Coexistence of micro-inflammatory and macrophage phenotype abnormalities in chronic kidney disease.

The heterogeneity of macrophages promotes renal fibrosis and plays an important role in the repair of kidney damage. The "microinflammation state" is closely related to accelerated mortality in patients with chronic kidney disease (CKD). The aim of this study was to investigate the relationship between microinflammation and macrophage polarization in CKD. The levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in peripheral blood of 30 non-dialysis CKD-5 patients (CKD group) and 20 healthy subjects (Con group) were measured. Peripheral mononuclear cells (PBMC) of each group were obtained, induced to differentiate into mature macrophages, and the expression of CD206 on the surface of macrophage M2 was detected. The expression of IL-10, TGF-β1 and TNF-α in the supernatant of macrophage culture medium was detected by real time RCR and ELISA. We found that the levels of hs-CRP, IL-6 and TNF-α in peripheral blood of patients with CKD were significantly higher than those of the control group. The expression of CD206 in macrophages was significantly decreased in CKD patients. The anti-inflammatory cytokines IL-10 and TGF-β1 in the supernatant of CKD macrophages decreased significantly, while the pro-inflammatory factor TNF-α did not change significantly. Our results demonstrate that the expressions of macrophage phenotype and anti-inflammatory cytokine in CKD patients are abnormal, which may be related to the microinflammation state prevalent in CKD patients.