Dr. Lakhia is on Doximity
As a Doximity member you'll join over two million verified healthcare professionals in a private, secure network.
- Gain access to free telehealth tools, such as our “call shielding” and one-way patient texting.
- Connect with colleagues in the same hospital or clinic.
- Read the latest clinical news, personalized to your specialty.
Office
5323 Harry Hines Blvd
Dallas, TX 75390Phone+1 214-645-1919Fax+1 214-645-0078
Education & Training
- University of Texas Southwestern Medical CenterFellowship, Nephrology, 2012 - 2014
- Baylor College of MedicineResidency, Internal Medicine, 2008 - 2011
- University of Texas Southwestern Medical SchoolClass of 2008
Certifications & Licensure
- TX State Medical License 2010 - 2025
- American Board of Internal Medicine Nephrology
Clinical Trials
- A Study of RGLS8429 in Patients With Autosomal Dominant Polycystic Kidney Disease Start of enrollment: 2022 Oct 06
Roles: Contact
Publications & Presentations
PubMed
- 136 citationsmicroRNA-17 family promotes polycystic kidney disease progression through modulation of mitochondrial metabolismSachin Hajarnis, Ronak Lakhia, Matanel Yheskel, Darren Williams, Mehran Sorourian
Nature Communications. 2017-02-16 - 86 citationsPPARα agonist fenofibrate enhances fatty acid β-oxidation and attenuates polycystic kidney and liver disease in miceRonak Lakhia, Matanel Yheskel, Andrea Flaten, Ezekiel B. Quittner-Strom, William L. Holland
American Journal of Physiology. Renal Physiology. 2018-01-01 - 34 citationsInterstitial microRNA miR-214 attenuates inflammation and polycystic kidney disease progressionRonak Lakhia, Matanel Yheskel, Andrea Flaten, Harini Ramalingam, Karam Aboudehen
JCI Insight. 2020-04-09
Journal Articles
- microRNA-17 Family Promotes Polycystic Kidney Disease Progression Through Modulation of Mitochondrial MetabolismJoshua A Johnson, Ronak Lakhia, Peter Igarashi, Vishal Patel, Nature
Viewing the full profile is available to verified healthcare professionals only.
Find your profile and take control of your online presence: