IL33 and acute kidney injury: Importantly, notably reduced acute tubular necrosis and apoptosis was observed in mice treated with a soluble IL-33 receptor (sST2), while administration of recombinant IL-33 (rIL-33) exacerbated CDDP-induced AKI [126], indicating pro-inflammatory role of IL-33 in the pathogenesis of CDDP-caused nephrotoxicity.