Abstract
Kidney injury in the course of chronic kidney disease (CKD) is a consequence of aggravated cell migration, inflammation, apoptosis, and fibrosis. However, the sequence of these phenomena, as well as of the reparatory mechanisms, are not fully known. Monocyte chemoattractant protein 1 (MCP-1) and macrophage colony-stimulating factor (MCSF) trigger monocyte migration to the sites of inflammation and their transition into macrophages. Tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) plays a protective role against excessive matrix remodeling, whereas survivin is known for its anti-apoptotic activity. To analyze the serum, urine and fractional excretion (FE) values of MCP1, MCSF, TIMP-2, and survivin in children at subsequent stages of CKD being treated conservatively, and to analyze the potential applicability of these markers in the evaluation of CKD-related renal damage and protective mechanisms against it. The study group consisted of 70 children with conservatively treated CKD, stages 1-5, and 12 controls. The serum and urine concentrations of MCP1, MCSF, TIMP-2, and survivin were assessed using enzyme-linked immunosorbent assay (ELISA). The FE of these parameters in the urine was also assessed. The serum values of all parameters were significantly elevated at CKD stage 1 compared to the controls. The urinary concentrations of MCP-1 and MCSF (stages 1-2) rose earlier than TIMP-2 and survivin (stage 4) concentrations. The FE values started increasing at CKD stage 3 (MCP-1) or stage 4 (other parameters). The complex analysis of serum/urinary/FE values of the selected parameters revealed a sequence of multifaceted CKD-related phenomena, when the migration of cells and inflammation were followed by delayed and insufficient anti-fibrotic and anti-apoptotic activity.
Highlights
Renal interstitial fibrosis is the final step in the progression of chronic kidney disease (CKD), irrespective of its origin, and confirms its irreversibility.[1]
The fractional excretion (FE) values started increasing at CKD stage 3 (MCP-1) or stage 4
The steep rise in CKD stage 1 was observed in the case of Monocyte chemoattractant protein 1 (MCP-1), macrophage colony-stimulating factor (MCSF) and Tissue inhibitor of matrix metalloproteinases-2 (TIMP-2), where the concentrations increased more than threefold, whereas those of survivin only by 30% (Fig. 2–5)
Summary
Renal interstitial fibrosis is the final step in the progression of chronic kidney disease (CKD), irrespective of its origin, and confirms its irreversibility.[1]. It is a consequence of an imbalance between tissue repair and damage.[2]. Chronic kidney disease triggers both destructive and protective mechanisms in the kidney, concerning immunocompetent cell activity, inflammation or apoptosis.[2]. Monocyte chemoattractant protein 1 (MCP-1) and macrophage colony stimulating factor (MCSF) are engaged in the early phase of injury: immunocompetent cell migration to the sites of inflammation. Kidney injury in the course of chronic kidney disease (CKD) is a consequence of aggravated cell migration, inflammation, apoptosis, and fibrosis. Tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) plays a protective role against excessive matrix remodeling, whereas survivin is known for its anti-apoptotic activity
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