Chronic kidney disease and inflammation in pediatric patients: from bench to playground.
Signs of an activated immune system can be observed already in the early stages of chronic kidney disease (CKD). Markers of a chronically activated immune system are closely linked to several complications of CKD, such as accelerated atherosclerosis, vascular calcification, insulin resistance, increased muscle catabolism, loss of appetite, bone remodeling, and increased peritoneal permeability. Interestingly, all the aforementioned pathological states resemble a state of accelerated ageing and are strongly associated with increased morbidity and mortality in CKD patients. In recent studies, signs of inflammation have been shown as predictors for mortality in dialysis patients, and the role of inflammation as a risk factor for complications of CKD in children has emerged. Although preliminary findings suggest that inflammation is highly prevalent in the pediatric population with CKD, information related pathogenic links and to clinical outcomes is lacking. For the future, it is crucial for investigations to address the mechanisms and complications of inflammation that are manifested in pediatric patients with CKD in all stages. Since early identification and intervention may generate the most efficient strategies for prevention and treatment of cardiovascular disease in CKD patients, the pediatric population deserves special attention in future studies. In this review, we discuss the mechanisms involved in the inflammatory activation and the main causes and consequences of the inflammatory state observed in the CKD patient, with special emphasis on the pediatric population.
Pecoits-Filho
Roberto
R
Division of Renal Medicine, Karolinska University Hospital at Huddinge, Karolinska Institute, Stockholm, Sweden. r.pecoits@pucpr.br
Sylvestre
Lucimary C
LC
Stenvinkel
Peter
P
D000375:Aging; D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000401:mortality; D002648:Child; D002908:Chronic Disease; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000503:physiopathology; D007674:Kidney Diseases / Q000150:complications*