Cytokine Dysregulation in Chronic Kidney Disease: How Can We Treat It?

Carrero, Juan Jesús; Yılmaz, Mahmut İlker; Lindholm, Bengt; Stenvinkel, Peter

doi:10.1159/000126926

Cited by 94 publications

(79 citation statements)

References 177 publications

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“…Increased expression and activity of macrophage scavenger receptors during ESRD might lead to enhanced oxLDL clearance and, as a consequence, to foam cell formation, an early step in atherogenesis (25). Alterations in pattern-recognition receptors could contribute to a state of hypercytokinemia, which is strongly associated with CVD and poor outcome in the ESRD population (19,62). The pro-inflammatory cytokines are thought to mediate PEW in ESRD patients (19) and are associated with indices of atherosclerosis (63,64) and with increased mortality rates (65).…”

Section: Associations With Atherosclerosis and Cvdmentioning

confidence: 99%

Aspects of Immune Dysfunction in End-stage Renal Disease

Kato

Chmielewski

Honda

et al. 2008

Clinical Journal of the American Society of Nephrology

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905

716

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End-stage renal disease (ESRD) is associated with significantly increased morbidity and mortality resulting from cardiovascular disease (CVD) and infections, accounting for 50% and 20%, respectively, of the total mortality in ESRD patients. It is possible that these two complications are linked to alterations in the immune system in ESRD, as uremia is associated with a state of immune dysfunction characterized by immunodepression that contributes to the high prevalence of infections among these patients, as well as by immunoactivation resulting in inflammation that may contribute to CVD. This review describes disorders of the innate and adaptive immune systems in ESRD, underlining the specific role of ESRD-associated disturbances of Toll-like receptors. Finally, based on the emerging links between the alterations of immune system, CVD, and infections in ESRD patients, it emphasizes the potential role of the immune dysfunction in ESRD as an underlying cause for the high mortality in this patient population and the need for more studies in this area.

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Section: Associations With Atherosclerosis and Cvdmentioning

confidence: 99%

Aspects of Immune Dysfunction in End-stage Renal Disease

Kato

Chmielewski

Honda

et al. 2008

Clinical Journal of the American Society of Nephrology

Self Cite

905

716

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“…In CKD, especially in ESRD, the systemic concentrations of both pro-and anti-inflammatory cytokines are several-fold higher as a result of both decreased renal clearance and increased production. Several factors, both dialysis-related (e.g., membrane bioincompatibility) and non-dialysis-related (e.g., infection, comorbidity, genetic factors, diet), may additionally contribute to a state of persistent inflammation (1).…”

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confidence: 99%

Persistent Inflammation as a Catalyst for Other Risk Factors in Chronic Kidney Disease

Carrero¹,

Stenvinkel²

2009

Clinical Journal of the American Society of Nephrology

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181

131

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Because inflammation by now is a "traditional" finding that predicts poor outcome and cardiovascular events in the vast majority of patients with ESRD, it could be argued that inflammatory biomarkers should not longer be considered "novel" risk factors. In this review, we forward the hypothesis that, in addition to putative direct proatherogenic effects, persistent inflammation may serve as a catalyst and, in the toxic uremic milieu, modulate the effects of other concurrent vascular and nutritional risk factors. We discuss some recent observational studies, suggesting that the presence of persistent inflammation magnifies the risk for poor outcome via mechanisms related to self-enhancement of the inflammatory cascade and exacerbation of both the wasting and the vascular calcification processes. Because persistent inflammation may be the silent culprit of other commonly observed pathophysiologic alterations in chronic kidney disease, it is imperative that inflammatory markers be regularly monitored and therapeutic attempts be made to target persistent low-grade inflammation in this patient group.

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“…They require the contribution of a variety of immune cells, especially T lymphocytes. 6 Treg and Th17 cells are both CD4 þ T cells while distinct from Th1 and Th2 cells. They are generated from a common precursor but are functionally antagonistic.…”

Section: Discussionmentioning

confidence: 97%