Current
therapy directed at delaying the progression of
diabetic nephropathy includes intensive glycemic and optimal blood pressure control, renin angiotensin-aldosterone system blockade and multifactorial intervention. However, the renal protection provided by these therapeutic modalities is incomplete. There is a scarcity of studies analysing the nephroprotective effect of antihyperglycaemic drugs beyond their
glucose lowering effect and improved glycaemic control on the prevention and progression of
diabetic nephropathy. This article analyzes the exisiting data about older and newer drugs as well as the mechanisms associated with
hypoglycemic drugs, apart from their well known
blood glucose lowering effect, in the prevention and progression of
diabetic nephropathy. Most of them have been tested in humans, but with varying degrees of success. Although experimental data about most of
antihyperglycemic drugs has shown a beneficial effect in kidney parameters, there is a lack of clinical trials that clearly prove these beneficial effects. The key question, however, is whether
antihyperglycemic drugs are able to improve renal end-points beyond their
antihyperglycemic effect. Existing experimental data are post hoc studies from clinical trials, and supportive of the potential renal-protective role of some of them, especially in the cases of dipeptidyl peptidase-4 inhibitors,
glucagon-like peptide-1 receptor agonists and
sodium-glucose cotransporter 2 inhibitors. Dedicated and adequately powered renal trials with renal outcomes are neccessary to assess the nephrotection of antihyperglycaemic drugs beyond the control of hyperglycaemia.