Abstract
Chronic kidney disease (CKD) is characterized by manifestations and symptoms involving systemic organs and apparatus, associated with elevated cardiovascular morbidity and mortality, bone disease, and other tissue involvement. Arterial hypertension (AH), diabetes mellitus (DM), and dyslipidemia, with glomerular or congenital diseases, are the traditional risk factors recognized as the main causes of progressive kidney dysfunction evolving into uremia. Acute kidney injury (AKI) has recently been considered an additional risk factor for the worsening of CKD or the development of CKD de novo. Evidence underlies the role of systemic inflammation as a linking factor between AKI and CKD, recognizing the role of inflammation in AKI evolution to CKD. Moreover, abnormal increases in oxidative stress (OS) and inflammatory status in CKD seem to exert an important pathogenetic role, with significant involvement in the clinical management of this condition. With our revision, we want to focus on and update the inflammatory mechanisms responsible for the pathologic conditions associated with CKD, with particular attention on the development of AKI and AKI-CKD de novo, the alteration of calcium-phosphorus metabolism with bone disease and CKD-MBD syndrome, the status of malnutrition and malnutrition–inflammation complex syndrome (MICS) and protein-energy wasting (PEW), uremic sarcopenia, the status of OS, and the different inflammatory pathways, highlighting a new approach to CKD. The depth comprehension of the mechanisms underlying the development of inflammation in CKD may present new possible therapeutic approaches in CKD and hopefully improve the management of correlated morbidities and provide a reduction in associated mortality.
Highlights
Alongside the recommended control of classical risk factors such as arterial hypertension (AH) and hyperglycemia with common pharmacological tools, in particular angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blocker (ARB), we explore the potential role of the new renin–angiotensin system (RAAS) blocker mediated by the novel nonsteroidal receptor antagonist finerenone and sodium–glucose cotransporter-2 (SGLT-2)
In another cross-sectional, observational study of our research group, 226 patients diagnosed with cystic fibrosis (CF), we reported a significant association between lower eGFR value and alteration of metabolic CV index, with a significant negative correlation between eGFR, triglycerides, and serum uric acid, which is involved in endothelial dysfunction by increasing inflammation and oxidative stress
We highlighted the role of inflammation as a linking condition present in all clinical, biological, and biochemical aspects of Chronic kidney disease (CKD), from traditional risk factors of renal disease, including AH, diabetes mellitus (DM), and dyslipidemia, to cellular and immunologic responses involving multiple proinflammatory processes
Summary
Uremic CV risk factors are chronic causes of a low-grade inflammatory status associated with alteration in calcium-phosphorus metabolism, hyperhomocysteinemia, malnutrition, uremic sarcopenia, and oxidative stress (OS) [1]. We aim to focus on and update the dynamic complex of inflammatory mechanisms responsible for the pathologic conditions associated with CKD, with particular attention on the development of AKI and hypoxia, the alteration of calciumphosphorus metabolism and bone disease, adipose tissue dysfunction, hyperhomocysteinemia, the status of malnutrition and uremic sarcopenia, gut microbiota alterations, and the status of OS. The role of OS, hypoxia-induced factors (HIFs), and other inflammatory mediators are considered and described, as the kidney represents one of the most metabolically active organs, which renders it vulnerable to oxidative damage, hypoxia, and inflammation.
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