Diana Zepeda-Orozco, MD

Portrait
Clinical Associate Professor of Pediatrics - Nephrology, Dialysis and Transplantation

Contact Information

Primary Office
SE 425 GH
200 Hawkins Drive
Iowa City, IA 52242
319-4675-5113

Lab
1257 CBRB
Iowa City, IA 52242
319-384-1771

Education

MD, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico
Resident, Pediatrics, University of Tennessee, LeBonheur Children's Medical Center, Memphis, Tennessee
Fellow, Pediatric Nephrology, Children's Medical Center, University of Texas Southwestern Medical Center, Dallas, Texas
Fellow, Pediatric Nephrology Transplant, University of Texas Southwestern Medical Center, Dallas, Texas

Licensure and Certifications

Pediatric Nephrology
Iowa Medical License
Pediatrics

Center, Program and Institute Affiliations

Fraternal Order of Eagles Diabetes Research Center, Holden Comprehensive Cancer Center

Research Summary

Acute kidney injury (AKI) is a condition with a mortality rate >50% in the intensive care unit, and current treatment remains supportive. The incidence of AKI has been increasingly related to incremental use of nephrotoxic agents in a population with higher prevalence of chronic kidney disease (CKD). The current treatment of AKI is supportive and trials of a variety of agents showing promise in experimental AKI models have failed to ameliorate clinical AKI in translational studies. Dr. Zepeda-Orozco is a pediatric nephrology physician scientist that encounters this problem all the time. The Zepeda-Orozco lab focuses on defining how impaired tubular epithelial cells mitochondrial metabolism causes oxidative stress, and their implications in maladaptive repair following AKI. Maladaptive repair is caused by incomplete resolution of kidney injury leading to residual abnormalities in kidney structure (tubular atrophy, interstitial fibrosis, reduction of interstitial capillaries) and function. Biochemical pathways involved in AKI maladaptive repair include hypoxia, oxidative stress, and mitochondrial dysfunction, which contribute to the development of progressive renal disease even in younger patients. Understanding how tubular epithelial cell mitochondrial metabolism and oxidative stress are implicated in AKI maladaptive repair is key to develop novel approaches for implementation in direct patient care to predict, prevent, and treat the AKI maladaptive repair.