Chronic kidney disease (CKD) is a growing medical problem, and the number of patients progressing to end-stage renal disease has increased by 95 percent over the last 10 years in the United States. There are currently over half a million Americans on dialysis, a procedure that severely reduces quality of life and comes with much comorbidity. Furthermore, the impact of CKD is not limited to impairments related to renal failure. CKD is also recognized as an important risk factor for other ailments such as cardiovascular disease, including myocardial infarction, atherosclerosis, stroke and hypertension. A critical and unavoidable contributor to CKD is normal kidney aging.
Our goal is to identify key genetic factors that contribute to the decline of function and damage in the aging kidney, to learn their role in the kidney, and to understand why variations of these factors lead to different outcomes. We do this by studying the natural genetic variation in mice and their association with different kidney phenotypes. Once causal genes are identified, we develop precision disease models for further study of the gene and to develop therapeutics that will slow down the decline of kidney function and development of disease.