Nephrology: New insight into common kidney disease
- Date:
- April 26, 2010
- Source:
- Journal of Clinical Investigation
- Summary:
- The kidney disease crescentic glomerulonephritis rapidly progresses to acute kidney failure and death within months if it is not treated. Even with treatment, many patients progress to end-stage kidney disease and require dialysis and sometimes a kidney transplant. New research in mice has identified a potential new drug target for the treatment of crescentic glomerulonephritis.
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The kidney disease crescentic glomerulonephritis rapidly progresses to acute kidney failure and death within months if it is not treated. Even with treatment, many patients progress to end-stage kidney disease and require dialysis and sometimes a kidney transplant.
New research in mice, performed by Alan Salama and colleagues, at Hammersmith Hospital, United Kingdom, has identified a potential new drug target for the treatment of crescentic glomerulonephritis.
In the study, mice lacking the mannose receptor protein were found to be protected from crescentic glomerulonephritis. This protection was associated with decreased kidney damage mediated by cells known as macrophages and mesangial cells. Further, macrophages lacking the mannose receptor actually became antiinflammatory in the kidney after they interacted with mesangial cells.
The authors therefore suggest that targeting the mannose receptor might provide a new approach to treating crescentic glomerulonephritis. Importantly, this approach would not have the wide-ranging immunosuppressive effects that many current therapies have.
The research appears in the Journal of Clinical Investigation.
Story Source:
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
Journal Reference:
- Konstantia-Maria Chavele, Luisa Martinez-Pomares, Jan Domin, Samantha Pemberton, Stuart M. Haslam, Anne Dell, H. Terence Cook, Charles D. Pusey, Siamon Gordon and Alan D. Salama. Mannose receptor interacts with Fc receptors and is critical for the development of crescentic glomerulonephritis in mice. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI41560
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