Abstract
Patients with chronic kidney disease (CKD) have significant cardiovascular morbidity and mortality as a result of risk factors such as left ventricular hypertrophy (LVH), oxidative stress, and inflammation. The presence of anaemia in CKD further increases the risk of LVH and oxidative stress, thereby magnifying the deleterious consequence in uraemic cardiomyopathy (UCM), and aggravating progression to failure and increasing the risk of sudden cardiac death. This short review highlights the specific cardio-renal oxidative stress in CKD and provides an understanding of the pathophysiology and impact of uraemic toxins, inflammation, and anaemia on oxidative stress.
Highlights
Oxidative stress refers to an imbalance in the reactive oxygen species (ROS) production/degradation ratio
Given that iron deficiency anaemia in chronic kidney disease (CKD) may exacerbate oxidative stress and worsen the poor cardiovascular outcome, how can parenteral iron therapy which is employed in current clinical practice modify oxidative stress at both the systemic and tissue level? This review aims to provide insight into these questions and highlight research questions that need to be answered in the future
Hypertension and increased oxidative stress in the animal model of CKD were both attenuated by antioxidant therapy [55,56]
Summary
Oxidative stress refers to an imbalance in the reactive oxygen species (ROS) production/degradation ratio. The association between renal and cardiac oxidative stress in chronic kidney disease (CKD) is poorly defined, and the impact of anaemia on the oxidant status of the kidney and heart is not completely characterized. HIangfloacmytmesa,tomryoncoeclyltses(/em.ga.c, ropphhaaggoecsy, teosr, mOpcao2oulynsaimontcgotyhrtpeoexshs/iiodtmneauotaicfcvlrieeonapflrshtalrmaeeugsmseksoaa,tcniyoodtrnepsRc)aoOurlyeSslmientahogsareoptx,rhieidonanactuttiiuvcvrleeensa,strurceblasesnsutaakinnnocdicteyiRsatetOsesuS)cintrhhetarlaeatsa,ciseOnell2utruelaaratnrc,tthsicvieagennsisaitnulelibitonisafgttaiennciafcnlesatcsrmaasdcmueeclalhtutihloaaansrt saicgtnivaaltliensgpcraos-icnafdlaemthmatataocrtyivgaetenseperxop-irneflssaimonm[3a9to].ryFogreenxeaemxpprlee,ssainonin[c3r9e]a.sFeoirneRxOamS pislea,sasnociinactreedasweitinh RthOeSinisduascstoiocniaotefdinwfliathmtmheatiinodnu, cctoionnseoqfuiennfltalymimncarteioansi,ncgonthseeqlueveneltslyoifnmcreedaisaintogrsthseulcehvealssionftemrleeduikaitno-r6s (IL-6) and tumour necrosis factor β (TGF-β) [40]. Inflammation and oxidative stress in CKD are interlinked, with synergy between them magnifying the deleterious consequences associated with. Inflammation4aonf 1d4 oxidative stress in CKD are interlinked, with synergy between them magnifying the deleterious ceoitnhseerqoufenthceesmasaslooncieat(esdeewFiitghuerieth3e)r. Hypertension and increased oxidative stress in the animal model of CKD were both attenuated by antioxidant therapy [55,56]
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