Uta Kunter

TL;DR: Data identify VEGF(165) as a factor of central importance for endothelial cell survival and repair in glomerular disease, and point to a potentially novel way to influence the course of glomerulonephritides, thrombotic microangiopathies, or renal transplant rejection.

TL;DR: Even low numbers of MSC can markedly accelerate glomerular recovery from mesangiolytic damage possibly related to paracrine growth factor release and not to differentiation into resident glomersular cell types or monocytes/macrophages.

TL;DR: In this GN model, the early beneficial effect of MSC of preserving damaged glomeruli and maintaining renal function was offset by a long-term partial maldifferentiation of intraglomerular MSC into adipocytes accompanied by glomerular sclerosis, suggesting that MSC treatment can be a valuable therapeutic approach only if adipogenic mald differentiated differentiation is prevented.

TL;DR: The data suggest that podocyturia may become a more sensitive means to assess the activity of glomerular damage than proteinuria, and not simply a reflection of proteinuria because it is limited to phases of ongoingglomerular injury.

TL;DR: It is shown that both hypercholesterolemia and hypertriglyceridemia aggravate renal injury primarily via podocyte rather than via mesangial cell damage, and both are accompanied by tubulointerstitial cell activation and injury.