Ulf Janssen

TL;DR: The usefulness of these rodent models to study renal involvement in type II diabetes is discussed with particular emphasis on confounding factors such as hyperlipidemia, hypertension, immunologic abnormalities, urogenital structural abnormalities and other associated pathological conditions.

TL;DR: In vitro studies have clearly demonstrated that exposure of cultured renal cells, such as glomerular mesangial cells and proximal tubular epithelial cells, to elevated glucose concentrations, may alter cell proliferation and/or extracellular matrix turnover and Identification of the mediators involved in the above processes will likely result in future novel therapeutic approaches to diabetic nephropathy.

TL;DR: Data indicate that ICAM-1 is a central mediator of glomerular and tubulointerstitial injury in murine nephrotoxic nephritis, and deficiency in nephritic mice led to significantly reduced (peri-)glomerular and/or interstitial macrophage influx, alpha-smooth muscle actin expression, and type IV collagen accumulation.

TL;DR: A pronounced dysregulation of pro-oxidative and antioxidative enzymes in mesangioproliferative GN is document for the first time, leading to a net increase in glomerular ROS levels.