These results align with a large body of evidence that has established insulin resistance as a consequence of increased 11β‐HSD1 activity in animal models and human disease.7, 23, 24, 26, 27, 28, 29 The absence of a correlation between urine (THF+5αTHF)/THE and HbA1c in the non‐diabetic subgroup can be explained by a lack of change in HbA1c regardless of insulin resistance, as accompanying insulin secretion increases sufficiently to maintain glycaemic control.18 Our data therefore remain consistent with a role for 11β‐HSD1 in insulin resistance in human CKD. This evidence concerns the gene INS and Insulin resistance.