Abstract
Ischemic acute kidney injury (IAKI) is a common but severe complication after a cardiopulmonary bypass (CPB). Multiple studies have demonstrated that peripheral CD133+ or differentiated cells are able to home and repair the damaged tissues, but the number of available CD133+ cells is limited, and no efficient method published previously to mobilize them immediately. We analyzed the relationship between CD133+ cells and renal function in CPB patients, in addition, the efficacy of granulocyte colony-stimulating factor (G-CSF) pre-mobilized CD133+ cells in treating of mouse IAKI model have been investigated. In the clinical study, the prospective cohort study analyzed the correlation between BUN/Crea level and the peripheral CD133+ cell numbers. CPB was associated with postoperative renal dysfunction. The significant negative correlation was observed between patients’ Crea and CD133+ cells (P < 0.05). The proposed mechanism studies were performed on the mouse IAKI model. The experimental mice were treated by G-CSF to mobilize CD133+ cells before implementing CPB. Data on cell count, inflammatory index, renal function/injury, and CD133+ cell mobilization were analyzed. The result demonstrated that pretreatment by G-CSF resulted in tremendous increase in the number of mouse peripheral blood and renal CD133+ cells, significantly reduces renal tissue inflammation and dramatically improves the renal function after CPB. In summary, we concluded that premobilization of CD133+ cells abated CPB induced IAKI, by promoting both repairing damaged epithelium and by its anti-inflammatory activity. Our findings stress the remarkable applications of CD133+ or differentiated cells-based therapies for potential preventing ischemic acute kidney injury.
Highlights
Ischemic acute kidney injury (IAKI) is a severe complication which occurs in about 30% of patients after implementing the cardiopulmonary bypass (CPB), and 2–7% of reported patients might need renal replacement therapy and associated with 50% mortality[1,2]
We tested the relationship with CD133+ cells and CPB induced postoperative renal dysfunction in patients, in addition, we test the efficacy of mobilization of cells by Granulocyte colony-stimulating factor (G-CSF) in treating of mouse IAKI model
There is no effective prevention methods nor treatments currently. Through this mouse model of IAKI induced by CPB, we demonstrated that pretreatment with G-CSF could significantly abate IAKI by increasing the number of CD133+ cells in kidney and www.nature.com/scientificreports cells in renal tissue, CD133 positive staining were shown in red fluorescence color, CD31 was used as the endothelial progenitor cells control displayed in green fluorescence color
Summary
Ischemic acute kidney injury (IAKI) is a severe complication which occurs in about 30% of patients after implementing the cardiopulmonary bypass (CPB), and 2–7% of reported patients might need renal replacement therapy and associated with 50% mortality[1,2]. IAKI often occurs within 24–48 hours after CPB surgery[43] In this project, we tested the relationship with CD133+ cells and CPB induced postoperative renal dysfunction in patients, in addition, we test the efficacy of mobilization of cells by G-CSF in treating of mouse IAKI model. We investigated a strategy to abated cardiopulmonary bypass-induced ischemic acute kidney injury by using premobilized CD133+ cells, which effectively reduces the CPB induced IAKI and improves renal function
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