About the speaker

Professor Ivan Tack, MD, PhD is a nephrologist, Head of the Dpt of Clinical Physiology in Rangueil hospital since 2006 and Chairman of the Dpt of Physiology at Paul Sabatier University – Toulouse School of Medicine, France. He experienced a post doctoral fellowship at University of Miami School of Medicine, Dpt of Nephrology (USA) working on pathophysiology of diabetic nephropathy. His clinical activity mostly focuses on water and electrolytes disorders, inherited tubular diseases and metabolic impact of nutritional disorders, including renal stone diseases and osteoporosis. Concomitantly he is involved in experimental research (INSERM Unity 1048, Toulouse) with a focus on early protection from renal diseases based on in vivo experimental modelling (main models: diabetic nephropathy, post-hemorrhagic acute kidney injury, renal stone disease in murine). He has authored/co-authored over 80 peer-reviewed scientific articles and regularly contributes to the development of French Health High Authority program. Professor Tack is a member of the American Society of Nephrology, American Physiological Society and also collaborates with Danone Nutritia Research since 2007 as a member of the Scientific Advisory Board (Water Division).

About the talk

Since the discovery of endocrine roles of the pituitary gland, at the turn of the 20th century, it took one century and two Nobel prizes to identify the small peptide arginine vasopressin (AVP) and to describe its main functions and regulatory pathways. Since the beginning, AVP has confused researchers by the duality of its actions.

This hormone is “classically” responsible for renal water saving at low concentration and for blood maintenance of pressure during hypovolemia at higher concentration. Indeed, AVP is involved in a wide range of physiological or clinical situations at the frontier of “stress”. Whereas beneficial in the short term, the impact of its prolonged and/or intense AVP secretion becomes questioned.

Due to the duality of vasopressin that becomes a stress hormone when increased, its marked and/or prolonged recruitment has a potential cost for the kidney, and likely for metabolic and cardiovascular health. This could be the case during various physiological and clinical circumstances such as prolonged renal water economy, especially in case of prior CKD, but also during poorly controlled diabetes or hypertension. Medical knowledge in this field is only emerging and a relationship is far from proving causality.

However, proofs of concept are already sufficient to encourage people to drink at least enough water to meet published dietary reference values, and to propose interventional randomized controlled hydration study in the most exposed situations. Two questions remain to answer: 1) Can improvement of hydration prevent health impact of AVP even in circumstances where its stimulation is independent of osmotic regulation? 2) What does drinking “enough” practically mean regarding potential health benefits?