Having in mind that aggravated AKI and impaired uptake of AGEs, observed in CDDP-treated Gal-3-/- kidneys (Figure 1A-D) corresponded with reduced immunosuppressive and nephroprotective function of Gal-3-/-DCs (Figure 6-7), we assume that Gal-3 deficiency resulted in unstable expression of AGE receptor complex and significantly impeded AGE receptor-dependent generation of tolerogenic phenotype in renal DCs. This evidence concerns the gene LGALS3 and acute kidney injury.