Purpose of review: The prevalence of diabetic kidney disease (DKD) is increasing worldwide. Despite major therapeutic advances in the last decades in DKD, the current standard of care let many people progress to severe stages. Vasopressin secretion is increased in diabetes, and its potential role in the onset and progression of DKD is being re-investigated.
Recent findings: Recently, observational studies evidenced an association between surrogates of vasopressin secretion (daily fluid intake or urine volume, and plasma copeptin concentration) and chronic kidney disease in the community, but also specifically in type 1 and in type 2 diabetes. Causality is strongly supported by a series of studies in rats conducted more than a decade ago, and by additional recent experimental data. The mechanism underlying these adverse effects likely involves the hyperfiltration induced indirectly as a consequence of the tubular effects of the hormone mediated by the V2 receptor.
Summary: If chronic vasopressin action on the kidney is detrimental in diabetes as suggested so far, intervention studies should be designed. Available tools include V2 receptor blockade, and changes in daily water intake in vulnerable patients. Safety and effectiveness should be tested, as it is currently done in patients with CKD (NCT01766687).