Purpose of review: Malnutrition and accelerated catabolism frequently complicate chronic kidney disease and end-stage renal disease. This review provides an update on the recent advances in the understanding of the mechanisms underlying protein-energy wasting, both in experimental and human models, and on the currently available therapeutic approaches.
Recent findings: Increased levels of circulating cytokines, metabolic acidosis, oxidative stress and insulin resistance all appear to be variably implicated in muscle protein breakdown during end-stage renal disease and dialysis. The individual role of each component in the pathogenesis of chronic kidney disease-related wasting is still unclear, but recent clinical data show a positive relationship between inflammation and muscle protein catabolism as a major contributing factor.
Summary: The basis for appropriate therapeutic approaches to protein-energy wasting in chronic kidney disease and end-stage renal disease relies entirely on the understanding of its pathophysiology. Our knowledge of the pathogenesis of malnutrition and hypercatabolism in renal disease is still limited and mostly based on experimental data, but the currently available evidence suggests that multimodal preventive and therapeutic strategies should be entertained.