In SOST-/- mice, for instance, it has been shown that kidney repair after unilateral urether obstruction is delayed [6] whilst in animal models of early CKD, incomplete recovery from acute kidney injury led to increased expression of Wnt inhibitors including DKK1 and sclerostin in the injured kidney and to increased levels in the systemic circulation [7]. The gene discussed is SOST; the disease is medical procedure.