Cardiorenal syndrome (CRS) is a progressive disorder involving reciprocal deterioration of cardiac and renal function. Kidney organoids derived from CRS patient-specific induced pluripotent stem cells (iPSCs) capture individual genomic backgrounds but often fail to reproduce physiologically relevant tubular architecture and apical–basolateral polarity, features essential for modeling disease mechanisms and patient-specific nephrotoxicity. To address this, we established a stepwise protocol to generate kidney tubule organoids from human pluripotent stem cells (hPSCs), including embryonic stem cells (ESCs) and iPSCs. Treatment with CHIR-99021 (6–9 μM) and Noggin (5–20 ng/mL) efficiently induced intermediate mesoderm markers (HOXD11, LHX1) in >90% of cells. By day 60, ~80% of cells expressed tubular markers such as Lotus Tetragonolobus Lectin (LTL) and E-cadherin (ECAD). To enhance architecture, we applied 3D bioprinting to pattern ESCs (H7 line) into tubular structures at varying cell densities (50–200 million cells/mL). All conditions yielded high mesodermal and nephron progenitor cell populations (80–90%). Constructs printed at 50M cells/mL showed long-term viability (>30 days) and robust expression of proximal and distal tubule markers (LTL, ECAD). Our ongoing work applies this strategy to CRS patient-derived iPSCs. We aim to establish a tubule-mimetic kidney organoid system as a physiologically relevant platform for CRS modeling and patient-specific nephrotoxicity assessment, thereby advancing drug testing and disease modeling