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The division has a long history of basic, clinical, and outcomes research. Basic research is predominantly housed in the modern UTHSC translational science buildings. A strong federal (NIH, VA, DOD) funding base exists.

Areas of strength include:

  1. Uremic metabolic bone disease
  2. Chronic inflammation and microbial biome in CKD morbidity and mortality
  3. Molecular and cellular approaches to metabolic syndrome
  4. Renal outcome research focusing on factors that effect and accelerate CKD

The Transplant Research Institute also has 3 PhD scientists and a PhD bioinformatics specialist working on projects that include:

  1. A biobank of kidney allograft biopsies (cold storage and reperfusion specimens), organ perfusate, recipient urine, and recipient blood
  2. Roles of non-coding RNAs in the transplant setting
  3. Machine learning tools applied to clinical and omics data
  4. Development of a novel tool for identification of APOL1 genotyping

Clinical Research Program: Clinical Outcomes and Clinical Trials Program (COCTP)

Csaba P. Kovesdy, MD, who is the Fred Hatch Professor of Medicine at UT Health Science Center, heads the group. Our group’s research interests are centered on epidemiology and outcomes research, and clinical trials in the fields of nephrology, transplantation medicine and general internal medicine.

Besides its main research mission, COCTP provides research training for fellows, residents, graduate and undergraduate students interested in pursuing careers in medicine and/or medical research, and also for young physician investigators from all over the world.

Basic Science Laboratory

The Quarles laboratory is interested in metabolic disorders, particularly those involving bone and mineral metabolism.   Our group of scientists focus on three major areas, including the FGF23-Bone-Kidney Network, the Osteocalcin-GPRC6A Bone Endocrine Network, and bone mechanosensing. 

We have made many of the seminal observations that have shaped the field of FGF23 research.  For example, we:

  • Discovered that Phex and FGF23 are co-expressed in the osteoblast lineage and were one of the first to propose a bone-kidney axis, implicating bone as an endocrine organ that regulates phosphate homeostasis to meet the needs for bone mineralization
  • Found that increased transcription of FGF23 is an important control mechanism leading to elevated FGF23 levels in Phex and Dmp1-deficient states
  • Identified osteocytes in bone as a source of FGF23, thereby discovering the endocrine function of these cells
  • Cloned the full length PHEX and assessed its enzymatic activity in vitro;
  • Isolated and cloned both the promoters for Phex and FGF23
  • Established that circulating levels of FGF23 were elevated in ESRD;
  • Created FGF23 null mice with knock-in of eGFP downstream of FGF23 promoter
  • Defined the separate roles of phosphate and 1,25(OH)2D in mediating the toxic effects of FGF23 deficiency in mic
  • Discovered that FGF23 is a counter regulatory hormone for 1,25(OH)2D
  • Established that treatment of Hyp mice with calcitriol further elevates FGF23
  • Investigated the role of FGF23 in mouse models of CKD and human CKD databases, leading to a reassessment of the respective roles of phosphate and Vitamin D in CKD, as recently published in Nature Clinical Practice
  • Collaborated with Drs. Bonewald, Feng, and White to discover that Dmp1 mutations are the genetic defect in ARHR published in Nature Genetics
  • Proposed an integrated model to explain the pathogenesis of XLH and ARHR and the function of other “phosphtonins”  in the Journal of Clinical Investigation and
  • Provided new insights into the location of the physiologically relevant receptor for FGF23 in the kidney and identified the possible presence of a distal to proximal tubule feedback mechanism.


Jan 30, 2024