While TSP-1 is primarily known for its canonical role in activating latent TGF-β and engaging downstream SMAD-dependent and SMAD-independent pathways (e.g., ERK1/2 MAPK) [33,34,35,36], our findings suggest that plasma TSP-1 levels in CAKUT may not directly correlate with the extent of local renal injury or fibrosis, but instead reflect broader systemic or remodeling processes. This evidence concerns the gene TGFB1 and congenital anomaly of kidney and urinary tract.