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Complement activation in the tubulointerstitium: AKI, CKD, and in between.
Jyoti E Brar1, Richard J Quigg1
1Division of Nephrology, Department of Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York, USA.
Kidney International
|October 1, 2014
Summary
Deleting the complement regulator Crry from kidney tubular cells did not affect healthy mice. However, it worsened injury after ischemia-reperfusion due to alternative pathway complement activation.
Area of Science:
- Immunology
- Nephrology
- Complement System Biology
Background:
- Complement activation is tightly regulated to prevent tissue damage.
- Aberrant complement activity contributes to kidney injury.
Purpose of the Study:
- To investigate the role of tubular cell complement regulator Crry in kidney injury.
- To determine the impact of Crry deletion in tubular cells on ischemia-reperfusion injury.
Main Methods:
- Generated mice with Crry specifically deleted from kidney tubular cells.
- Assessed kidney injury following ischemia-reperfusion in these mice.
Main Results:
- Crry deletion in tubular cells had no effect in unmanipulated mice.
- Following ischemia-reperfusion, Crry-deleted mice exhibited exacerbated kidney injury.
- This increased injury was linked to alternative pathway activation of C5.
Conclusions:
- Tubular cell complement regulation is crucial for mitigating kidney injury.
- Imbalance favoring complement activation over regulation leads to pathologic outcomes in the kidney.
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