The Unit was created in 1965 by Professor G. Richet with the title “Néphrologie normale et pathologique” when kidney research was weakly developed and all research themes could be embraced at once. Continuity was ensured by Professor R. Ardaillou in 1985. When Professor P. Ronco took over in 1998, there were 6 different teams and more than 12 themes of research which was explained by the way G. Richet and R. Ardaillou were so successful in attracting new, talented research groups and by the diverse origin of the clinical investigators who came from different renal divisions and hospital clinical investigation laboratory. To adapt to the constraints of modern research, we reduced the number of research teams down to 3 then to 2 (since 2008), in parallel to the reduction of the number of themes which was made possible by the paradigm shift from glomerular physiology to the pathophysiology of chronic kidney disease (CKD) progression based on the implication of the same peptides in these different processes. This resulted in augmenting the critical mass of researchers devoted to more focused projects, which led to a major increase in the number of competitive grants (8 National Research Agency grants, 3 European grants) and in the levels of publications and productions (5 patents and 5 more still pending) during the last years.


The Unit is currently organized with 2 teams directed by P. Ronco and C. Chatziantoniou respectively and 4 well-equipped platforms including animal facilities with a dedicated, well trained staff for each of them. Our research activities are devoted to pathophysiology of kidney diseases, being bi-directionally oriented from the bench to the bedside (translational research) and from the bedside to the bench (clinical research). These activities are basically aimed at developing new knowledge beyond the frontiers of medical science with always clinical applications always in mind. Good examples are the identification of 2 antigens and 2 predisposing genes in membranous nephropathy (MN), the description of a new systemic disease related to COL4A1 mutations, and the elucidation of novel mechanisms and targets of CKD progression and repair. Our basic research strategy is based either on the use of genetically modified mice to investigate the role of a pre-defined protein, or on applying therapy-driven hypotheses in standard mouse strains to uncover the underlying mechanisms and mediators.


One main objective is the identification of novel biomarkers and druggable molecular targets, particularly in the field of membranous nephropathy and kidney disease progression. Beyond kidney diseases, we hope that our results will contribute to unravel the mechanisms of auto-immune diseases, cysts formation, alterations of vascular reactivity (a major cardiovascular risk factor), and muscle cramps.