Regarding the first mechanism, we were able to retrieve one, recent observation, highlighting age as a potential confounder of a relationship between eGFRcre and brain atrophy.33 On the other hand, cardiovascular BS, constructed from the combined levels of GDF15 and NT-proBNP, was another significant mediator identified by us, and there is increasing literature regarding the involvement of these proteins in arteriosclerotic processes. The gene discussed is NPPB; the disease is Brain atrophy.