Polycystic kidney disease (PKD) affects nearly 600,000 people in the United States and it is caused by mutations in the genes that encode polycystin-1 (PC1) and polycystin-2 (PC2). These modifications are responsible for the growth of fluid-filled renal cysts that can impair kidney function over time, and lead to end stage renal disease. PC1 and PC2 have also been localized to the mitochondria, suggesting that they are responsible for regulating cellular metabolism and energy production, which can lead to mitochondrial dysfunction and increased PKD progression. Our lab uses human pluripotent stem cells (hPSCs) to generate kidney organoids that can be used to study the advancement of PKD, which contain the major proximal structures of the nephron including podocytes, proximal tubules, distal tubules, and endothelial cells. Orgnaoids that lack both PC1 and PC2 will develop cysts that can grow large enough to be seen by eye. Unfortunately, these organoids lack a collecting duct (CD) system, a crucial component of the kidney that expands greatly in PKD. To address this need, we developed a protocol to differentiate hPSCs into ureteric bud (UB) cells, the precursors of CD cells. First, we identified Dolichos biflorus agglutinin (DBA) as a key CD lineage marker in developing kidneys through immunofluorescence analysis on human kidney tissue. Then, we took undifferentiated hPSCs and investigated their ability to express DBA by treating them with a concentration gradient of small molecules known to induce kidney lineage cells. The resulting cells were stained with DBA and GATA 3, an additional, early CD marker, and we found that both markers were expressed in vitro. We will continue modifying this protocol to better study the increased metabolic rates seen in PKD, its effects in CD cells, and the mechanism behind the PC1 and PC2 pathway that leads to cyst formation.