Kidney failure is relatively common but potentially fatal, developing as a complication in about 5 percent of all hospitalized patients and up to 50 percent of patients in intensive care units.
Kidneys fail when the cells in the tubules, a component of the kidney’s basic structural unit, become dysfunctional. Although research has shown that immune cells that infiltrate renal tissue exacerbate and promote tubule dysfunction and structural injury, work done by Vanderbilt researchers Raymond Harris, M.D., Ming-Zhi Zhang, M.D., and colleagues suggests that local macrophages and dendritic cells might in turn promote repair.
The researchers demonstrate in a recent paper in Kidney International how colony-stimulating factor 1 (CSF-1), a type of signaling molecule, secreted in the proximal tubules is essential for recovery after acute kidney injury. They showed that tubular secretion of CSF-1 not only increases the population of renal tissue-repairing lymphocytes that are necessary for recovery, but that abolishing its expression leads to delayed recovery time and increased scarring.
This work was supported by National Institute of Health grants CA122620, DK095785, DK051265, DK062794, AG045040 and by funds from the Department of Veterans Affairs.
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