OUR RESEARCH
Division of nephrology and hypertension is actively engaged in translational, and outcomes research. Our translational research headed by Dr. Reiser focuses on podocyte biology and glomerular diseases. His laboratory has been developing therapies and assays to combat renal diseases and its many complications since 2004. His contributions range from identification of a common circulating blood protein —soluble urokinase plasminogen activator receptor (suPAR)— in the pathogenesis of focal segmental glomerulosclerosis (FSGS)[15] to suPAR's emerging role as earliest known biomarker for incident and progressive chronic kidney disease (CKD)[3] as well as for acute kidney injury (AKI).[4] suPAR may link the innate immune system.
Previously research in our laboratory has focused on cellular and molecular mechanisms regulating renal tubule electrolyte transport, with emphasis on regulation of acid-base transport in the thick ascending limb. This research was supported continuously by NIDDK/NIH funding for more than 25 years. The Division has been funded since 1987 to study the Regulation of Thick Ascending Limb Acid-Base Transport. The goal of this project is to study the cellular, biochemical, and molecular mechanisms involved in the regulation of HCO3 absorption by the renal medullary thick ascending limb.
Our transplant outcomes studies have focused on access to transplant, high risk transplants, as well as transplant monitoring. Our Glomerulonephritis clinic actively participates in glomerulonephritis studies and trials. We are also partners in industry trials.
Research in our laboratory is focused on cellular and molecular mechanisms regulating renal tubule electrolyte transport, with emphasis on regulation of acid-base transport in the thick ascending limb. The goals of our current research are to define how innate immune signaling pathways affect renal tubule function and to determine the role of these pathways in the impairment of thick ascending limb bicarbonate absorption and the pathogenesis of metabolic acidosis in sepsis. Our studies use an integrative approach that combines methods for direct study of ion transport and cell signaling in microdissected renal tubules with a clinically-relevant sepsis model to advance understanding of the molecular mechanisms underlying sepsis-induced renal tubule dysfunction. In addition, we are investigating cellular mechanisms by which a novel therapeutic agent prevents sepsis-induced thick ascending limb dysfunction. These studies are designed to uncover new therapeutic targets that may aid in protecting renal tubule function during sepsis and a variety of inflammatory kidney disorders. This research has been supported continuously by NIDDK/NIH funding for more than 25 years.
The Division has been funded since 1987 to study the Regulation of Thick Ascending Limb Acid-Base Transport. The goal of this project is to study the cellular, biochemical, and molecular mechanisms involved in the regulation of HCO3 absorption by the renal medullary thick ascending limb. We are in the early stages of discussions with several companies to conduct registries of patient outcomes from kidney transplants. The addition of Interventional Nephrology presents opportunities to add additional research components.