As soon as I started to work in a research laboratory, I became passionate and could no longer think of another job. My mentor (the well-known nephrologist Jean-Pierre Grünfeld in Paris) introduced me to kidney physiology and antidiuretic hormone (ADH = vasopressin). My early studies focussed on the adaptations of the kidney that allow mammals to excrete electrolytes and nitrogen endproducts in a concentrated urine. I studied various aspects of kidney anatomy and function in both desert-adapted rodents and Brattleboro rats with hereditary diabetes insipidus (that we could treat or not with chronic infusions of ADH). After some years, I understood that ADH induced in the kidney the same effects as those induced by a protein-rich diet, and that, besides its advantageous effects on water economy, ADH might have the same adverse consequences as proteins on kidney disease progression. I started to get a small group of students and post docs, two of them, Marie-Marcelle Trinh-Trang-Tan and Nadine Bouby have been working with me after their Ph.D. for more than 20 years. We confirmed the adverse effects of vasopressin in chronic kidney disease, diabetic nephropathy and hypertension (and more recently also in diabetes mellitus itself). Most studies were carried in rats. But I was also able to initiate a few clinical investigations in humans comparing the influence of low or high hydration on several aspects of renal function. My interest in urea handling came from the fact that dietary proteins lead the kidney to not only excrete urea, but also concentrate it markedly in the urine. The characterization and regulation of urea transporters was thus an obvious topic of interest, as well as the influence of glucagon on renal hemodynamics and urea and electrolyte excretion. I am very pleased today to see the growing interest of clinicians in hydration, vasopressin and urine osmolarity, and to be able to collaborate with them in epidemiological studies and in the design and interpretation of clinical investigations and trials.