Our lab is focused on 2 projects at this time, both exploring the link between the alternative pathway of complement and vascular outcomes in chronic kidney disease (CKD). In one, we are measuring biomarkers of the alternative pathway of complement and evaluating if these predict future cardiovascular events and/or kidney disease progression. Common and rare genetic variants of complement will be evaluated as contributors to alternative pathway activation and adverse cardiovascular and kidney outcomes. In another, we have established an animal model of CKD. This includes wild type mice and mice with genetic deficiency of factor H. The latter group have underlying complement activation. We are evaluating if CKD contributes to complement lability and if activation of the alternative pathway results in vascular dysfunction in these mice. Future model development will include obese mice with single nephrectomy to evaluate the impact of alternative pathway activation on kidney disease progression.