Stuart J. Shankland MD, MBA

Medicine/Nephrology
Belding H Scribner Chair of Medicine

Email: stuartjs@uw.edu | Phone: 206.543.2346

Kidney disease, which impacts one in nine Americans, leads to loss of certain cell types. Our lab studies both aging and diseases of the glomerulus, the kidney’s filtering units. The glomerular cell called the podocyte is lost in disease, and in the healthy aging kidney. Podocyte loss underlies scarring of the kidney, with loss of kidney function, accompanied by leakage of protein into the urine (proteinuria). However, podocytes are unable to proliferate and thus cannot self-renew. This, their replacement relies on regeneration by neighboring stem/progenitor cells. We have identified that parietal epithelial cells and renin producing cells are podocyte stem/progenitor cells. Ongoing studies in our lab are identifying which small molecules and drugs can increase the regenerative capacity of podocyte stem/progenitor cells to replace podocytes in disease, why regeneration is decreased in the healthy aged kidney and unable to regenerate adequately, and how we can deliver specific therapies to parietal epithelial cells to increase efficiency while minimizing off target effects. The end goal of our studies is to translate these results to the patient with kidney disease by enhancing regeneration in order to restore cell number, integrity and function.