Page 760 - Small Animal Clinical Nutrition 5th Edition

788 Small Animal Clinical Nutrition

(Brown et al, 1991). Specifically, in this study, progression and
VetBooks.ir death were associated with interstitial fibrosis, tubular atrophy
and dilatation and mineralization of cortical basement mem-
branes, tubular epithelia and vascular and tubular lumina. The
association of progression with tubulointerstitial lesions and
nephrocalcinosis,however,does not necessarily establish a causal
role for nephrocalcinosis. A similar study was conducted by
investigators in the same laboratory to evaluate effects of dietary
phosphorus restriction (0.48 vs. 1.46% DM) when a higher pro-
tein food (32% DM) was fed (Finco et al, 1992). In contrast to
the previous study, improved survival was not observed in the
group fed low-phosphorus food. An additional study compared
the effects of feeding four foods of varying phosphorus and pro-
Figure 37-8. The effect of dietary phosphorus on serum parathyroid tein content (low phosphorus/low protein; high phosphorus/low
hormone (PTH) concentrations in dogs with experimentally induced protein; low phosphorus/high protein; high phosphorus/high
kidney disease. Note that consumption of higher levels of phospho- protein) to four groups of dogs with CKD (remnant kidney
rus resulted in excessive PTH secretion. High phosphorus means
model). In this study, survival was significantly increased by
dogs ingested 60 to 80 mg phosphorus/kg body weight/day, Low
feeding either of the low-phosphorus foods (0.44 to 0.49% DM
phosphorus means dogs ingested 15 to 40 mg phosphorus/kg body
weight/day. (Adapted from Rutherford WE, Bordier P, Marie P, et al. phosphorus) and was not affected by the amount of dietary pro-
Phosphate control and 25-hydroxycholecalciferol administration in tein (16.7 to 32% DM) (Finco et al, 1992a).
preventing experimental renal osteodystrophy in the dog. Journal of Beneficial effects of limiting dietary phosphorus intake, by
Clinical Investigation 1977; 60: 332-341.)
feeding a veterinary therapeutic renal food, have also been
demonstrated in cats and dogs with naturally occurring CKD
(Elliott et al, 2000; Barber et al, 1999; Jacob et al, 2002; Ross et
al, 2006). In one study, feeding a dry or moist veterinary thera-
e
peutic renal food with low phosphorus (0.29 or 0.41% DM)
was associated with significantly decreased plasma phosphorus
and PTH concentrations compared with results from cats fed a
typical maintenance food with higher phosphorus (1.9% DM)
(Barber et al, 1999). In three additional studies, dogs and cats
managed by feeding a veterinary therapeutic renal food with
decreased phosphorus had significantly prolonged survival
times compared with patients that were fed a higher phospho-
rus maintenance food (Elliott et al,2000; Jacob et al,2002; Ross
et al, 2006) (Box 37-3).
The minimum recommended allowance for dietary phos-
phorus is 0.3% DM in foods for healthy adult dogs and 0.26%
DM for healthy adult cats (NRC, 2006).The mean DM phos-
phorus contents of several grocery brand dog and cat foods
were 1.39 and 1.54%, respectively (Allen et al, 2000). To
Figure 37-9. Plasma parathyroid hormone (PTH) concentrations in
cats with chronic kidney disease that were fed either a veterinary achieve beneficial effects, the recommended phosphorus levels
therapeutic renal food with decreased phosphorus (blue line) (n=14) for foods used to manage CKD are 0.2 to 0.5% DM for dogs
or a maintenance food with higher phosphorus (red line) (n=8). and 0.3 to 0.6% DM for cats.
Results expressed as mean ± SEM. NS = not significant.
P values represent statistical significance of each value compared Sodium and Chloride
with pre-treatment value (Day 0).
*No significant difference between groups at baseline (Day 0). As renal function deteriorates, fractional sodium excretion
(Adapted from Barber PJ, Rawlings JM, Markwell PJ, et al. Effect of increases to maintain sodium balance and preserve extracellular
dietary phosphate restriction on renal secondary hyperparathyroidism fluid volume. The fractional excretion of sodium must change
in the cat. Journal of Small Animal Practice 1999; 40: 62-70.)
markedly to maintain sodium balance when dietary sodium
intake changes (Klahr and Slatopolsky, 1973). Patients with
Survival rate was significantly higher in the low-phosphorus decreased renal function can only vary sodium excretion over a
group (75%) compared with the high-phosphorus group (33%) limited range, which narrows progressively as GFR declines.
(Figure 37-11). Kidney function also deteriorated at a more Thus, patients with CKD may not tolerate excessively high or
rapid rate in the high-phosphorus group. Decrements of renal low dietary sodium levels. If excessive sodium is ingested, sodi-
function were more closely related to nephrocalcinosis and um retention with expansion of extracellular fluid volume can
tubulointerstitial lesions than to glomerular abnormalities occur and produce or worsen preexisting hypertension, fluid