Therefore, sAH patients with severe cholestasis will likely have impaired hepatic activation of endogenous GC by HSD11β1 and the resultant impaired hepatic GR signaling, whereas these sAH patients may have defective renal inactivation of prednisolone by HSD11β2 and the resultant activation of MR and aggravated risk of acute kidney injury (AKI) [32]. This evidence concerns the gene NR3C2 and cholestasis.