Eryptosis in Patients with Chronic Kidney Disease: A Possible Relationship with Oxidative Stress and Inflammatory Markers.
CKD
eryptosis
inflammation
oxidative stress
red blood cells
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
02 Dec 2022
02 Dec 2022
Historique:
received:
20
10
2022
revised:
24
11
2022
accepted:
30
11
2022
entrez:
11
12
2022
pubmed:
12
12
2022
medline:
12
12
2022
Statut:
epublish
Résumé
Background. Eryptosis is the programmed death of red blood cells; it may contribute to worsening anemia in chronic kidney disease (CKD). In this clinical condition, different factors induce eryptosis, such as oxidative stress, energy depletion and uremic toxins. In our study, we investigated if the progression of CKD may influence erythrocyte death levels and its relationship with oxidative stress and inflammation. Methods. We evaluated eryptosis levels in 25 CKD patients (five for each stage), as well as markers of oxidative stress and inflammation: myeloperoxidase (MPO), copper/zinc superoxide dismutase (Cu/Zn SOD) and interleukin-6 (IL-6) were evaluated in plasma samples. Results. Higher cell death rate was reported in the highest CKD stages (p < 0.05). Furthermore, we divided CKD patients into two groups (eGFR< or ≥60 mL/min/1.73 m2). Patients with eGFR < 60 mL/min/1.73 m2 had higher eryptosis levels (p < 0.001). MPO, CU/Zn SOD and IL-6 resulted significantly differently between groups (p < 0.001). Significant positive correlations were reported between eryptosis and MPO (Spearman’s rho = 0.77, p = 0.01) and IL-6 (Spearman’s rho = 0.52, p = 0.05) and Cu/Zn SOD. Spearman’s rho = 0.6, p = 0.03). Conclusions. In patients with CKD, different factors are involved in the pathogenesis of eryptosis, in particular uremic toxins and oxidative stress and inflammatory markers. The progressive impairment of renal function may be associated with the increase in eryptosis levels, probably due to the accumulation of oxidative stress factors, inflammatory cytokines and uremic toxins.
Identifiants
pubmed: 36498741
pii: jcm11237167
doi: 10.3390/jcm11237167
pmc: PMC9737176
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Front Cell Dev Biol. 2020 Jul 08;8:597
pubmed: 32733893
Arch Biochem Biophys. 2007 Jun 15;462(2):189-94
pubmed: 17316548
Kidney Int. 2004 Nov;66(5):1988-93
pubmed: 15496170
Antioxidants (Basel). 2020 Sep 27;9(10):
pubmed: 32992565
J Clin Med. 2022 Sep 10;11(18):
pubmed: 36142976
Cell Physiol Biochem. 2019;53:794-804
pubmed: 31661199
BMC Nephrol. 2013 Nov 04;14:244
pubmed: 24188099
Transfus Med Hemother. 2012 Oct;39(5):308-14
pubmed: 23801921
Kidney Blood Press Res. 2022;47(6):375-390
pubmed: 35114677
Kidney Blood Press Res. 2013;37(2-3):158-67
pubmed: 23712027
Blood Purif. 2016;41(4):317-23
pubmed: 26848873
Antioxidants (Basel). 2020 Sep 28;9(10):
pubmed: 32998418
Toxins (Basel). 2015 Oct 28;7(11):4390-403
pubmed: 26516916
World J Nephrol. 2013 May 6;2(2):31-7
pubmed: 24175263
Ann Intern Med. 2009 May 5;150(9):604-12
pubmed: 19414839
J Am Soc Nephrol. 1999 Sep;10(9):1982-90
pubmed: 10477151
Lipids Health Dis. 2010 Sep 03;9:93
pubmed: 20815897
Nephrol Dial Transplant. 2003 Jul;18(7):1272-80
pubmed: 12808161
Blood Purif. 2012;33(1-3):125-30
pubmed: 22269222
Blood Purif. 2019;48(4):351-357
pubmed: 31291616
Mol Cell Biochem. 2011 Nov;357(1-2):171-9
pubmed: 21625956
Int Urol Nephrol. 2022 Nov;54(11):2919-2928
pubmed: 35469112
J Biol Chem. 1987 Jul 15;262(20):9555-60
pubmed: 3036865
Am J Kidney Dis. 2001 Apr;37(4):807-14
pubmed: 11273881