dogs) or 1-2 mg/cat orally or 0.1-0.5 mg/cat given intravenously; or oxazepam at a dose rate of 2 mg/cat orally) may encourage eating in anorectic patients (). Diets claiming good palatability should be selected carefully to avoid those containing high levels of nutrients (e.g. salt) that might be contraindicated in the presence of renal disease.
Studies in man have demonstrated an improvement in ability to mainnitrogen equilibrium by increasing the calorie intake of uraemic patients on a low-protein, high biological value protein diet ().
A high calorie-dense diet reduces the amount of food that has to be eaten to meet daily energy needs, and this can be helpful in reducing the total intake of specific nutrients that have to be controlled, e.g. phosintake will be less if less food is eaten.
Cats, being obligate carnivores, have a high requirement for energy from dietary protein. In the presence of inadequate protein-calories a cat will breakdown its own body protein to produce energy, hence severe dietary protein restriction is not as feasible in the cat as it is in the dog.
Renal blood flow
Loss of renal function is commonly slow and progressive with a profall in glomerular filtration rate (GFR) caused by increasing loss of functional nephrons. One mechanism by which this progress is believed to occur is the ‘hyperfiltration theory’ (). This theory is based upon the increased workload on functioning nephrons, in kidneys in which renal reserve has been lost due to injury. Under such circumstances surviving nephrons are subjected to intraglomerular hypertension and hyperperfusion which can result in glomerular injury (sclerosis) and further loss of function.
Ingestion of a meal causes a postprandial increase in renal perfusion and filtration and by cumulative effect this is thought to be responsible for hyperfiltration and the<renal hypertrophy seen in animals maintained on high protein diets. In the dog changing from a carbohydrate to a meat diet increases renal blood flow and filtration rates by as much as 100% (). This increase in renal blood flow is thought to be mediated by a hormone (e.g. glucagon) or other factor ().
In the presence of decreasing renal function, therefore, feeding a low protein diet is indicated to decrease further glomerular damage caused by the above effects on renal haemodynamics.
It has also been suggested that augmented intrarenal pressures and flows associated with ad libitum feeding might contribute to age-related glomerular sclerosis (), but whether or not diet induced changes can result ultimately in disease, remains controversial.
In experimental models reducing dietary protein intake has been assowith decreased progression of renal haemodynamics () and improved longevity (). Other studies have demonstrated accelerated glomerulosclerosis in uninephrectomised rats fed high protein diets () and retardation of the progression of renal failure in rats (), and in mice (), by feeding a protein restricted diet.
Increasing glomerular pathology as evaluated by light microscopy (including glomerulosclerosis) has been reported in nephrectomised dogs fed increasing levels of dietary protein (). Several studies in dogs with renal failure have shown that dietary protein restriction reduces proteinuria, an indicator of glomerular injury () and recent studies show that glomerular hyperfiltration may promote the development of glomerular sclerosis in dogs with chronic renal failure ().
In humans a prospective, randomised study has recently been reported () after which the authors concluded that dietary protein restrictions was effective in slowing the rate of progression of chronic renal failure.
Protein malnutrition has been shown to be unlikely to occur on a protein intake of more than 1.9 g protein/kg body weight per day in dogs with chronic renal failure (). Protein intake below this amount did not further reduce hyperfiltration and hence would be of no additional benefit in reducing glomerular injury.
Systemic hypertension has been reported in dogs with acute and subinterstitial nephritis () and in 58-93% of dogs with renal failure (). The presence of systemic hypertension may result in intraglomerular hypertension, although it is not necessarily present for the development of the laffer. Animals with renal insufficiency are unable to regulate sodium excretion properly, however net loss of sodium (sodium dumping) was not demonin one study in which sodium intake was decreased abruptly in nephrectomised dogs (). Currently it is recommended that the sodium intake for dogs and cats with renal disease be limited to 0.1-0.3% in dry mailer, which is considerably less than the levels in most commercial pet foods ().
Sodium supplementation is contraindicated, though this was once commonly recommended.
Maintaining blood haemodynamics to avoid hypoperfusion and ischaemia is an important objective in the management and prevention of acute renal failure, and interestingly it has recently been suggested that limiting protein intake might reduce the susceptibility of renal tubular cells to nephrotoxic or ischaemic stress, such as occurs in renal failure ().
Uraemia is a common occurrence in renal disease, and urea itself may increase renal blood flow, thus having an effect on renal haemodynamics.
The uraemic syndrome results from an inability of the kidney to excrete nitrogenous waste products including urea, and other toxins. Reduction of dietary intake of protein reduces the quantity of circulating proteinaceous waste products and has been shown in many studies in rats, people and dogs to result in marked clinical improvement, increased survival and preserved renal function. A comprehensive reference list has been published ().
It has been shown that people () and dogs () with renal failure have a higher requirement for protein than normal individuals and the amount of protein needed will depend upon the severity of the renal dysfunction and the digestibility and quality of the protein in the food. The aim therefore is to feed sufficient high biologic value protein to meet the animal’s requirements, but to maintain a blood urea level of 60 mg/dl (10 mmol/l) or less. Approximations of the amount of protein needed in dogs with renal failure to achieve this have been published ().
Clinical signs attributable to uraemia should be controlled at a BUN of less than 60 mg/dl (10 mmol/l).
With decreasing renal function the kidney becomes less able to:
- · degrade parathyroid hormone
- · excrete phosphorus
- · convert vitamin D to its active form.
Reduction in these activities results in bone demineralisation or osteodystrophy and mineral deposition in soft tissues, including the kidneys themselves, which further reduces function. This mineral deposition can occur at normal plasma calcium and phosphorus concentrations in damaged renal tissue, and it can be an early morphological abnormality in animals with renal insufficiency.
Dietary phosphorus restriction has been reported to reduce nephrocalcinosis and osteodystrophy even in mild renal insufficiency before increased plasma phosphorus levels (). Plasma phosphorus concentrations should be kept at 5.0 mg/dl (1.6 mmol/l) or less, and plasma calcium levels at 10 mg/dl (2.5 mmol/l) or more, with a solubility factor for the two of less than 55 ().
Phosphorus restriction significantly reduced the degree of tissue mineralisation in nephrectomised cats when compared with cats fed a normal diet (), and high phosphorus intake in nephrectomised dogs resulted in hyperparathyroidism and severe bone deminerialisation as compared with dogs with reduced phosphorus intake ().
Studies in cats and dogs have demonstrated that phosphate binders are ineffective at the commonly used dosages if diets with unrestricted phosphorus content are fed.
Acidosis may occur with oliguria or severe polyuric renal failure and is due to reduced excretion of sulphates, phosphorus, organic acids, hydrogen and ammonium ions. Metabolic acidosis enhances osteodystrophy and protein catabolism.
Acidifying diets should be avoided in animals with renal failure.
When considering the most appropriate dietary regimen for an individual case it is important to perform a full and detailed clinical examination, because renal disease may be associated with concomitant disease in other organ systems, e.g. pyometra () and heart failure () which may influence dietary choice.
Renal disease increases in incidence with increasing age () and so it frequently occurs in individuals that also have compromised cardiac, hepatic or other organ function. The most serious disorder will usually be managed first.
Complications may even occur within the urinary tract itself. For example, renal failure precipitated by urinary tract obstruction due to a struvite urolith, presents the clinician with a dilemma, because the diet of choice for renal failure is not ideal for the management of struvite urolithiasis. In such circumstances the clinician needs to use his/her clinical judgement to manage the case most effectively.
Summary of dietary management
1. Chronic renal failure
Feed a diet that is:
- · high in energy-density
- · low in protein content (contains high biological value protein)
- · low in phosphorus content
- · low in sodium content
- · buffered against acidosis.
e.g. Prescription Diet Canine or Feline k/d; Prescription Diet Canine u/d (Hill’s Pet Nutrition).
2. Glomerular Disease (nephrotic syndrome)
Protein loss into the urine accompanies glomerular disease and may lead to hypoproteinaemia. Feed a diet with the same profile as that listed above for chronic renal failure. It used to be advised that extra high biological value protein in the form of whole egg or cottage cheese should be added if the animal developed hypoproteinaemia, however recent evidence suggests that increasing dietary intake of protein only results in increased urinary excretion. Furthermore the effect of the increased protein on renal haemodynamics () might make this practice more harmful than beneficial.