Page 764 - Small Animal Clinical Nutrition 5th Edition
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792 Small Animal Clinical Nutrition
study design and differences between groups (e.g., age of cats,
VetBooks.ir plasma creatinine concentrations) and foods (e.g., potassium,
phosphorus) used, it is not possible to conclude that differences
in survival times were due to increased amounts of EPA. In
(number) addition, EPA content was not determined for all foods used in
the study.
Although the recommended amount of omega-3 fatty acids
Dogs for foods for CKD patients has not been definitively deter-
mined, the amounts in the aforementioned studies in dogs
(Brown et al, 1998, 2000; Brown, 2008) ranged from 0.41 to
4.37% DM. With a 5:1 omega-6:omega-3 fatty acid ratio, the
lower end of the range (0.41%) was effective in reducing the
magnitude of glomerular hypertension and renal generation of
Figure 37-13. Survival of dogs with experimentally induced chronic inflammatory eicosanoids (Brown, 2008). The omega-
kidney disease fed foods with three different fat sources (fish oil, tal-
low, safflower oil). Note that survival was increased in those dogs 6:omega-3 ratio was not reported in the earlier studies (Brown
consuming foods with either tallow or fish oil compared to safflower et al,1998,2000).To date,studies like these have not been done
oil. Dietary fatty acid composition appears to affect hemodynamic in cats but it seems likely that similar levels would be effective.
adaptations to renal disease in dogs. (Adapted from Brown SA, Based on results of canine studies described above, the recom-
Brown CA, Crowell WA, et al. Dietary lipid composition alters chronic mended range for total omega-3 fatty acid content in foods for
course of canine renal disease (abstract). Journal of Veterinary
Internal Medicine 1996; 10: 168.) canine and feline CKD patients is 0.4 to 2.5% DM. Until there
is definitive work, a somewhat broad range for the omega-
the other two groups, the group receiving the food supplement- 6:omega-3 fatty acid ratio is recommended (1:1 to 7:1). These
ed with safflower oil had greater glomerular enlargement and recommendations are similar to omega-3 fatty acid content and
mean glomerular capillary pressure. Dietary fatty acid compo- omega-6:omega-3 ratios recommended for dogs and cats with
sition appeared to alter hemodynamic responses to renal insuf- cancer, osteoarthritis and inflammatory skin diseases.
ficiency. Final mean exogenous creatinine clearance was 1.3 Dietary omega-3 fatty acid supplementation in combination
ml/min./kg body weight for the menhaden fish oil group, 0.9 with antioxidants (See Antioxidants below.) can further reduce
ml/min./kg body weight for the beef tallow group and 0.5 renal oxidant injury. In a study in dogs with the remnant model
ml/min./kg body weight for the safflower oil group. Mean of CKD, dietary supplementation with omega-3 fatty acids and
UPC ratios were 0.6 in the menhaden fish oil group, 1.5 in the antioxidants (vitamin E, carotenoids and lutein), both were
beef tallow group and 2.1 in the safflower oil group. Survival independently renoprotective; when combined, their effects
was similar in groups receiving menhaden oil and beef tallow; were additive (Brown, 2008). In this model, addition of antiox-
however, four of seven dogs in the safflower oil group were idants reduced proteinuria, glomerulosclerosis and interstitial
euthanized. In other studies in dogs with a remnant kidney fibrosis independent of the ratio of dietary omega-6 to omega-
model of CKD, dietary supplementation with either omega-3 3 fatty acids (Brown, 2008).
fatty acids or antioxidants was renoprotective and their effects
were additive when used together (Brown, 2008). Antioxidants:Vitamins E and C
However, in normal and CKD dogs fed foods supplemented Oxidative damage is a component in the progression of renal
with safflower and menhaden fish oil, the oil supplement had injury in several types of kidney disease (Figure 37-7)
no significant effect on the ratio of urinary eicosanoids (Diamond et al, 1986; Agarwal, 2003; Vasavada and Agarwal,
(Crocker et al, 1996). The ratio of the urinary eicosanoids 2005). Unquenched ROS may damage proteins, lipids, DNA
thromboxane B (a stable urinary metabolite of thromboxane and carbohydrates, resulting in structural and functional abnor-
2
A ) and prostaglandin E has been used as an index of renal malities and progressive renal injury. Renal oxidative stress
2
2
vascular tone in normal and CKD dogs. Failure to demonstrate occurs when production of ROS exceeds quenching capacity of
a change in the ratio may be related to the length of the antioxidant defense mechanisms (Brown, 2008). As previously
washout period (three weeks) and uncertain stability of lipid discussed (See Etiopathogenesis above.), increased renal oxida-
supplements in this study. tive stress has been linked to proteinuria as a potential media-
A retrospective CKD study was conducted to evaluate sur- tor of tubulointerstitial damage and to progression of CKD
vival times in 146 cats fed one of seven commercial veterinary (Brown, 2008; Agarwal, 2003; Agarwal et al, 2004; Vasavada
therapeutic renal foods, compared with survival times in 175 and Agarwal, 2005). Specifically, overloading tubular mecha-
cats fed regular maintenance foods (Plantinga et al, 2005). The nisms for resorption of filtered albumin by proximal tubular
median survival time for cats fed maintenance foods was seven cells can stimulate production of proinflammatory and profi-
months whereas the median survival time for cats fed veteri- brotic cytokines by activation of the redox-sensitive gene nu-
nary therapeutic renal foods was 16 months. The group with clear factor-κB thereby contributing to tubulointerstitial dam-
the longest median survival time (23 months) was fed the food age (Agarwal, 2003; Rossert and Froissart, 2006).
with the highest reported content of EPA. However, because of Numerous antioxidant defense mechanisms are designed to