Galectin-3, a member of the multigene family of beta-galactoside binding lectins, is mainly expressed in epithelial cells. The distribution of galectin-3 depends on cell type and cell differentiation. We previously showed that galectin-3 is transiently associated with the centrosome, and more specifically with the basal body at the basis of the primary cilium of MDCK cells. In the present study, we use galectin-3 null (Gal3-/-) mutant mice to investigate the functional consequences of our observations in the context of kidney regeneration after subtotal nephrectomy. Three months after surgery, renal functions were more severely affected in Gal3-/- mutant than in wt animals. Upon sacrifice, we found that Gal3-/- mutant kidneys were bigger and heavier, and this hypertrophy was associated with large tubular dilatations. Interestingly, in wt mice, galectin 3 intracellular distribution was altered in response to injury, displaying a distinct centrosomal localization in epithelial cells lining the collecting ducts close to the wound, whereas in cells away from the wound galectin-3 remained uniformly cytosolic. The impact of nephron reduction on primary cilium growth was examined by 3D reconstruction of wt and Gal3-/- renal tubules stained for acetylated alpha-tubulin. This analysis revealed that mutant primary cilia are irregular, bent, twisted and longer than wt primary cilia, indicating that Galectin-3 is essential for primary cilium growth. This suggests that the failure in kidney regeneration observed in Gal3-/- mutant mice may be due to defects in primary cilium biogenesis.