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Intestinal regulation of urinary sodium excretion and the pathophysiology of diabetic kidney disease: a focus on glucagon‐like peptide 1 and dipeptidyl peptidase 4

What is the topic of this review? This review describes how hyperglycaemia and attendant increases in proximal tubular growth and sodium reclamation form the mechanistic basis for the tubular hypothesis of hyperfiltration and nephropathy in the kidneys of patients with diabetes. The review highlights how signals arising from the gastrointestinal tract may be capable of modulating this response and how pharmacological enhancement of these signals may ameliorate the progression of diabetic kidney disease. What advances does it highlight? The review highlights the potential of glucagon‐like peptide 1 analogues, glucagon‐like peptide 1 receptor agonists and dipeptidyl peptidase 4 inhibitors to exercise renoprotective effects in diabetes independent of their classical effects on endocrine pancreas.