Staff, Department of Inflammation & Immunity
Professor, Cleveland Clinic Lerner College of Medicine
Location: Cleveland Clinic Main Campus
Dr. Bruggeman's lab is studying the etiology of chronic kidney disease using a variety of basic and translational methods including cell culture, preclincal models, and clinical specimens. Chronic kidney diseases of the glomerulus frequently cause nephrotic syndrome and generally involve injury to the primary epithelial cell of the glomerulus, the podocyte. Her lab's focus is on genetic and environmental causes of nephrotic syndrome, in particular, those assoicated with viral infection of the podoycte and risk attributed to polymorphisms in the APOL1 gene.
Dr. Bruggeman is a Professor of Molecular Medicine in the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University School of Medicine. She is a native Ohioan, growing up in a small farming community in west-central Ohio. She was fascinated by the natural world at a young age, and always knew she would become a scientist. She attended Bowling Green State University, completing undergraduate degrees in Biology and Chemistry, followed by a PhD in Biochemistry at West Virginia University. Her PhD training was at the start of the modern era of molecular biology, learning all of the basic skills in cloning and sequencing, which landed her a postdoc at the prestigious National Institutes of Health. Her work at the NIH was exciting and intense, and was her first exposure to working with physicians on clinically-relevant problems, an experience that impacted her career trajectory to continue working in medical departments. Her first faculty appointment was in the Nephrology Division at New York's Mount Sinai School of Medicine, working on the devastating kidney complications associated with the HIV/AIDS pandemic. Dr. Bruggeman has had an outstanding career in translational research, including over 90 manuscripts, and her work has been funded by NIH, including a recent R01 that aims to understand the connection between viral infection and genetic variations for some common causes of nephrotic syndrome. Dr. Bruggeman returned to Ohio in 2001 joining the faculty of Case Western Reserve University, and transitioned to the Lerner Research Institute in 2017 joining the Departments of Inflammation & Immunity and Kidney Medicine.
PhD, Department of Biochemistry, West Virginia University, 1987
Postdoctoral Fellow, Laboratory of Developmental Biology, National Insititute of Dental Research, 1989-1991
Staff/Senior Staff Fellow, Laboratory of Developmental Biology, National Insititute of Dental Research, 1991-1994
Assistant Professor, Division of Nephrology, Mount Sinai School of Medicine, 1994-2001
Associate Professor/Professor, Divison of Nephrology, MetroHealth Medical Center, Case Western Reserve University, 2001-2017
Staff, Department of Inflammation & Immunity, Cleveland Clinic and Professor of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, 2017 to present
Genetic polymorphisms in the gene for apolipoprotein L1 (APOL1) contribute significant risk for several forms of kidney disease associated with the pathologic changes characterized as focal segmental glomerulosclerosis (FSGS).
Several viral infections such as HIV-1 and SARS-CoV-2 are known triggers for FSGS.
View publications for Leslie Bruggeman, PhD
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Selected recent publications
Hong, C., F. Eichinger, M. Atta, M. Estrella, D. Fine, M.J. Ross, C. Wyatt, T.H. Hwang, M. Kretzler, J.R. Sedor, J.F. O’Toole, A.W. Miller, and L.A. Bruggeman. Viral associations with kidney disease diagnosis and altered metatranscriptome by kidney function. Kidney Int. 103:218-222 (2023).
Azhibekov, T., R. Durodoye, A.K. Miller, C.L. Simpson, R.L. Davis, S.M. Williams, L.A. Bruggeman. Fetal high risk APOL1 genotype increases risk for small for gestational age in term infants affected by preeclampsia. Neonatology Apr 14: 1-5 (2023).
Bruggeman, L.A., T. Azhibekov, J.F. O’Toole. Moving toward a common mechanism and treatments for APOL1 nephropathies. Am. J. Kidney Dis. 79:901-903 (2022).
Bruggeman, L.A., J.R. Sedor, J.F. O’Toole. APOL1 and mechanisms of kidney disease susceptibility. Curr. Opin. Nephrol. Hypertension. 30:317-323 (2021).
Blessing, N.A., Z. Wu, L. S.M. Madhavan, J.W. Choy, M. Chen, M.K. Shin, M. Hoek, J.R. Sedor, J.F. O’Toole, L.A. Bruggeman. Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys. PLoS One 16(6):e0253197 (2021).
Chen, D., Z. Zaky, J. D. Schold, L. C. Herlitz, R. El-Rifai, P.E. Drawz, L.A. Bruggeman, L. Barisoni, S. L. Hogan, Y. Hu, J.F. O’Toole, E. D. Poggio, J.R. Sedor. Podocyte density is reduced in kidney allografts with high-risk APOL1 genotypes at transplantation. Clin. Transplant. 35:e14234 (2021).
Miller, A.K, T. Azhibekov, J. F. O’Toole, J. R. Sedor, S. M. Williams, R.W. Redline, L. A. Bruggeman. Association of preeclampsia with infant APOL1 genotype in African Americans. BMC Med. Genet. 21:110 (2020).
Bruggeman, L.A., Z. Wu, L. Lou, S. M. Madhavan, P. Drawz, D. B. Thomas, L. Barisoni, J. F. O'Toole, J. R. Sedor. APOL1-G0 protects podocytes in a mouse model of HIV-associated nephropathy. PLoS One. 14(10):e0224408 (2019).
Bruggeman, L.A. Common mechanisms of viral injury to the kidney. Adv. Chron. Kid. Dis. 26: 164-170 (2019).
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Dr. Bruggeman and team use sequencing data to identify novel factors that cause kidney diseases of unknown origin.
Drs. Bruggeman, Sedor and O’Toole will investigate the pathogenic mechanisms of chronic kidney disease to develop greater understanding of genetic susceptibility and develop new treatment strategies.
Dr. Bruggeman shows in a new study that genetic variants to the APOL1 gene are associated with increased risk for pregnancy-induced hypertension in African American women.
By studying a model of HIV-associated nephropathy, a group of kidney disease researchers and clinicians discovered that in patients with the APOL1 risk gene, the presence of an environmental stressor, like a virus, can trigger cell changes that lead to chronic kidney diseases.