Retinoids reduce renal damage in rat experimental glomerulonephritis. It is unknown, however, how local and systemic retinoid pathways respond to renal injury. We, therefore, examined the extrarenal and glomerular expression of the retinol (RoDH) and retinal (RalDH) dehydrogenases 1 and 2 as well as the expression of the retinoic acid (RAR) and retinoid X (RXR) receptor subtypes , , and at several times in acute anti-Thy1.1-nephritis (THY-GN). Furthermore, we investigated serum and glomerular retinoid concentration patterns. On day 3, 7, and 14 we compared non-nephritic rats (control group; CON) to THY-GN rats. Systolic blood pressure and glomerular cell count were significantly higher in THY-GN rats on day 7 and 14 (p<0.001). We found an approximately 60% reduction in expression levels for retinoid receptors and dehydrogenases in nephritic glomeruli on day 3, but a 3-fold increase on day 7 (p<0.001 vs. CON). Similar applies to protein RAR. Hepatic expression of retinoid receptors was not influenced. On day 14 glomerular expression levels for retinoid receptors and retinoid metabolizing enzymes had returned to a normal level, glomerular cell count being still increased. Administering 13-cis retinoic acid (13-cis RA, isotretinoin) lowered blood pressure and glomerular cell count in nephritic rats but failed to influence the glomerular expression of retinoid receptors or of retinoid metabolizing enzymes. Our data document a stimulation of glomerular retinoid synthesizing enzymes and expression of retinoid receptors in the early repair phase of THY-GN suggesting activation of this system in acute renal disease.