Page 754 - Small Animal Clinical Nutrition 5th Edition

782 Small Animal Clinical Nutrition

VetBooks.ir Table 37-10. Summary of evidence for treatments of chronic kidney disease.

Dogs
Cats
Grade I
Some therapeutic renal foods (for prolonging survival time and Grade I
Some therapeutic renal foods (for prolonging survival time and
increasing quality of life when serum creatinine [SCr] >2 mg/dl) increasing quality of life when SCr >2 mg/dl)
Calcitriol (for prolonging survival) ACE inhibitor (benazepril) (for reducing proteinuria; increasing
ACE inhibitor (enalapril) (for reducing proteinuria)* appetite in cats with urine protein-creatinine ratios ≥1)*
Grade II Grade II
ACE inhibitor (enalapril) (for delaying progression)* –
Grade III Grade III
Recombinant human erythropoietin (for correcting anemia) Some therapeutic renal foods (for prolonging survival time)
Dietary phosphorus restriction (IRIS stages 3 and 4) Dietary phosphorus restriction (IRIS stages 3 and 4)
Omega-3 fatty acid supplementation (IRIS stages 3 and 4) Recombinant human erythropoietin (for correcting anemia)
Amlodipine (for controlling hypertension)
Potassium supplementation (for correcting hypokalemia)

Grade IV Grade IV
Therapeutic renal foods (for delaying progression when Therapeutic renal foods (for delaying progression when
SCr is <2 mg/dl) SCr is <2 mg/dl)
Subcutaneous fluid therapy (for maintaining hydration) Subcutaneous fluid therapy (for maintaining hydration)
ACE inhibitors (non-proteinuric) (for delaying progression) ACE inhibitor (benazepril) (for cats without proteinuria)
Antihypertensive therapy (confirmed hypertension) Alkalinizing therapy (acidemia)
Alkalinizing therapy (acidemia) Assisted feeding (anorexia and malnutrition)
Assisted feeding (anorexia and malnutrition) Calcitriol therapy
Phosphate binders (for hyperphosphatemia) Phosphate binders (for hyperphosphatemia)
Others (e.g., enteric dialysis) Potassium supplementation (for cats with normokalemia)
Others (e.g., enteric dialysis)
Key: ACE = angiotensin-converting enzyme, IRIS = International Renal Interest Society, SCr = serum creatinine.
*Combined with feeding a veterinary therapeutic renal food. See Chapter 2 and Table 46-20 for more information about evidence grades
I through IV.

erally results in increased total water intake compared with dry ed to slow progression of CKD on the basis of studies in rats,
food consumption. which revealed that excessive dietary protein consumption was
associated with glomerular capillary hypertension and hyperfil-
Protein tration (Brenner et al, 1982). Decreased dietary protein intake
There is general consensus that avoiding excessive dietary pro- prevents these hemodynamic changes and preserves normal
tein intake is indicated to control clinical signs of uremia in glomerular structure in rats (Brenner et al, 1982). The role of
dogs and cats with CKD; uremic signs most often occur in decreased dietary protein in delaying progression of CKD in
stage 4 disease but may be observed earlier (Polzin et al, 2005; dogs and cats is less clear and has been the subject of numerous
Elliott et al, 2006). Many of the extrarenal clinical and meta- studies and a topic of considerable debate (Polzin et al, 2000;
bolic disturbances associated with uremia are direct results of Finco et al, 1998a) (Box 37-1).
the accumulated waste products derived from protein catabo- Despite the lack of clarity about the effects of dietary protein
lism. Early studies in laboratory animals showed rapid improv- on progression of CKD in dogs and cats, potential benefits
ement when dietary protein was reduced (Klahr et al, 1983; should be considered. Decreased dietary protein intake inhibits
Brenner, 1983). However, urea by itself does not account for all, secretion of TGF-β, a cytokine that may be involved in pro-
if any, of the clinical signs of uremia. Serum urea nitrogen gen- gression of kidney disease (Fukui et al, 1993). (See Etio-
erally is considered to simply be a marker for other more pathogenesis of Chronic Kidney Disease, Tubulointerstitial
important uremic toxins. Excessive dietary protein is catabo- Changes.) Decreased protein intake potentially reduces tubular
lized to urea and other nitrogenous compounds that normally hyperfunction by decreasing the renal acid load and decreasing
are excreted by the kidneys. And, as mentioned above, endoge- renal ammoniagenesis. In general, protein metabolism is the
nous proteins will be degraded if amino acid intake is insuffi- major source of hydrogen ions. Consequently, avoiding excess
cient to maintain nitrogen balance. The goal of managing dietary protein and decreasing endogenous protein catabolism
patients with CKD is to achieve nitrogen balance and limit for energy contribute markedly to the maintenance of acid-base
accumulation of nitrogenous waste products by proportionally balance (Relman et al, 1961). Primary dietary protein contribu-
decreasing protein intake as renal function declines. tions to the renal acid load are from the sulfur-containing
The role of decreased dietary protein intake is less clear in amino acids (methionine and cysteine). Animal proteins tend
patients with CKD that do not have clinical signs of uremia to be higher in sulfur-containing amino acids than plant pro-
(Polzin et al, 2005). Limiting protein intake has been advocat- tein sources. This is true whether the source of the animal pro-