Research

Acute kidney injury and kidney fibrosis research within the division focuses on uncovering the cellular and molecular mechanisms that drive kidney injury, repair, and progression to chronic kidney disease. Investigators employ in vivo and in vitro models to study pathways such as Wnt/β-catenin, Muc1, Nrf2/Keap1, and matrix metalloproteinases that regulate inflammation, fibrosis, and epithelial integrity following ischemic or toxic injury. Ongoing work explores glomerular-tubular crosstalk in disease pathogenesis and identifies molecular targets to prevent or reverse fibrosis. Clinical research complements these mechanistic studies, with large multicenter trials examining strategies to prevent contrast-induced acute kidney injury and improve quality of life and symptom management for patients receiving maintenance hemodialysis. Together, these efforts aim to translate mechanistic insights into therapeutic approaches that improve kidney outcomes across the spectrum of acute and chronic disease.

Research in chronic kidney disease (CKD) spans clinical, translational, and basic science efforts aimed at improving outcomes and slowing disease progression. Investigators are studying patient-centered interventions to address fatigue, sleep disorders, and quality of life in CKD and dialysis populations, as well as strategies using health information technology to enhance care delivery and reduce disparities. Ongoing work examines the impact of aging, diabetes, and obesity on kidney function, and evaluates novel models of CKD management that integrate lifestyle and behavioral approaches. Basic research explores the molecular pathways linking tubular and glomerular injury, such as β-catenin/MCP-1 signaling, to identify new therapeutic targets for proteinuric CKD. Collectively, these studies aim to personalize CKD care and improve long-term kidney and patient outcomes.

Research in epithelial cell biology and physiology within the Renal-Electrolyte Division explores the molecular and cellular mechanisms governing ion transport, membrane trafficking, and epithelial function in the kidney and related organ systems. Investigators employ electrophysiology, molecular biology, live-cell imaging, and animal models to study sodium, potassium, and chloride channel regulation, including epithelial sodium (ENaC) and BK channels, and their roles in maintaining fluid and electrolyte balance, blood pressure, and renal physiology. Additional projects examine the biology of the urothelium, mechanisms of stretch-regulated membrane trafficking, and the structural and functional organization of tight junctions. Researchers also investigate renal lymphatic biology, apical membrane endocytosis in proximal tubule cells, and the genetic and proteolytic regulation of ion channels under physiological and disease conditions. Together, these studies aim to define new molecular pathways that control epithelial transport and to identify mechanisms underlying disorders such as hypertension, nephrotic syndrome, and congenital kidney disease.

Research in hypertension and electrolyte regulation seeks to elucidate the molecular and physiological mechanisms that control sodium, potassium, and chloride balance and their impact on blood pressure regulation. Central to this work is the epithelial sodium channel (ENaC), which mediates sodium absorption in the kidney, lung, and colon and plays a key role in maintaining fluid and electrolyte homeostasis. Investigators are defining how ENaC activity is regulated by proteases, sodium concentration, and mechanical forces, and how mutations or dysregulation of this pathway contribute to salt-sensitive hypertension and kidney disease. Complementary studies explore how WNK kinases and other ion channels facilitate adaptive responses to dietary electrolyte changes and fluid stress. Through integrated approaches combining electrophysiology, molecular modeling, animal studies, and human genetics, this research aims to uncover new therapeutic targets for hypertension and related renal disorders.

Researchers focused on lower urinary tract biology and dysfunction are investigating the cellular, molecular, and physiological mechanisms that maintain urinary tract function and contribute to disease. Investigators study the urothelium – the epithelial lining of the bladder and ureters – to understand how it regulates membrane trafficking, tight junction integrity, and signaling during stretch and injury. Work in this area has revealed that urothelial cells exhibit sensory and neuron-like properties, communicating with underlying interstitial cells, smooth muscle, and sensory nerves to coordinate bladder filling and voiding. Complementary studies examine the role of transmembrane proteins such as Mucin 1 (MUC1) in host defense and infection, as well as mechanisms underlying bladder dysfunction caused by benign prostatic hyperplasia, radiation injury, and spinal cord trauma. Using approaches spanning molecular biology, electrophysiology, imaging, and in vivo functional assays, researchers aim to define how epithelial and neural pathways interact to maintain lower urinary tract health and identify new therapeutic targets for disorders such as overactive bladder, urinary tract infection, and radiation cystitis.

Research in transplantation and immunology focuses on understanding the cellular and molecular mechanisms that drive kidney transplant rejection and long-term allograft injury. Investigators study the roles of memory T cells, B cell-T cell interactions, and innate immune activation in the development of chronic rejection, while also identifying immunologic and clinical predictors of poor transplant outcomes. Ongoing work explores antibody-mediated rejection, subclinical and acute rejection, and the use of biomarkers, such as regulatory B cell cytokine ratios, to detect and prevent graft dysfunction. Clinical studies examine cardiovascular risk assessment, infection management, drug disposition, and outcomes in special populations including elderly and non-renal solid organ transplant recipients. Together, these efforts aim to improve patient selection, personalize immunosuppression, and enhance long-term kidney allograft survival.