Plasma calprotectin in chronically dialyzed end-stage renal disease patients

Malíčková, Karin; Brodská, Helena; Lachmanová, J; Sulková, S; Janatková, I; Marecková, H; Tesař, Vladimı́r; Zima, Tomáš

doi:10.1007/s00011-009-0103-x

Cited by 11 publications

(8 citation statements)

References 24 publications

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“…In addition, calprotectin was more strongly and independently associated with CV outcome and mortality than CRP. Our results, in accordance with previous reports (17,19,20,24), suggest that the regulation of calprotectin and CRP respond to different mechanisms and that calprotectin may be a more sensitive marker of the chronic inflammatory state than CRP. In our 5/6 Nx mouse model, increased plasma calprotectin was strongly correlated to renal function decline and monocyte count.…”

Section: Discussionsupporting

confidence: 93%

“…Calprotectin is a marker of disease activity in many autoimmune and inflammatory diseases, including rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematous, or, more recently, COVID-19 (14)(15)(16). Some reports have shown that circulating calprotectin was increased in dialysis patients compared with healthy individuals (17,18) and that serum calprotectin was associated with overall mortality in hemodialysis patients with elevated serum phosphorus or patients on peritoneal dialysis (19,20). In addition, increased circulating calprotectin has been associated with a higher incidence of CV events in patients without CKD, including coronary events, peripheral arterial disease, and acute ischemic stroke (21)(22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

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Calprotectin is a contributor to and potential therapeutic target for vascular calcification in chronic kidney disease

Amaya-Garrido,

Brunet,

Buffin-Meyer

et al. 2023

Sci. Transl. Med.

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Vascular calcification is an important risk factor for cardiovascular (CV) mortality in patients with chronic kidney disease (CKD). It is also a complex process involving osteochondrogenic differentiation of vascular smooth muscle cells (VSMCs) and abnormal deposition of minerals in the vascular wall. In an observational, multicenter European study, including 112 patients with CKD from Spain and 171 patients on dialysis from France, we used serum proteome analysis and further validation by ELISA to identify calprotectin, a circulating damage-associated molecular pattern protein, as being independently associated with CV outcome and mortality. This was confirmed in an additional cohort of 170 patients with CKD from Sweden, where increased serum calprotectin concentrations correlated with increased vascular calcification. In primary human VSMCs and mouse aortic rings, calprotectin exacerbated calcification. Treatment with paquinimod, a calprotectin inhibitor, as well as pharmacological inhibition of the receptor for advanced glycation end products and Toll-like receptor 4 inhibited the procalcifying effect of calprotectin. Paquinimod also ameliorated calcification induced by the sera of uremic patients in primary human VSMCs. Treatment with paquinimod prevented vascular calcification in mice with chronic renal failure induced by subtotal nephrectomy and in aged apolipoprotein E–deficient mice as well. These observations identified calprotectin as a key contributor of vascular calcification, and increased circulating calprotectin was strongly and independently associated with calcification, CV outcome, and mortality in patients with CKD. Inhibition of calprotectin might therefore be a promising strategy to prevent vascular calcification in patients with CKD.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Calprotectin is a contributor to and potential therapeutic target for vascular calcification in chronic kidney disease

Amaya-Garrido,

Brunet,

Buffin-Meyer

et al. 2023

Sci. Transl. Med.

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“…Plasma levels of S100A8/A9 predicted risk of future myocardial infarction, stroke or death in post-menopausal healthy women [ 25 ]. Elevated S100A8 levels have also been found in other inflammatory disorders which are associated with abnormalities of vascular and cardiac function, particularly diastolic dysfunction, such as diabetes [ 46 – 48 ], end-stage renal disease [ 49 , 50 ], and inflammatory bowel disease [ 51 , 52 ]. This is the first association of S100A8 with HFpEF, yet its role in the disease process still needs be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Combining patient proteomics and in vitro cardiomyocyte phenotype testing to identify potential mediators of heart failure with preserved ejection fraction

et al. 2016

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BackgroundHeart failure with ejection fraction (HFpEF) is a syndrome resulting from several co-morbidities in which specific mediators are unknown. The platelet proteome responds to disease processes. We hypothesize that the platelet proteome will change composition in patients with HFpEF and may uncover mediators of the syndrome.Methods and resultsProteomic changes were assessed in platelets from hospitalized subjects with symptoms of HFpEF (n = 9), the same subjects several weeks later without symptoms (n = 7) and control subjects (n = 8). Mass spectrometry identified 6102 proteins with five scans with peptide probabilities of ≥0.85. Of the 6102 proteins, 165 were present only in symptomatic subjects, 78 were only found in outpatient subjects and 157 proteins were unique to the control group. The S100A8 protein was identified consistently in HFpEF samples when compared with controls. We validated the fining that plasma S100A8 levels are increased in subjects with HFpEF (654 ± 391) compared to controls (352 ± 204) in an external cohort (p = 0.002). Recombinant S100A8 had direct effects on the electrophysiological and calcium handling profile in human induced pluripotent stem cell-derived cardiomyocytes.ConclusionsPlatelets may harbor proteins associated with HFpEF. S100A8 is present in the platelets of subjects with HFpEF and increased in the plasma of the same subjects. We further established a bedside-to-bench translational system that can be utilized as a secondary screen to ascertain whether the biomarkers may be an associated finding or causal to the disease process. S100A8 has been linked with other cardiovascular disease such as atherosclerosis and risk for myocardial infarction, stroke, or death. This is the first report on association of S100A8 with HFpEF.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0774-3) contains supplementary material, which is available to authorized users.

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“…Attempts to measure calprotectin levels in patients with ESKD have been reported by others with conflicting results. Malickova et al 27 found calprotectin levels elevated in patients with ESKD predialysis and unchanged after dialysis; intradialytic levels were not obtained. The focus of their study was not on neutrophil activation per se and the multiple parameters we assessed were not measured.…”

Section: Discussionmentioning

confidence: 98%

Neutrophil Activation and Neutrophil Extracellular Trap Formation in Dialysis Patients

2020

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Plasma calprotectin in chronically dialyzed end-stage renal disease patients

Abstract: Significantly elevated levels of plasma calprotectin in ESRD patients occur without an acute infectious cause and are not affected by the presence of diabetes. By analogy to plasma beta-2 microglobulin, a close relation of plasma calprotectin to HD vintage was shown.

Cited by 11 publications

References 24 publications

Calprotectin is a contributor to and potential therapeutic target for vascular calcification in chronic kidney disease

Calprotectin is a contributor to and potential therapeutic target for vascular calcification in chronic kidney disease

Combining patient proteomics and in vitro cardiomyocyte phenotype testing to identify potential mediators of heart failure with preserved ejection fraction

Neutrophil Activation and Neutrophil Extracellular Trap Formation in Dialysis Patients

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