Mann Lab
Approximately 20-30% of children with chronic kidney disease have an underlying genetic cause of their disease. Our lab is interested in better understanding the genetic landscape of kidney disease and the mechanisms by which these genetic changes affect kidney development and function.
We apply human genetics and basic cell biology techniques to study how genetic changes impact kidney function. Dr. Mann also co-directs the Kidney Genetics Clinic at Nationwide Children's Hospital, and we integrate clinical genetics with basic research with the goal of improving diagnosis, care and future treatments for children with inherited kidney conditions.
Inside Mann Lab
Featured Publications
- Mechanisms of Podocyte Injury in Genetic Kidney Disease
- Genetic Contributions to Lower Urinary Tract Dysfunction
- Mutations in PRDM15 Are a Novel Cause of Galloway-Mowat Syndrome
- CAKUT and Autonomic Dysfunction Caused by Acetylcholine Receptor Mutations
- Whole-Exome Sequencing Enables a Precision Medicine Approach for Kidney Transplant Recipients
Join Our Team
The Mann Lab is actively recruiting undergraduate and post-doctoral researchers. If you are interested in joining our team or collaborating, please email Nina Mann at Nina.Mann@NationwideChildrens.org.
Featured Research Projects
Lower urinary tract dysfunction can cause significant distress for patients. Our previous studies discovered that mutations in an acetylcholine receptor, CHRNA3, can cause recurrent urinary tract infections and bladder dysfunction. We are applying genomic tools to discover novel genetic causes for lower urinary tract dysfunction and to understand the functional consequences of these genetic changes.
WT1, or wilms tumor 1, is a protein that plays an important role in kidney development and health, and mutations in WT1 can cause a spectrum of diseases, including wilms tumor, proteinuria and end-stage kidney disease. We are interested in better understanding the clinical spectrum of WT1-related disease as well as the mechanisms by which patient mutations may impact WT1 function.
