Chemerin levels in chronic kidney disease: A systematic review and meta-analysis

Abstract

IntroductionChemerin as an inflammatory biomarker has gained attention in its biomarker capability. Several studies measured its levels in chronic kidney disease (CKD), as one of the common non-communicable causes of mortality and morbidity. Hence, this systematic review and meta-analysis aimed to investigate this association.MethodsPubMed, Scopus, Embase, and the Web of Science databases were systematically searched for studies investigating chemerin levels in any CKD stage (including end-stage renal disease patients undergoing hemodialysis (HD)) and comparing it with healthy controls. Random effect meta-analysis was performed to calculate the standardized mean difference (SMD) and 95% confidence interval (CI).ResultsA total of eight studies were included, comprised of 875 individuals, with a mean age of 56.92 ± 11.78 years. All studies had high quality based on the New Castle-Ottawa Scale (NOS). Meta-analysis revealed significantly higher levels of chemerin in CKD patients compared to healthy controls (SMD 2.15, 95% CI 0.83-3.48, p-value<0.01). Additionally, HD patients had statistically higher levels of chemerin than controls (SMD 2.10, 95% CI 0.58-3.62, p-value=0.01). In meta-regression, publication year accounted for 23.50% and 24.17% of heterogeneity for these analyses, respectively.ConclusionChemerin can be potentially used as a biomarker in CKD patients, which can suggest the inflammatory pathways for the disease. Further research is warranted for the assessment of its clinical applications and enlightening its role in the pathophysiology of CKD.

Comprehensive assessment of cardiovascular-kidney-metabolic (CKM) syndrome: Novel tools for assessment of cardiovascular risk and kidney outcomes in long-term kidney transplant patients

“…Others have also demonstrated a relationship with renal function in diabetics [41]. We observed a significant relationship between higher chemerin and KDIGO stage in KTRs, which falls in line with pooled observation for the general population [18].…”

“…Due to the 16kDA polypeptide size, increased chemerin may be derived from reduced excretion or increased stimulation of adipokine levels, which is consistent with decline in concentrations after KTx [18,43]. Alternatively, excessive activation of inflammatory, endothelial and oxidative cascades following renal insult may also contribute to higher chemerin levels [18]. In the present study, we observed serum chemerin concentrations showed an increase with higher CKM (numerical) and CKD stage, but also exhibited a prognostic role for dialysis therapy risk.…”

“…The role of adipose tissue as a major source of chemerin in CKD remains unclear [42]. Due to the 16kDA polypeptide size, increased chemerin may be derived from reduced excretion or increased stimulation of adipokine levels, which is consistent with decline in concentrations after KTx [18,43]. Alternatively, excessive activation of inflammatory, endothelial and oxidative cascades following renal insult may also contribute to higher chemerin levels [18].…”

“…It is mainly secreted by the liver and white adipose tissue, but also immune cells and endocrine organs [16]. Pooled data from multiple cohorts of CKD patients indicates higher chemerin concentrations parallel a decline in renal filtration [18]. While enhanced expression has been observed in experimental chemerin-related models of kidney disease, whether local production alone translates to marked shifts in circulating levels remains uncertain [19,20].…”

Hypoxia-Induced Insulin Resistance Mediates the Elevated Cardiovascular Risk in Patients with Obstructive Sleep Apnea: A Comprehensive Review

“…OSA independently increases the risk of insulin resistance [32]. Systematic reviews and meta-analyses confirm an association between OSA and insulin resistance determined via an elevated HOMA-IR [33] or the atherogenic index of plasma, calculated according to the formula: log (serum triglyceride level/serum HDL-c level) [34]. Compared to usual care, OSA therapy with continuous positive airway pressure (CPAP) [35][36][37][38][39][40] or implantation of a mandibular advancement device [41], improves insulin resistance without changing BMI, supporting a role for tissue hypoxia in the pathogenesis of insulin resistance.…”