Hemodialysis-Induced Regional Left Ventricular Systolic Dysfunction and Inflammation: A Cross-sectional Study

Assa, Solmaz; Hummel, Yoran M.; Voors, Adriaan A.; Kuipers, Johanna; Westerhuis, Ralf; Groen, Henk; Bakker, Stephan J. L.; Kobold, Anneke C. Muller; Oeveren, Wim van; Struck, Joachim; Jong, Paul E. de; Franssen, Casper F. M.

doi:10.1053/j.ajkd.2013.11.010

Cited by 31 publications

(31 citation statements)

References 30 publications

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“…Inflammatory biomarkers are substantially increased in uremic patients and are associated with increased risks of all-cause and cardiac mortalities in dialysis patients (60, 61) . Several studies reported increase in circulating inflammatory markers including interleukin-6 and pentraxin during single session hemodialysis (62, 63) . A recent study also reported that predialysis inflammatory markers including high sensitivity C-reactive protein, and the ratio of interleukin-6 and 10 levels were independently associated with hemodialysis-induced regional LV systolic dysfunction (63) .…”

Section: Introductionmentioning

confidence: 99%

“…Several studies reported increase in circulating inflammatory markers including interleukin-6 and pentraxin during single session hemodialysis (62, 63) . A recent study also reported that predialysis inflammatory markers including high sensitivity C-reactive protein, and the ratio of interleukin-6 and 10 levels were independently associated with hemodialysis-induced regional LV systolic dysfunction (63) . Another possibility is hemodialysis-induced systemic circulatory stress and recurrent regional ischemia of gut leading to endotoxin translocation.…”

Section: Introductionmentioning

confidence: 99%

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Cardiovascular impact in patients undergoing maintenance hemodialysis: Clinical management considerations

Chirakarnjanakorn

Navaneethan

Francis

et al. 2017

International Journal of Cardiology

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Patients undergoing maintenance hemodialysis develop both structural and functional cardiovascular abnormalities. Despite improvement of dialysis technology, cardiovascular mortality of this population remains high. The pathophysiological mechanisms of these changes are complex and not well understood. It has been postulated that several non-traditional, uremic-related risk factors, especially the long-term uremic state, which may affect the cardiovascular system. There are many cardiovascular changes that occur in chronic kidney disease including left ventricular hypertrophy, myocardial fibrosis, microvascular disease, accelerated atherosclerosis and arteriosclerosis. These structural and functional changes in patients receiving chronic dialysis make them more susceptible to myocardial ischemia. Hemodialysis itself may adversely affect the cardiovascular system due to non-physiologic fluid removal, leading to hemodynamic instability and initiation of systemic inflammation. In the past decade there has been growing awareness that pathophysiological mechanisms cause cardiovascular dysfunction in patients on chronic dialysis, and there are now pharmacological and non-pharmacological therapies that may improve the poor quality of life and high mortality rate that these patients experience.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cardiovascular impact in patients undergoing maintenance hemodialysis: Clinical management considerations

Chirakarnjanakorn

Navaneethan

Francis

et al. 2017

International Journal of Cardiology

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“…In patients with ESRD, several mediators of inflammation share a link with cardiovascular disease [34,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63] (Table 1). Indeed, this is quite dubious for C reactive protein (CRP), either in terms of mere association or from a pathogenic perspective.…”

Section: Mechanisms By Which Inflammation May Increase Cardiovascularmentioning

confidence: 99%

“…In fact, while in some trials CRP did not merge as a strong independent cardiovascular risk factor (instead of IL-1, IL-6, TNF-α, albumin, and body mass index) [52,53,55,60], the genetic analysis of polymorphisms leading to a gain of function of gene transcription of CRP failed to demonstrate a dose-dependent effect of this marker [64] and a possible causal role. Other biomarkers (sTWEAK, MIC-1, CD4 + CD28-null T-cells, RANKL, pentraxin3, CCR5, GAL-3, myeloperoxidase, Lp-PLA 2 , and sCD14) , have also been linked to cardiovascular risk in ESRD [32,34,45,46,47,48,51,57,61,62,63]. Besides studies of association, there are evidences that uremic serum directly causes vascular damage [65] via activation of pro-inflammatory endothelial pathways (e.g., TLR4, NF-κB, NALP3 [NACHT, LRR and PYD domains-containing protein 3] and p38 MAPK [p38 mitogen-activated protein kinase]), which induce increased endothelial expression of ICAM-1, VCAM-1 (vascular cell adhesion molecule-1), von Willebrand factor [66,67], reduced nitric oxide availability, generating endothelial dysfunction [68].…”

Section: Mechanisms By Which Inflammation May Increase Cardiovascularmentioning

confidence: 99%

Targeting Immunity in End-Stage Renal Disease

2017

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Background: Despite the stable incidence of end-stage renal disease (ESRD), it continues to be associated with an unacceptably high cardiovascular risk. Summary: ESRD is characterized by enhanced oxidative stress and severe inflammation, which boost cardiovascular risk, thus increasing cardiovascular-associated mortality rate. While substantial effort has been made in the technological innovation of dialytic techniques, few significant advances have been made to reduce inflammation in patients with ESRD. Indeed, this contrasts with the extensive scientific breakthroughs made in the basic field of science in targeting inflammation. There is thus a pressing need for clinical trials to test the effect of reducing inflammation in patients with ESRD. Here, we will revisit the negative effect of ESRD on inflammation and explore the impact of enhanced inflammation on cardiovascular outcomes and survival in patients with ESRD. Finally, we will discuss the need for clinical trials that target inflammation in ESRD, as well as weigh potential disadvantages and offer novel innovative approaches. Key Message: We will try to understand why the issue of inflammation has not been successfully addressed thus far in patients with ESRD, while at the same time weighing the potential disadvantages and offering novel innovative approaches for targeting inflammation in patients with ESRD.

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“…A third possibility, also raised by Lines et al [21], is that complement activation could well be induced by dialysis treatment in itself, for instance, due to the use of bioincompatible materials including the dialysis membrane [23]. It is well established that hemodialysis in itself inflicts cardiovascular stress, which could be mediated by hemodynamic effects [24], but also by a pro-inflammatory profile of patients prone to experience hemodialysis-induced cardiac stress [25]. This pro-inflammatory state may, in turn, be related to dialysis (membrane)-induced complement activation in this category of patients.…”

Section: Figmentioning

confidence: 99%

The Complement System in Hemodialysis Patients: Getting to the Heart of the Matter

Borst

2016

Nephron

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Hemodialysis-Induced Regional Left Ventricular Systolic Dysfunction and Inflammation: A Cross-sectional Study

Cited by 31 publications

References 30 publications

Cardiovascular impact in patients undergoing maintenance hemodialysis: Clinical management considerations

Cardiovascular impact in patients undergoing maintenance hemodialysis: Clinical management considerations

Targeting Immunity in End-Stage Renal Disease

The Complement System in Hemodialysis Patients: Getting to the Heart of the Matter

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