The Role of Inflammation in CKD

Abstract

Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD.

Nlrp2 deletion ameliorates kidney damage in a mouse model of cystinosis

“…These in vivo observations are in full agreement with our previous in vitro data, demonstrating in PTEC that NLRP2 overexpression upregulates the expression and production of many proinflammatory and profibrotic genes by modulating the activity of the transcription factor NF-κB ( 19 ). Indeed, it has been widely demonstrated that the local production of inflammatory mediators by hematopoietic and non-hematopoietic cells, including Cxcl1 , Saa1 , Il6 and Mcp1 , which we found modulated in cystinotic kidney by Nlrp2 deletion, plays an important role in promoting immune and inflammatory responses which, in turn, may contribute to the exacerbation of kidney damage ( 29 , 30 ). Contrary to results obtained in vitro showing a role for NLRP2 in promoting anti-apoptotic responses in PTECs, Nlrp2 deficiency in cystinotic mice induced a significant decrease in renal apoptotic rate, as assessed by cleaved Caspase-3 staining.…”

Systemic immune inflammation index is a valuable marker for predicting hemodialysis patients with depression: a cross-sectional study

“…During dialysis, contact between blood and foreign objects can lead to acute and chronic in ammatory reactions through complement activation, cytokine or nitric oxide (NO) production, oxidant stress, carbonyl stress, activation of T-cell, B-cell and monocyte et al [16]. In addition, MHD patients can also experience sustained in ammatory activation due to factors such as oxidative stress, hypoxia, uid and sodium overload, dysbiosis of gut microbiota, and uremic toxins including indoxyl sulphate [6,17]. High levels of in ammation in MHD patients can further mediate the occurrence of depression through cytokines.…”

Immune cell signatures and inflammatory mediators: unraveling their genetic impact on chronic kidney disease through Mendelian randomization

“…Chronic kidney disease is frequently accompanied by a persistent, low-grade inflammatory state, implicated in disease progression and linked to a spectrum of comorbid conditions including atherosclerosis, cardiovascular diseases, cachexia, malnutrition, and anemia [ 53 ]. At the core of this inflammatory milieu is IL-17A, a cornerstone cytokine within the IL-17 family, renowned for its proinflammatory actions in synergy with cytokines like IL-1-β and TNF.…”