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allowances for dietary protein where common dietary protein sources are used. Allowances for growing dogs are 22% protein (DMB), adult dogs are 22% protein (DMB), growing kittens are 30% (DMB), and adult cats are 26% (DMB).
The kidney is a highly metabolic organ; therefore,
CKD would be expected to have a variety of adverse systemic effects in addition to renal effects. In general terms, renal function includes filtration, reabsorption, and secretion of endogenous and exogenous substances; maintaining homeostasis of water, acid-base, minerals, electrolytes, and other substances; neurohumoral regulation of vitamins (such as vitamin D), red blood cell production, blood pressure, and others; and energy metabolism including gluconeogenesis and reabsorption of amino acids. There is little to no information on protein metabolism in dogs and cats with chronic kidney disease or the incidence of cachexia and sacropenia in these patients although it is assumed to occur in at least some. It has been shown that dogs with CKD that are under- conditioned have a decreased survival compared to dogs who are optimally or over conditioned;(2) however, no information was provided in this study as to muscle condition scoring and lean body mass (LBM).
In uremic rodent models, 3-methylhistidine release, an index of myofibrillar protein degradation, is elevated to a greater degree than in rodents without CKD. During in vivo infusion of 14C leucine, protein synthesis following fasting was less in rats with CKD than in healthy
rats. Muscle protein synthesis was lower in rats with
CKD following a period of stress than in rats without CKD. There is also increased muscular alanine and glutamine release and a decrease in leucine incorporation in rats with CKD and increased muscular tyrosine and phenylalanine release. It has been shown in rodent studies that metabolic acidosis, excess angiotensin II, and inflammation increases muscular protein degradation and decreases muscular protein synthesis primarily through insulin resistance and impaired insulin/IGF-I signalling. Data in human beings suggest that CKD, even when advanced, does not in itself engender net protein breakdown. Many nitrogen balance studies in human beings with CKD who are not undergoing chronic dialysis have demonstrated that they are able to maintain neutral or positive nitrogen balance studies with low protein intakes. Thus, uremia, per se, does not stimulate net protein catabolism and human pre-dialytic patients fed low protein diets are able to conserve protein if metabolic academia is not present or if there is no concurrent illness. Protein turnover kinetic studies suggest that
the mechanism of protein conservation include down- regulation of protein degradation, and amino acid oxidation and maintenance of protein synthesis at near
An Urban Experience
normal levels. If chronic inflammation, increased cytokine levels and activity, and/or metabolic acidosis exists, then protein requirements may be increased.
So, if protein restriction is not detrimental with CKD
in many patients, the question is whether there is an advantage over not restricting dietary protein with
CKD. In evaluating the veterinary literature, no clear consensus is derived. There are potentially several reasons for this. Studies evaluating only a dietary protein effect have used induced CKD models in dogs and cats, which may or may not adequately represent naturally occurring disease. Some studies demonstrate histologic changes while others have only evaluated blood biochemical parameters. Most induced CKD studies evaluated a small number of animals. Finally, CKD is
a complex disease and optimal treatment of patients with CKD involves modifying multiple dietary factors. Nonetheless, dietary protein restriction if not detrimental has potential benefits. Decreased dietary protein
intake inhibits secretion of TGF-β a cytokine involved in progression of CKD. Decreased dietary protein intake reduces tubular hyperfunction by decreasing renal
acid load and renal ammoniagenesis. Sulfur-containing amino acids in dietary protein contributes to renal acid load. If proteinuria is present, dietary protein restriction is beneficial as proteinuria induces inflammatory and fibrogenic pathways and increases oxidative stress.
Two studies evaluated effects of dietary protein on progression of induced CKD for one year in cats.(3, 4) In one study, renal function did not progressively decrease, regardless of dietary protein amount and caloric intake; however, cats fed the higher protein diet had more severe glomerular and tubulointerstitial changes.(3) The cats in the higher protein diet group also consumed more calories. In the other study, no difference in renal function or glomerular lesions were found in cats consuming the high protein diet.(4) These studies were of short duration and progression of spontaneous CKD in cats may occur slowly.
Clinical trials of naturally occurring CKD in pet dogs and cats have utilized dietary modification including but not limited to dietary protein restriction. The effectiveness of diet therapy in minimizing uremic episodes and mortality in dogs and cats with naturally occurring IRIS CKD stages 2 and 3 have been established in double-blinded randomized controlled clinical trials.(5-7) These studies compared a renal diet to a maintenance diet. The renal diets contained reduced quantities of dietary protein,
but also contained reduced quantities of phosphorous and sodium and were supplemented with omega-3 fatty acids when compared with the maintenance diet. In the canine study, the risk of developing a uremic crisis was reduced by approximately 75% in dogs fed the renal diet when compared with dogs fed the adult maintenance diet.(5) The median symptom-free interval in dogs fed

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