Page 750 - Small Animal Clinical Nutrition 5th Edition

778 Small Animal Clinical Nutrition

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Figure 37-7. Increased generation of reactive oxygen species (ROS) occurs in chronic kidney disease and may play a role in disease progres-
sion. (Adapted from Brown SA. Oxidative stress and chronic kidney disease. Veterinary Clinics of North America: Small Animal Practice 2008;
38: 157-166).

reaction is shifting of the corticomedullary blood flow to the Antioxidant defense mechanisms are designed to minimize
medulla when renal blood flow is reduced. Because the work of damage by ROS including superoxide dismutase, catalase,
concentrating urine predisposes a patient to medullary hypoxic nitric oxide synthase, glutathione peroxidase, vitamins E and C
injury, reducing the need for concentration of urine may pre- and carotenoids (Brown, 2008). Erythrocytes and albumin may
vent medullary injury. Reducing transport activity protects also play important roles in minimizing oxidative injury to tis-
medullary tubules from hypoxic injury. Dehydration, volume sues (Agarwal, 2003; Brown, 2008; Rossert and Froissart,
depletion and renal hypoperfusion stimulate urine concentra- 2006). Erythrocytes represent a major antioxidant component
tion; avoiding these conditions reduces the work of urine con- of blood through enzymes such as superoxide dismutase, cata-
centration and stimulates intrarenal protective mechanisms, lase and glutathione peroxidase. Also, erythrocyte glutathione
such as prostaglandin and dopamine production. reductase can regenerate reduced glutathione from its oxidized
form (Rossert and Froissart, 2006).
Renal Oxidative Stress Renal tissue damage occurs when production of ROS exceeds
ROS are examples of free radicals that are produced at low lev- capacity of antioxidant defense mechanisms and is called renal
els by normal aerobic metabolism in the kidney (Brown, 2008). oxidative stress (Brown, 2008). Oxidative damage has been
Examples of ROS produced in the kidney include hydrogen incriminated as a cause of progressive renal injury in several
peroxide (H O ), hydroxyl radical (OH), superoxide anion types of kidney disease (Diamond et al, 1986; Agarwal, 2003;
2 2
-
(O ), lipid peroxy radicals, lipid and DNA hydroperoxides, Vasavada and Agarwal, 2005; Brown, 2008) (Figure 37-7). In
2
hypochlorous acid and peroxynitrite. These ROS may damage rats with remnant kidneys, increased oxygen consumption asso-
proteins, lipids, DNA and carbohydrates, resulting in structur- ciated with increased dietary protein is accompanied by in-
al and functional abnormalities and progressive renal injury. creased urinary clearance of oxidative products (Nath et al,