LAUSR

According to the International Society of Renal Nutrition and Metabolism (ISRNM), protein energy wasting (PEW) in chronic kidney disease (CKD) is defined as a Bstate of nutritional and metabolic derangements characterized by simultaneous loss of systematic body protein and energy stores, leading to loss of muscle and fat mass and, ultimately cachexia^ [1]. PEW describes a pathological state characterized by anorexia and a high metabolic rate in the face of a negative energy balance resulting in abnormal body composition of decreased muscle mass, with or without decreased fat [2]. CKD staging has been associated with PEW prevalence. In adults with moderate to severe CKD, PEW prevalence is between 18 and 48%, going up to 75% in patients on dialysis [3, 4]. Children with CKD are also at risk for PEW. PEW prevalence is difficult to ascertain since there is no consensus for its definition and assessment. In this regard, of particular interest, Abraham et al. [5] using data from 528 children enrolled in the Chronic Kidney Disease in Children (CKiD) study, have shown that PEW prevalence ranged from 7 to 20% depending on the definitions used. A number of epidemiological and cohort studies have demonstrated the association of PEW with high morbimortality and low quality of life [6]. On the other hand, the association between this wasting syndrome and adverse outcomes in children with CKD has not been established, again mainly due to the absence of consensus regarding the diagnosis of these nutritional disorders. ThepathophysiologyofPEW/cachexiasyndromeinCKDis multifactorial. BThe proposed criteria to establish the diagnosis of PEW includes four categories: (1) biochemical indexes; (2) bodyweightparameters, including reducedbodyfat andweight loss; (3) reduced muscle mass; (4) low protein/energy intake^ [2]. Anorexia is included as a criterion for cachexia [7], while poorprotein/energy intake is a criterion for PEW[1].Anorexia, defined as the loss of appetite and early satiety, is prevalent in adults and pediatric CKD patients [8]. Anorexia in these patients is multifactorial, including an abnormal sense of taste, abnormal gastric emptying, and increased circulatory inflammatory cytokines [2, 9]. Perturbations in anorexigenic/ orexigenic hormones, including leptin, ghrelin, and obestatin, may also be important [10].