Abstract
Accumulating evidence indicates that oxidative stress plays a role in the pathophysiology of chronic kidney disease (CKD) and its progression; during renal replacement therapy, oxidative stress-derived oxidative damage also contributes to the development of CKD systemic complications, such as cardiovascular disease, hypertension, atherosclerosis, inflammation, anaemia, and impaired host defence. The main mechanism underlying these events is the retention of uremic toxins, which act as a substrate for oxidative processes and elicit the activation of inflammatory pathways targeting endothelial and immune cells. Due to the growing worldwide spread of CKD, there is an overwhelming need to find oxidative damage biomarkers that are easy to measure in biological fluids of subjects with CKD and patients undergoing renal replacement therapy (haemodialysis, peritoneal dialysis, and kidney transplantation), in order to overcome limitations of invasive monitoring of CKD progression. Several studies investigated biomarkers of protein oxidative damage in CKD, including plasma protein carbonyls (PCO), the most frequently used biomarker of protein damage. This review provides an up-to-date overview on advances concerning the correlation between plasma protein carbonylation in CKD progression (from stage 1 to stage 5) and the possibility that haemodialysis, peritoneal dialysis, and kidney transplantation improve plasma PCO levels. Despite the fact that the role of plasma PCO in CKD is often underestimated in clinical practice, emerging evidence highlights that plasma PCO can serve as good biomarkers of oxidative stress in CKD and substitutive therapies. Whether plasma PCO levels merely serve as biomarkers of CKD-related oxidative stress or whether they are associated with the pathogenesis of CKD complications deserves further evaluation.
Highlights
Chronic kidney disease (CKD) has a worldwide prevalence of around 8-16%, and it is declared by the World Health Organization (WHO) as an ever-increasing public health problem [1]
CKD is usually characterized by albuminuria and/or decreased glomerular filtration rate (GFR), which is the volume of plasma filtered by the glomeruli per unit of time
Colombo et al [41] divided ESRD patients on HD into two groups according to sex, and they reported that pre-HD and post-HD plasma protein carbonyls (PCO) levels in females were significantly different while in males were not
Summary
Chronic kidney disease (CKD) has a worldwide prevalence of around 8-16%, and it is declared by the World Health Organization (WHO) as an ever-increasing public health problem [1]. Several biomarkers of oxidative stress, such as malondialdehyde, oxidized low-density lipoprotein, advanced glycation end products, and 7,8-dihydro-8-oxo-2′-deoxyguanosine, have increased levels in patients with CKD [11] Their specificity as a biomarker of oxidative stress can be questionable, as in the case of oxidized low-density lipoprotein, which is most commonly measured in plasma or isolated lipoprotein by immunological methods using one of three different antibodies, each of which has methodological limitations [22]. CKD is characterized by the accumulation of uremic toxins released from the intestinal tract, which have become clinically relevant in CKD progression and are tightly related to many CKD-associated systemic complications, including inflammation, oxidative stress, and decreased production of nitric oxide by endothelial cells [23]. We summarize and discuss the main studies that have assessed plasma PCO levels in CKD, dialysis, and kidney transplantation and the potential role of protein carbonylation in driving CKD progression
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