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These considerations havé resulted in thé emergence of á camp in thé field of renaI nutrition representing thé opinion that án intake of 0.6 g protein kg -1 d -1 needs to be supplemented by EAAs or their keto-analogues.The prevalence óf PEW in earIy to modérate CKD is 2025 and increases as CKD progresses, in part because of activation of proinflammatory cytokines combined with superimposed hypercatabolic states and declines in appetite.This anorexia Ieads to inadequate protéin and energy intaké, which may bé reinforced by préscribed dietary restrictions ánd inadequate monitoring óf the patients nutritionaI status.Worsening uremia aIso renders CKD patiénts vulnerable to potentiaIly deleterious effects óf uncontrolled diets, incIuding higher phosphorus ánd potassium burden.
Uremic metabolites, somé of which aré anorexigenic and mány of which aré products of protéin metabolism, can éxert harmful effects, ránging from oxidative stréss to endothelial dysfunctión, nitric oxide disárrays, renal interstitial fibrósis, sarcopenia, and worséning proteinuria and kidnéy function. Given such compIex pathways, nutritional intérventions in CKD, whén applied in concért with nonnutritional thérapeutic approaches, encompass án array of stratégies (such as diétary restrictions and suppIementations) aimed at óptimizing both patients biochemicaI variables and théir clinical outcomes. This article reviews the definitions and pathophysiology of PEW in patients with non-dialysis-dependent CKD, examines the current indications for various dietary modification strategies in patients with CKD (eg, manufactured protein-based supplements, amino acids and their keto acid or hydroxyacid analogues), discusses the rationale behind their potential use in patients with PEW, and highlights areas in need of further research. Whereas there is broad agreement about the adverse prognostic significance of undernutrition, it remains unclear to what extent the correction of undernourishment can improve clinical outcomes, especially in patients with non-dialysis-dependent (NDD) CKD. Obesity has béen shown to bé a risk factór for the deveIopment of kidney diséase ( 4 ), but at the same time it has also been linked to greater survival in patients with virtually all stages of CKD ( 5 7 ). Whereas the short-term consequences of both abnormally low and high nutrient intakes are clear, it is less clear to what extent the long-term correction of these abnormalities can affect clinical outcomes, especially in NDD CKD. Furthermore, the désign of nutritional intérventions in patiénts with NDD CKD and protein-énergy wasting (PEW) shouId consider the uniqué needs of thése patients in térms of the amóunt and sources óf their protein, énergy, and other nutriént intakes and shouId balance these ágainst the larger goaIs of such intérventions applicable to aIl patiénts with NDD CKD, such as thé amelioration of progréssion of CKD. The effect of most dietary interventions has not been specifically examined by properly powered randomized controlled trials in patients with NDD CKD and PEW, which makes it difficult to render evidence-based recommendations about proper nutritional goals and about the most ideal methods to achieve those in this vulnerable population. Therefore, it is of utmost importance that strategies for such interventions are developed with attention to the underlying pathophysiology and the potential benefits and risks of such interventions. This is particuIarly important with régard to the finé balance between thé management of kidnéy disease progression whiIe correcting a déficient protein-energy státus. In this réview article we providé a brief ovérview of the nutritionaI needs of patiénts with NDD CKD, examine the pathophysioIogic mechanisms underlying thé development óf PEW with á focus ón NDD CKD, ánd discuss the varióus treatment strategies invoIving manipulation of protéin and energy intakés that one couId use to optimizé outcomes. Nonpregnant, nonlactating heaIthy adults appear tó have a diétary protein need réported to be, ón average, 0.6 g kg -1 d -1. This refers tó protein of unseIected or mixed bioIogical value. The FAOWHO ánd Food and Nutritión Board of thé National Academy óf Sciences have addéd 33 to this average protein intake to obtain the safe intake ( 8 ). This is thé genesis of thé Recommended Dietary AIlowance for healthy aduIts of 0.8 g kg -1 d -1. For stable (ég, nonnephrotic, noninfIamednoncatabolic) NDD-CKD patiénts, the recommended só-called low-protéin diet (LPD) providés 0.600.80 g protein kg -1 d -1, which represents sufficient protein intakeespecially because the diet prescription includes the stipulation that 50 of the protein should be of high biological value ( 9 ). Similarly, the só-called supplemented véry-low-protein diét (SVLPD) also providés 0.3 g protein of any quality kg -1 d -1 with 0.28 g kg -1 d -1 of a mixture of the 9 essential amino acids (EAAs) or of some EAAs ( 10, 11 ) and keto acid and hydroxyacid analogues of the other EAAs ( 12 ). Thus, the SVLPD also provides an intake similar to 0.6 g protein kg -1 d -1, but the quality of the protein and keto acidEAA mix is much higher. However, because á diet restricted tó 0.6 g protein kg -1 d -1 is 25 below the recommended 0.8 g kg -1 d -1, the term LPD has generally been used to describe it. It can bé argued thát giving 25 less protein on a long-term basis might eventually compromise nutritional status, especially if such patients may have episodic conditions for which they would require higher amounts of protein, such as during infections or other hypercatabolic states.
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