Section of Mineral Metabolism

The UAB Section of Mineral Metabolism is a multidisciplinary research program within the Division of Nephrology dedicated to advancing the understanding of mineral metabolism and its role in kidney disease and overall human health.

We bring together basic scientists, clinical investigators, and translational researchers to study the regulation of phosphate, calcium, magnesium, and iron metabolism, and how disruptions in these pathways contribute to kidney disease, aging, and dysfunction in other organ systems. Through collaborative research, innovative methodology, and shared scientific expertise, we aim to accelerate discovery and improve patient outcomes.

What We Study

• The physiology underlying the regulation of minerals, including phosphate, calcium, magnesium, and iron
• The biology underlying the effects of these minerals on cells and tissues
• Pathologies caused by acute and chronic imbalance in these minerals

Our Focus

• Understanding how phosphate disorders influence kidney health and aging
• Investigating the pathologic effects of hyperphosphatemia in chronic kidney disease (CKD)
• Exploring the protective role of magnesium in CKD
• Examining the relationship between phosphate and iron metabolism
• Identifying how iron metabolism becomes dysregulated in acute kidney injury (AKI) and CKD

Mission & Goals

• We aim to advance the science of mineral metabolism, identifying and addressing the major barriers in the field, and attracting investigators to build on and enhance our collective expertise.
• We provide a communication platform for investigators with interests in mineral metabolism.
• We work collaboratively to address important scientific questions in the field of mineral metabolism from multiple angles and with progressive depth, catalyzing the development of grant proposals and collaborations.

Our Team

We are an integrated, multidisciplinary team of investigators from across UAB and the Division of Nephrology, bringing together basic scientists, clinical researchers, and translational investigators with expertise spanning patient-oriented research, human physiology, clinical trials, epidemiology, informatics, statistics, molecular and cell biology, animal physiology, and computational biology. Our collaborative work extends beyond the kidney to explore the role of mineral metabolism in the heart, skeletal muscle, lungs, and other organ systems.

Faculty

Christian Faul, Ph.D.
Director of the Section of Mineral Metabolism

Orlando Gutierrez, M.D.

Javier Neyra, M.D., MSCS

Jorge Gamboa, M.D., Ph.D.

Abolfazl Zarjou, M.D., Ph.D.

Associated Faculty

Tanecia Mitchell, Ph.D.
Kidney stone disease and inflammation

Stefanie Krick, M.D., Ph.D.
Mineral metabolism and lung disease

Matthew Alexander, Ph.D.
Mineral metabolism and skeletal muscle

Vinoy Thomas, Ph.D.
Mineral chemistry

Jin Chen, Ph.D.
Bioinformatics

Current Trainees

Tanima Chatterjee, Ph.D. (Postdoc)

Suri Tangchitthavorngul, M.D., MPH, (Visiting Scholar)

Jospeh Crivelli, M.D., Assistant Professor, UAB Department of Urology

Madison Thomas (Ph.D. Student)

Qing Li (Ph.D. Student)

Research Core Facilities

Our investigators leverage UAB's nationally recognized core facilities to access advanced technologies, specialized expertise, and collaborative resources that enhance the quality and impact of our research through Core Facilities. These shared facilities support innovative discoveries across basic, translational, and clinical science while helping accelerate research from the laboratory to patient care.

• High Resolution Imaging Facility (HRIF)
• Small Animal Imaging Shared Facility (SAIF)
• O'Brien Center for AKI Research

Key Publications

• Chatterjee T, Machado S, Cowen K, Miller M, Zhang Y, Volpicelli-Daley L, Fielding L, Pattanayak R, Rosenblum F, Potor L, Balla G, Balla J, Faul C, Zarjou A. Macrophage ferritin heavy chain/α-synuclein regulatory axis modulates ferroptosis during kidney injury. JCI Insight 2026; 11(8): e196521.
• Heitman K, Li Q, Fajol A, Denniff M, Peng D, Thomas SM, Czaya B, Yanucil C, Westbrook D, Wasiuddin S, Rowe GC, Zarjou A, Gutierrez OM, White KE, Gamboa JL, Watson EL, Alexander MS, Faul C. Systemic phosphate elevations induce FGF23 production in skeletal muscle to reduce renal phosphate reabsorption in mice. J Am Soc Nephrol. 2026; 37: 1160-73.
• Mitchell T, Verma V, Fajol A, Faul C. The effects of elevated phosphate on the kidney - damaging the gatekeeper. Pflugers Arch. 2026; 478: 34.
• Fajol A, Li Q, Thomas SM, Sloan A, He L, Xie X, Heitman K, Kentrup D, Yanucil C, Grabner A, Merscher S, Fornoni A, Gutierrez OM, Faul C. Nephrotic syndrome in mice elevates FGF23 levels and leads to cardiac hypertrophy in the absence of hyperphosphatemia. Nephrol Dial Transplant. 2025; in press.
• Fajol A, Heitman K, Thomas SM, Li Q, Mitchell T, Gamboa J, Zarjou A, Gutierrez OM, Faul C. Soft tissue accumulations of phosphate are not always associated with serum phosphate or with calcifications in mouse models of hyperphosphatemia. J Physiol. 2025; 603: 7323-43.
• Chatterjee T, Zarjou A. Navigating the Complex Pathogenesis of Acute Kidney Injury: Exploring Macrophage Dynamics, Mitochondrial Dysfunction, and Ferroptosis Pathways. Adv Kidney Dis Health 2025; 32(2):122-32.
• Fajol A, Faul C. Soft tissue calcifications in chronic kidney disease - beyond the vasculature. Pflugers Arch. 2025; 477: 1037-59.
• Fajol A, Faul C. The pathologic actions of phosphate in chronic kidney disease. Kidney360 2025; 6: 1040-49.
• Campos C, Faul C. Elevated phosphate levels in CKD - a direct threat for the heart. Nephrol Dial Transplant. 2025; 40: 1294-1309.
• Mrug M, Mrug E, Rosenblum F, Chen J, Cui X, Agarwal A, Zarjou A. Distinct developmental reprogramming footprint of macrophages during acute kidney injury across species. Am J Physiol Renal Physiol. 2024; 326(4): F635-41.
• Heitman K, Bollenbecker S, Bradley J, Czaya B, Fajol A, Thomas SM, Li Q, Komarova S, Krick S, Rowe GC, Alexander MS, Faul C. Hyperphosphatemia contributes to skeletal muscle atrophy in mice. Int J Mol Sci. 2024; 25: 9308.
• Heitman K, Alexander MS, Faul C. Skeletal muscle injury in chronic kidney disease - from histologic changes to molecular mechanisms and to novel therapies. Int J Mol Sci. 2024; 25: 5117.
• Bollenbecker S, Heitman K, Czaya B, Easter M, Hirsch M, Vang S, Helton ES, Barnes JW, Faul C, Krick S. Phosphate induces inflammation and exacerbates injury from cigarette smoke in the bronchial epithelium. Sci Rep. 2023; 13: 4898
• Yanucil C, Kentrup D, Campos I, Czaya B, Heitman K, Westbrook D, Osis G, Grabner A, Wende AR, Vallejo J, Wacker MJ, Navarro-Garcia JS, Ruiz-Hurtado G, Zhang F, Song Y, Linhardt RJ, White K, Kapiloff MS, Faul C. Soluble klotho and heparin modulate the pathologic cardiac actions of FGF23 in chronic kidney disease. Kidney Int. 2022; 102: 261-79.
• Czaya B, Heitman K, Campos I, Yanucil C, Kentrup D, Westbrook D, Gutierrez O, Babitt JL, Jung G, Salusky IB, Hanudel MR, Faul C. Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signaling. eLife 2022; 11: e74782.

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