Immune-mediated glomerular diseases are a major cause of end stage renal disease and are associated with significant morbidity and mortality. Most forms of glomerulonephritis (GN) are characterized by a pathogenic immune response against renal autoantigens or by manifestations of systemic autoimmunity in the kidney.
This results in renal injury clinically ranging from proteinuria of various degrees to rapid loss of renal function. We aim to advance current understanding and bridge the translational gap with the CRC 1192 by combining elaborated experimental models, single cell OMICs and deep molecular mapping of human kidney tissue, we will generate a multidimensional atlas of GN.
Campus Research N27
20246 Hamburg Germany