The term sarcopenia was first introduced in 1988 by Irwin Rosenberg to define a condition of muscle loss that occurs in the elderly. Since then, a broader definition comprising not only loss of muscle mass, but also loss of muscle strength and low physical performance due to ageing or other conditions, was developed and published in consensus papers from geriatric societies. Sarcopenia was proposed to be diagnosed based on operational criteria using two components of muscle abnormalities, low muscle mass and low muscle function. This brought awareness of an important nutritional derangement with adverse outcomes for the overall health. In parallel, many studies in patients with chronic kidney disease (CKD) have shown that sarcopenia is a prevalent condition, mainly among patients with end stage kidney disease (ESKD) on hemodialysis (HD). In CKD, sarcopenia is not necessarily age-related as it occurs as a result of the accelerated protein catabolism from the disease and from the dialysis procedure per se combined with low energy and protein intakes. Observational studies showed that sarcopenia and especially low muscle strength is associated with worse clinical outcomes, including worse quality of life (QoL) and higher hospitalization and mortality rates. This review aims to discuss the differences in conceptual definition of sarcopenia in the elderly and in CKD, as well as to describe etiology of sarcopenia, prevalence, outcome, and interventions that attempted to reverse the loss of muscle mass, strength and mobility in CKD and ESKD patients.

Recent studies have highlighted the close relationship between the kidney and the gastrointestinal (GI) tract--frequently referred to as the kidney--gut axis--in patients with chronic kidney disease (CKD). In this regard, two important pathophysiological concepts have evolved: (i) production and accumulation of toxic end-products derived from increased bacterial fermentation of protein and other nitrogen-containing substances in the GI tract, (ii) translocation of endotoxins and live bacteria from gut lumen into the bloodstream, due to damage of the intestinal epithelial barrier and quantitative/qualitative alterations of the intestinal microbiota associated with the uraemic milieu. In both cases, these gut-centred alterations may have relevant systemic consequences in CKD patients, since they are able to trigger chronic inflammation, increase cardiovascular risk and worsen uraemic toxicity. The present review is thus focused on the kidney-gut axis in CKD, with special attention to the alterations of the intestinal barrier and the local microbiota (i.e. the collection of microorganisms living in a symbiotic coexistence with their host in the intestinal lumen) and their relationships to inflammation and uraemic toxicity in CKD. Moreover, we will summarize the most important clinical data suggesting the potential for nutritional modulation of gut-related inflammation and intestinal production of noxious by-products contributing to uraemic toxicity in CKD patients.

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Acute kidney disease (AKD) -which includes acute kidney injury (AKI) e and chronic kidney disease (CKD) are highly prevalent among hospitalized patients, including those in nephrology and medicine wards, surgical wards, and intensive care units (ICU), and they have important metabolic and nutritional consequences.Moreover, in case kidney replacement therapy (KRT) is started, whatever is the modality used, the possible impact on nutritional profiles, substrate balance, and nutritional treatment processes cannot be neglected.The present guideline is aimed at providing evidence-based recommendations for clinical nutrition in hospitalized patients with AKD and CKD. Due to the significant heterogeneity of this patient population as well as the paucity of high-quality evidence data, the present guideline is to be intended as a basic framework of both evidence and -in most cases -expert opinions, aggregated in a structured consensus process, in order to update the two previous ESPEN Guidelines on Enteral (2006) and Parenteral (2009) Nutrition in Adult Renal Failure. Nutritional care for patients with stable CKD (i.e., controlled protein content diets/low protein diets with or without amino acid/ketoanalogue integration in outpatients up to CKD stages four and five), nutrition in kidney transplantation, and pediatric kidney disease will not be addressed in the present guideline.

The presence of intestinal dysbiosis, along with increased intestinal permeability and high circulating levels of lipopolysaccharides, a condition known as "endotoxemia," characterize T2DM, CKD, and ESRD on dialysis. The hallmark of intestinal dysbiosis is a reduction of saccharolytic microbes mainly producing short-chain fatty acids (SCFA) and, in the case of CKD/ESRD, an increase in proteolytic microbes that produce different substances possibly related to uremic toxicity. Dysbiosis is associated with endotoxemia and chronic inflammation, with disruption of the intestinal barrier and depletion of beneficial bacteria producing SCFAs. T2DM and CKD/ESRD, whose coexistence is increasingly found in clinical practice, share similar negative effects on both intestinal microbiota and function. More studies are needed to characterize specific alterations of the intestinal microbiota in diabetic nephropathy and to assess possible effects of probiotic and prebiotic treatments in this setting.