The nephrology division has an active research presence. We have a number of NIH funded investigators, and many other faculty engaging in clinical research or other projects.
Within our fellowship we have elective time the fellows can dedicate to research if they choose.
Our faculty publish in prominent peer reviewed journals, and are happy to mentor fellows in a research project of their choosing. We also have a listing of our recent fellow publications online for your review.
Principal Investigator Faculty
Dr. Bushinsky has published over 100 peer-reviewed articles and over 60 invited reviews, chapters and editorials focusing on disorders of divalent ion metabolism. His has developed a strain of rats that exhibit genetic hypercalciuria, the most common metabolic abnormality in humans with nephrlithiasis, and spontaneously form kidney stones. The pathophysiology of the hypercalciuria closely parallels that of man and is thus a useful model to study stone formation in humans. He has also extensively studied the mechanism by which acid induces physicochemical bone dissolution and cell-mediated resorption. Dr. Bushinsky has lectured throughout the world on stone formation, effects of acid on bone and other disorders of divalent ion metabolism.
Dr. Le is Professor of Medicine, and Chief of the Division of Nephrology. Her clinical practice focuses on the care of patients with hypertension and chronic kidney disease. She applies her knowledge and extensive research experience in renal physiology to her clinical practice. She has an active research program in mechanisms of hypertension and genetics of chronic kidney disease.
Dr. Le is John J. Kuiper Distinguished Professor of Medicine. In October 2018, Dr. Le became Chief of the Division of Nephrology at the University of Rochester. She graduated from George Washington University with a major Chemistry and a minor in Philosophy, and received her MD from George Washington University School of Medicine where she graduated as valedictorian. Dr. Le undertook her Internal Medicine and Nephrology training at Duke University Medical Center. She was a faculty at Duke from July 2000 –June 2009, and faculty at the University of Virginia from July 2009–September 2018. As a clinical investigator, she is dedicated to patient care as well as research. Her research has been funded by the NIH. She served on the study sections for the American Heart Association and the National Kidney Foundation, and was a regular member of the NIH Genetics of Health and Disease Study Section from 2012-2018. She is regular member for NIDDK Kidney, Urology, and Hematology (KUH) study section (2019 –2025). She has been serving as Associate Editor of the American Journal of Physiology–Renal Physiology (July 1, 2013 -June 30, 2020).
Scientific Approach: My laboratory studies renal mechanisms of hypertension and genetic determinants of susceptibility to kidney disease progression. We use the mouse as a model system, and translate our findings in human cohorts.
Collectrin (Tmem27) in hypertension and salt-sensitivity.
The goal of this project is to define the physiological role of collectrin, Tmem27, a chaperone of amino acid transporters, in blood pressure homeostasis. We previously reported that collectrin, by regulating arginine uptake, regulates nitric oxide and superoxide balance. We will use a tissue-specific knockout approach to delineate the tissue-collectrin-nitric oxide synthase axis and renal mechanisms (tubular epithelial regulation versus renal blood flow) by which collectrin influences blood pressure and the adaptive response to high salt intake. In addition, using a translational approach, we will be the first to comprehensively examine the effect of genetic variants of collectrin on blood pressure in 4 different human populations. In the context of debates in the field of hypertension, our findings may be able to address the decades-old question whether vascular dysfunction in general, and specifically that in the kidney, is a prerequisite for salt sensitivity and/or hypertension.
Role of GSTM1 deficiency in chronic kidney disease progression.
Our work identified that glutathione-S-transferase mu-1 gene, Gstm1, is a candidate gene for renal vascular remodeling in a mouse model. The translational work in my laboratory from mouse to human identified that the common null allele of GSTM1 gene in humans is associated with accelerated kidney disease progression in the African American Study of Hypertension and Kidney Disease (AASK) Trial participants. We have further assessed the joint effects of GSTM1 and APOL1 in AASK, and found that the GSTM1 null allele and APOL1 high risk alleles have additive deleterious effect on the composite outcomes of decline in eGFR, dialysis, and death. A similar effect was observed in the Atherosclerosis Risk in Communities (ARIC) study in African Americans and European Americans. Using mouse models, our ongoing work seeks to identify the mechanisms by which deficiency of GSTM1 enzyme accelerates kidney disease, and how it may interact with other genetic factors and the environment. Furthermore, in pursuit of personalized and precision medicine, our goal is to determine factors that may mitigate kidney disease progression in GSTM1 deficient patients who are genetically most at risk.
We have also become interested in the relationship between the type of vascular access and the development or progression of right heart dysfunction and pulmonary hypertension in hemodialysis patients. We are proposing a clinical study to examine this relationship. Plan is also underway to develop a mouse model to be able to address this phenomenon mechanistically.
Dr. Le Publications
Our laboratory studies mechanisms by which external cues regulate systems functions. Integrative approaches in the nematode C. elegans and mammalian cardiac models focus on how membrane electrolyte flux and pH regulation exhibit environmental responses to inform metabolism, physiology, and ultimately survival. Funded projects center around the role of mitochondria in oscillatory calcium signaling, metabolic plasticity, and sensitivity to ischemia-reperfusion injury.
Dr. Saeed is a practicing nephrologist and palliative care physician-scientist. He studies dialysis decision-making and examines the role of palliative care in improving patients' and caregivers’ quality of life and end-of-life experiences.
Dr. Saeed also investigates the nuances of physician-patient communication, health care utilization and health-related decision making in clinical contexts of chronic kidney disease and cancer.
Dr. Zand's research program is focused the role of B cells in alloimmune responses in solid organ transplantation and the adaptive immune response to biopathogens. NIH funded work includes:
The University of Rochester’s Clinical and Translational Science Institute: The major goal of this project is to improve the health of the population by advancing basic, translational and clinical research through providing education and training, supporting trans-disciplinary teams, and engaging community stakeholders.
Modeling Immune Desensitization in Renal Transplantation: This project will develop and validate an ordinary differential equation model to predict the effects of plasma exchange therapy, intravenous immunoglobulin, and anti-B cell agents on anti-ABO blood group antibodies in patients undergoing immune desensitization prior to kidney transplantation from an ABO incompatible donor.
Modeling B Cell Vaccine Responses in Transplant Recipients: The goal of this study is to model plasma cell differentiation using data generated from an in vitro system and a branching stochastic process method, and vaccine responses in kidney transplant recipients. The work involves both murine and human experiments using FACS and transcriptome analysis to test the hypothesis that circulating Bc populations in renal transplant recipient vaccine responders and non-responders have different activation kinetic rates and phenotypes.