Chronic kidney disease (CKD) is a growing public health issue. The Centers for Disease Control and Prevention estimates that one in seven Americans, about 35.5 million people, have CKD. A serious form of the disease is antibody-mediated glomerulonephritis (AGN), where antibodies attack the kidney’s glomeruli and cause inflammation and tissue injury.
Researchers reported new results in the Journal of Clinical Investigation Insight using a murine model of AGN. The work was led by Partha Biswas of the Renaissance School of Medicine at Stony Brook University. The team observed immune cells inside the kidney and focused on metabolically reprogrammed neutrophils.
They found that neutrophils in the nephritic kidney increase expression and function of the glucose transporter Glut1. The researchers showed that Glut1 activity in inflammatory cells is necessary for AGN to progress. Disabling Glut1 in neutrophils reduced tissue-damaging effector molecules in both early and late stages, while renal cytokine and chemokine production fell only in the late stage.
Treatment with a Glut1 inhibitor improved kidney pathology in AGN mice. The authors say targeting neutrophil metabolism may be a promising therapeutic strategy for AGN and possibly other forms of CKD. The research was supported in part by the National Institutes of Health.
Difficult words
- glomerulonephritis — inflammation of the kidney's tiny filtering units
- neutrophil — a white blood cell that fights infectionsneutrophils
- reprogram — to change how a cell works or behavesreprogrammed
- glucose transporter — a protein that moves sugar into cells
- inhibitor — a substance that stops or reduces activity
- cytokine — a small protein cells use to send signals
- pathology — damage or disease seen in an organ
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