“…They found upregulation of genes associated with the immune response, which correlated inversely with estimated glomerular filtration rate. Several of the differentially expressed genes in their study were also identified in our analysis, most notably including CC‐chemokine ligand 19 ( Ccl19 ) and its receptor 7 ( Ccr7 ), which are essential in establishing dendritic cell and T cell recruitment 44 ; several members of the C‐type lectin family (eg, Clec5a , Clec7a ), which have been strongly linked with activation of the nucleotide‐binding oligomerization domain‐like receptor protein 3 inflammasome and pyroptotic cell death 23 , 24 ; SLAM family member 6 ( Slamf6 ) and glycoprotein CD2 ( Cd2 ), both of which belong to the immunoglobulin superfamily and are expressed on natural killer, T, and B lymphocytes 45 ; interferon regulatory factor 4 ( Irf4 ), which has been implied in kidney fibrosis as it may regulate the migration and activation of macrophages 46 ; surface receptor sialic acid binding Ig‐like lectin 1 ( Siglec1 ), which regulates monocyte–macrophage activation and has been linked to increased frequency of kidney complications in patients with systemic lupus erythematosus 47 ; and members of the matrix metalloproteinase family (eg, Mmp2 , Mmp7 , MMp12 ), which play and important role in the degradation of the extracellular matrix and have been linked to CKD progression. 48 These findings are also well in accordance with the study by Tajti et al, 39 who confirmed the role of inflammation across a wide spectrum of CKD entities.…”