Induction of T regulatory cells attenuates idiopathic nephrotic syndrome.

Buffalo/Mna rats spontaneously develop FSGS and nephrotic syndrome as a result of an immune disorder. Similar to some humans with FSGS, the disease recurs after renal transplantation, suggesting the involvement of a circulating factor. Here, we tested the effect of several immunosuppressive treatments on these rats.

Renal macrophage activation and Th2 polarization precedes the development of nephrotic syndrome in Buffalo/Mna rats.

Background: At 8 weeks, Buffalo/Mna rats spontaneously develop a nephrotic syndrome associated with focal segmental glomerulosclerosis (FSGS). We have previously demonstrated that this glomerulopathy recurs after renal transplantation, thus supporting the relevance of this rat model to human idiopathic nephrotic syndrome [1]. In this study, we describe renal immune abnormalities which appear in parallel to the initiation and progression of the spontaneous Buffalo/Mna nephropathy.

Loss of NOS1 expression in high-grade renal cell carcinoma associated with a shift of NO signalling.

In normal human kidney, NOS1 and soluble guanylate cyclase (sGC) are expressed in tubular epithelial cells, suggesting a physiological autocrine NO signalling pathway. Therefore, we investigated both NOS1 and sGC expressions in benign and malignant renal tumours. In addition, we examined the pattern of protein tyrosine nitration in normal and tumour tissue.

Expression of NOS1 and soluble guanylyl cyclase by human kidney epithelial cells: morphological evidence for an autocrine/paracrine action of nitric oxide.

Background: Nitric oxide plays an important role in the kidney through effects on both renal hemodynamics and tubular functions. Tubular epithelial cells are thus a target for nitric oxide. However, as to whether tubular epithelial cells endogeneously produce nitric oxide under physiologic conditions in human kidney is currently unknown.