Chronic systemic inflammation in dialysis patients: an update on causes and consequences.
Despite marked improvements in dialysis technology during the last 20 years, the age-adjusted mortality rate in end-stage renal disease (ESRD) patients treated by 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 early stages of chronic kidney disease as compared to the general population. Although traditional risk factors for CVD 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 progressive atherosclerotic CVD and malnutrition, itself an important risk factor for the development of CVD, by several pathogenetic mechanisms. The causes of inflammation in dialysis are multifactorial and include both dialysis-related and unrelated factors. While the long-term effects of chronic inflammation may be most important in the pathogenesis of CVD, the acute-phase reaction may also cause vascular damage by several pathogenic mechanisms. Indeed, it seems logical to speculate that suppression of the vicious cycle of malnutrition, inflammation, and atherosclerosis (MIA syndrome) in ESRD would improve survival and decrease co-morbidity in dialysis patients. As there are currently no established guidelines for the treatment of chronic inflammation in ESRD patients, more 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 clearly warranted and will be helpful in identifying precisely which pathways are most involved in the pathogenic process.
Yao
Qiang
Q
Divisions of Baxter Novum and Renal Medicine, Department of Clinical Science, Karolinska Institutet, Stockholm, Sweden.
Axelsson
Jonas
J
Stenvinkel
Peter
P
Lindholm
Bengt
B
D002908:Chronic Disease; D016207:Cytokines / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000209:etiology* / Q000235:genetics; D007676:Kidney Failure, Chronic / Q000628:therapy*; D006435:Renal Dialysis / Q000009:adverse effects*; D014511:Uremia / Q000150:complications
D016207:Cytokines