Neopterin, MCP-1, and MCSF as New Markers of Tubular Damage in Children with Chronic Kidney Disease on Conservative Treatment - European Medical Journal

Neopterin, MCP-1, and MCSF as New Markers of Tubular Damage in Children with Chronic Kidney Disease on Conservative Treatment

2 Mins
*Kinga Musiał,1 Agnieszka Bargenda,1 Dorota Drożdż,2 Danuta Zwolińska1

The authors have declared no conflicts of interest.

EMJ Nephrol. ;5[1]:64-65. Abstract Review No. AR11.

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

Chronic kidney disease (CKD) is characterised by enhanced migration of immunocompetent cells to the sites of inflammation, renal fibrosis, and irreversible tubular damage. Monocyte chemoattractant protein (MCP)-1, macrophage colony stimulating factor (MCSF), and macrophage migration inhibitory factor (MIF) control early-stages of cell migratory activity, such as the movement of monocytes to the sites of inflammation and their transition into macrophages. However, these have not been put into the focus of CKD progression in children. Neopterin was the only parameter in this group produced by monocytes and macrophages upon stimulation. Thus, it may mirror cellular immune response; however, it has never been analysed as a marker of inflammation or macrophage activity in children with CKD.

The analysis of fractional excretion (FE) as a substitute for tubular dysfunction in CKD patients was studied in the case of heat shock protein (Hsp)-27 in adults1 and concerned markers of epithelial-mesenchymal transition in children from our previous study.2 The aim of this study was to analyse the usefulness of FE of MCP-1, MCSF, MIF, and neopterin as pluripotent markers of inflammation, monocyte-macrophage interplay, and tubular damage in the course of CKD. The study group consisted of 20 children at CKD Stages 1–2, 41 pre-dialysis patients at CKD Stages 3–5, and 23 age-matched controls. The serum and urine concentrations of MCP-1, MCSF, MIF, and neopterin were assessed by enzyme linked immunosorbent assay (ELISA). The FE of analysed parameters was then calculated according to the formula: ([parameter urine concentration] x [creatinine serum concentration])/([parameter serum concentration] x [creatinine urine concentration]) x 100%.

The serum and urine concentrations of MCP-1, MCSF, MIF, and neopterin were significantly elevated in CKD children versus controls, although no correlations were noticed. The values of MCSF and neopterin in urine were higher than those in serum, both in CKD and control groups. In healthy controls, the FE of MCP-1 and MIF did not exceed 1%, whereas it reached 5% in the case of MCSF and neopterin. FE MCP-1 remained <1% in children at CKD Stages 1–2 and FE MIF <1% was seen in all children with CKD. Only FE MCP-1 and MCSF values were significantly elevated in children at CKD Stages 1–2 versus controls, whereas all FE values were higher in patients at CKD Stages 3–5 than in CKD Stages 1–2.

The values of FE MCP-1 in CKD Stages 1–2 were significantly higher in comparison to controls but did not exceed 1%, which seemed to confirm the early inflammatory process in the tubules, preceding their damage. The increase in FE MCSF values, together with the decline in MCSF urine levels in CKD Stages 3–5, could signify early macrophage overactivity in renal parenchyma of CKD Stages 1–2 and progression to tubular damage in CKD Stages 3–5. Elevated FE neopterin values, accompanied by increasing neopterin urine concentrations in advanced CKD, suggested tubular damage due to persistent inflammation.

FE of the examined markers may serve as a useful tool in the assessment of CKD related to tubular dysfunction and may help distinguish between early inflammatory and late destructive processes in renal parenchyma of children with CKD.

Lebherz-Eichinger D et al. HSP27 and HSP70 serum and urine levels in patients suffering from chronic kidney disease. Clin Chim Acta. 2012;413:282-6. Bargenda A et al. Fractional excretion of survivin, EMMPRIN, and MMP-7 in children with chronic kidney disease. EMJ Nephrol. 2016;4(1):113-9.

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