Page 757 - Small Animal Clinical Nutrition 5th Edition
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Chronic Kidney Disease 785
ly more calories.Therefore, changes in renal morphology could to a new food if it is offered before clinical signs of uremia occur
VetBooks.ir have resulted from differences in protein and/or caloric intake. and it may delay onset of uremic signs as CKD progresses
(Polzin et al, 2005). On a practical note, it is difficult to achieve
In the other study, no difference in renal function or glomeru-
the degree of phosphorus restriction desired in veterinary ther-
lar lesions were found in cats consuming high-protein foods
(52% DM) compared with lower protein foods (28% DM) apeutic renal foods using typical ingredients without limiting
(Finco et al, 1998). Phosphorus amounts were similar for all the amount of dietary protein (Burkholder, 2000).
study groups (0.87 to 0.96% DM).There were mild and signif- In regards to determining how much protein to recommend
icant increases in cellular infiltrate and tubular lesions in cats for dogs and cats with CKD, all patients should be monitored
that consumed more calories, but no differences were detected for signs of protein insufficiency and nutritional management
based on amount of dietary protein. The authors concluded adjusted to maintain ideal body condition (Box 37-4). For cats
that protein intake was not a risk factor for progression of renal with CKD, the minimum dietary protein requirement identi-
lesions and that the practice of severe protein restriction was fied in one study was 20% of calories (Kirk and Hickman,
questionable. However, because renal function remained stable 2001); this translates to approximately 24% DM protein.
throughout both studies, it was not possible to assess the role of Similar studies have not been reported for dogs.The minimum
limiting dietary protein in decreasing progression of CKD. recommended allowances for DM dietary protein in foods for
Four clinical studies of cats or dogs with naturally occurring healthy adult dogs and cats are 10 and 20%, respectively (NRC,
CKD compared effects of feeding a commercial veterinary 2006). The minimum DM levels recommended by the
therapeutic renal food with either a control or regular mainte- Association of American Feed Control Officials are 18% for
nance food that contained more protein (Harte et al, 1994; dog foods and 26% for cat foods (AAFCO, 2007). A report of
Elliott et al, 2000; Jacob et al, 2002; Ross et al, 2006). In a six- the mean DM protein content of several popular U.S. grocery
month study, mean serum creatinine and urea nitrogen concen- brand dog foods was 41.7% for moist foods and 25% for dry
trations progressively increased in 10 cats receiving more foods. For grocery brand cat foods it was 51.5% for moist foods
dietary protein (39.4% DM) and declined or remained stable in and 35.1% for dry foods (Allen et al, 2000). The recommend-
f
25 cats that were fed a lower protein food (25.2% DM) (Harte ed range for DM protein levels in foods intended for most
et al, 1994). In a non-randomized, prospective study, cats patients with CKD is 14 to 20% for dogs and 28 to 35% for
g
receiving a lower protein food (22 to 24% protein) had signif- cats. Foods with less protein may be needed to control signs of
icantly prolonged median survival time compared with cats that uremia in patients with more advanced CKD; in these patients,
continued eating different maintenance cat foods with higher it’s important to monitor for signs of protein deficiency. In
protein (48% DM) (Elliott et al,2000).In a two-year study,cats addition to the amount of protein, patients with CKD should
h
eating a commercial veterinary therapeutic renal food with 28 receive protein of high biologic value.The concept of ideal pro-
to 29% DM protein had no uremic episodes or renal-related tein is useful when considering biologic value (Baker and
deaths whereas 26% of cats in the control group consuming a Czarnecki-Maulden, 1991). Lysine is the limiting amino acid
food with higher protein (46 to 48% DM protein) had a ure- in practical foods for dogs and cats (Baker and Czarnecki-
mic crisis and 22% died as a result of CKD (Ross et al, 2006). Maulden, 1991). However, experience with typical ingredients
Finally, dogs receiving a commercial veterinary therapeutic used in commercial veterinary therapeutic foods suggests that
e
renal food with 14% DM protein had delayed time to onset of tryptophan is more frequently limiting.Therefore, based on the
uremic crisis, slower decline in renal function and improved concept of ideal protein, foods that meet the requirement for
survival compared to parameters in dogs receiving a control lysine and tryptophan can be assumed to meet the requirement
food that contained 25% DM protein (Jacob et al, 2002). Based for all indispensable amino acids.
on these findings, it is clear that foods with less protein in these
studies were associated with significantly improved quality and Phosphorus
quantity of life in dogs and cats with naturally occurring CKD. Decreased dietary phosphorus intake is indicated in dogs and
However, because the protein amount was not the only nutri- cats with CKD to limit phosphorus retention, hyperphos-
ent difference between the veterinary therapeutic renal foods phatemia, secondary renal hyperparathyroidism (Figures 37-8
and comparison foods, it is not possible to conclude that limit- and 37-9) and progression of kidney disease (Polzin et al, 2005;
ing dietary protein alone was the sole reason for beneficial Rutherford et al, 1977; Barber at al, 1999).The mechanism for
effects. Box 37-3 provides detailed information about long- the protective effect of limiting phosphorus intake is unknown.
term studies that evaluated effects of veterinary therapeutic Possible factors include reduced nephrocalcinosis, suppression
renal foods on survival time of dogs and cats with CKD. of hyperparathyroidism, reduced cellular energy metabolism
In summary, limiting dietary protein intake is indicated to and altered renal hemodynamics. It is possible that these mech-
control clinical signs of uremia in dogs and cats with CKD. anisms may synergistically contribute to the beneficial effects of
Although currently available evidence fails to support a recom- lowering phosphorus intake.
mendation for or against limiting dietary protein intake alone Several studies evaluated effects of limiting dietary phospho-
in non-uremic patients with CKD, there are potential benefits, rus intake in cats and dogs with induced kidney disease. In cats,
assuming that patients maintain adequate caloric intake and high dietary phosphorus intake (1.56% DM phosphorus) for 65
body condition. Patients may be more likely to accept a change to 343 days was associated with renal mineralization, fibrosis