Systemic inflammation in dialysis patients with end-stage renal disease: causes and consequences.
Despite rapid improvements in dialysis technology during the last 20 years, the mortality rate in end-stage renal disease (ESRD) patients treated with dialysis is still unacceptably high and comparable to that of many cancer patients with metastases. The main cause of the increased mortality in ESRD patients is cardiovascular disease (CVD), which is twice as common and advances at twice the rate already in patients with earlier stages of chronic kidney disease as compared to the general population. Although traditional risk factors are common in dialysis patients, they can only in part explain the very high prevalence of CVD in this patient group. Recent evidence demonstrates that chronic inflammation, a non-traditional risk factor which is a commonly observed in dialysis patients, may cause malnutrition and progressive atherosclerotic CVD by several pathogenetic mechanisms. Available data suggest that pro-inflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. While the long-term effects of chronic inflammation may be most important in the pathogenesis of CVD, the acute-phase reaction may also be a direct cause of acute vascular injury by several pathogenetic mechanisms. The cause(s) of inflammation in dialysis are multifactorial and include both dialysis-related and unrelated factors. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation, and atherosclerosis (MIA syndrome) would improve survival in dialysis patients. As there are currently no established guidelines for the treatment of chronic inflammation in ESRD patients, studies on the long-term effects of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as outcome in this patient group are warranted.
Yao
Q
Q
Division of Baxter Novum and Renal Medicine, Department of Clinical Science, Karolinska Institutet, Stockholm, Sweden.
Axelsson
J
J
Heimburger
O
O
Stenvinkel
P
P
Lindholm
B
B
D006801:Humans; D007249:Inflammation / Q000150:complications / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000628:therapy*; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D006435:Renal Dialysis / Q000009:adverse effects*