¹Divisions of Baxter Novum and Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden

Correspondence: P Stenvinkel, K56, Karolinska University Hospital at Huddinge, 141 86 Stockholm, Sweden. E-mail: peter.stenvinkel@ki.se

Abstract

Protein energy malnutrition (PEM) is often present in patients with chronic kidney disease with or without ongoing renal replacement therapy. Muscle wasting (sarcopenia) is one of the hallmarks of PEM in these patients and recent studies have reported a link between sarcopenia and inflammation. The low-grade inflammation often observed in end-stage renal disease (ESRD) can lead to sarcopenia through an increase in protein catabolism, a decrease in protein syntheses or both. The activation of the ATP-ubiquitin-proteasome pathway, insulin resistance, hypermetabolism, and decreased appetite are all plausible pathophysiological pathyways whereby inflammation can contribute to sarcopenia and PEM. In the present review we discuss these interactions between inflammation and wasting in ESRD patients and explore putative pathways involved in this condition.