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Vasopressin and diabetic nephropathy.
Ronan Roussel1, Gilberto Velho, Lise Bankir
1aINSERM, UMRS 1138, Centre de Recherche des Cordeliers, 15 rue de l'Ecole de Médecine bAssistance Publique Hôpitaux de Paris, Bichat Hospital, DHU FIRE, Department of Diabetology, Endocrinology and Nutrition cUniversité Paris Diderot, Sorbonne Paris Cité, UFR de Médecine dUniversité Pierre et Marie Curie, Centre de Recherche des Cordeliers, Paris, France.
Current Opinion in Nephrology and Hypertension
|April 14, 2017
Summary
Vasopressin may worsen diabetic kidney disease (DKD) progression. Research suggests blocking its V2 receptor or modifying water intake could be new therapeutic strategies for DKD.
Area of Science:
- Nephrology
- Endocrinology
- Diabetology
Background:
- Diabetic kidney disease (DKD) prevalence is rising globally, with current treatments often failing to halt disease progression.
- Elevated vasopressin secretion in diabetes is increasingly recognized, prompting re-investigation of its role in DKD onset and advancement.
Purpose of the Study:
- To review the potential role of vasopressin in the development and progression of diabetic kidney disease.
- To explore emerging therapeutic strategies targeting the vasopressin system for DKD management.
Main Methods:
- Review of recent observational studies linking vasopressin secretion surrogates (fluid intake, urine volume, copeptin) to chronic kidney disease in diabetic populations.
- Analysis of experimental data, including rodent studies, supporting a causal link between vasopressin and kidney damage.
- Examination of the proposed mechanism involving V2 receptor-mediated tubular effects and hyperfiltration.
Main Results:
- Observational studies show associations between vasopressin surrogates and kidney disease in the general population and specifically in type 1 and type 2 diabetes.
- Experimental data strongly suggest a causal role for vasopressin in kidney injury.
- The V2 receptor pathway is implicated, potentially leading to hyperfiltration and adverse kidney effects.
Conclusions:
- Chronic vasopressin activity in the kidney appears detrimental in diabetes.
- Intervention studies targeting V2 receptor blockade or water intake modification are warranted.
- Clinical trials are needed to assess the safety and efficacy of these novel approaches in patients with DKD.