Page 766 - Small Animal Clinical Nutrition 5th Edition

794 Small Animal Clinical Nutrition

with uremic signs or endstage disease (Lulich et al, 1992; function. Calcitriol acts by decreasing PTH messenger RNA
VetBooks.ir Elliott and Barber, 1998; Elliott et al, 2003, 2003a). The kid- expression, increasing expression of vitamin D receptors and
controlling the “set point” of chief cells, which determines
neys play an important role in regenerating bicarbonate and
responsiveness to negative feedback by ionized serum calcium
excreting dietary acids, which may be derived from several
sources. Sulfuric acid is formed when sulfur-containing amino concentrations. Decreased circulating calcitriol levels in CKD
acids (i.e., methionine and cysteine) are oxidized to sulfate. In lead to chief-cell hyperplasia and increased secretion of PTH.
general, animal-source proteins are higher in sulfur-contain- Increased PTH levels have been suggested to play a role in the
ing amino acids than are plant-source proteins. Exogenous- severity of clinical signs and progression of CKD (Nagode and
and endogenous-source proteins are equally important. Chew, 1992).
Insufficient energy intake results in protein catabolism and Avoiding excessive dietary phosphorus and using phosphate
increased hydrogen ion production. Urinary urea production binders reduce the inhibitory effects of hyperphosphatemia on
and total urinary hydrogen ion excretion are directly propor- renal 1-α-hydroxylase activity, thereby increasing calcitriol pro-
tional. Organic acids are produced from partial oxidation of duction by tubular cells. Oral administration of low doses of
carbohydrates, fats, proteins and nucleic acids. Phosphoric calcitriol is associated with decreased serum PTH concentra-
acid can be ingested in the food or it can be produced endoge- tions. Strong evidence supports the use of calcitriol therapy for
nously. Phosphoric acid is used in some cat foods as a palata- slowing progression of CKD in dogs but not in cats (Polzin et
bility enhancer, either separately or as a component of topical- al, 2005a; Polzin, 2007). The effect of varying vitamin D levels
ly applied animal digests. Phosphoric acid can be derived in foods has not been studied; therefore, it is not included as a
from hydrolysis of phosphate esters in proteins and nucleic key nutritional factor.
acids, if they are not neutralized by mineral cations (e.g., sodi-
um, potassium and magnesium). The contribution of dietary B Vitamins
phosphate to acid production depends on the type of protein Limited information exists concerning vitamin nutrition in
ingested. Some proteins generate phosphoric acid, whereas dogs and cats with CKD; however, these patients are at risk for
others generate only neutral phosphate salts. Hydrochloric B-vitamin deficiency because of decreased appetite, vomiting,
acid is generated when positively charged cationic amino diarrhea and polyuria. Human patients with CKD apparently
acids (e.g., lysine and arginine) are broken down into neutral are especially prone to pyridoxine and folate deficiency
products. (Gilmour et al, 1993).Thiamin and niacin deficiency may con-
Some commercial veterinary therapeutic renal foods are for- tribute to anorexia associated with renal failure. Empirical
mulated with combinations of ingredients that will alkalinize administration of vitamins seems appropriate in anorectic pa-
the urine and blood, which minimizes dietary acid load tients with CKD. However, care must be taken to avoid exces-
(Burkholder et al, 2000). These foods are limited in protein sive amounts of fat-soluble vitamins. Patients eating adequate
ingredients, particularly those that are high in sulfur-containing amounts of commercial veterinary therapeutic renal foods are
amino acids. For patients with CKD, the serum total CO 2 unlikely to need B-vitamin supplementation.
should be maintained within the reference range for healthy
patients. Ideally, blood gas analysis should be done to more Trace Minerals
accurately confirm the presence of metabolic acidosis. As CKD Presumably, CKD alters metabolism of trace minerals. For
progresses and acidosis becomes more severe, alkali therapy example, nutrients such as copper and zinc that are highly
(e.g., sodium bicarbonate, potassium citrate) should be consid- bound to protein may be lost with severe proteinuria.
ered in addition to nutritional management. Although urinary Aluminum may accumulate in human patients with CKD
pH may be used as an indirect assessment of acid/base status, who are treated with aluminum-containing phosphate
monitoring venous blood gases is a more sensitive method to binders. Aluminum toxicity can cause metabolic bone disease,
evaluate effectiveness of alkalinization therapy. encephalopathy and anemia. However, exact data are not
available to support making a routine recommendation for
Vitamin D dietary trace mineral modification for dogs and cats with
Calcitriol (1,25-dihydroxyvitamin D) plays an important role CKD. There are no reports of trace mineral problems in dogs
in the pathogenesis of secondary renal hyperparathyroidism. and cats with CKD that eat commercial veterinary therapeu-
Patients with severe CKD have decreased circulating levels of tic renal foods.
1,25-dihydroxyvitamin D because of decreased synthesis by the
kidney. Hyperphosphatemia and the progressive loss of renal Soluble Fiber
epithelial cells inhibit conversion of 25-hydroxyvitamin D to It is well established that soluble fiber causes bacterial prolifer-
calcitriol by renal 1-α-hydroxylase. At earlier stages of CKD, ation in the colon. Bacterial growth requires a source of nitro-
circulating levels of 1,25-dihydroxyvitamin D may be normal gen. Although dietary protein provides some nitrogen, blood
due to the compensatory effect of increased concentrations of urea is the largest and most available source of nitrogen for bac-
PTH on renal 1-α-hydroxylase activity and tubular synthesis of terial protein synthesis in the colon (Younes et al, 1995). Urea
1,25-dihydroxyvitamin D. is the major end product of protein catabolism in mammals.
Calcitriol is an important regulator of parathyroid chief-cell When blood urea diffuses into the large bowel it is broken