Current treatments of diabetic nephropathy (DN) are limited to Renin-Angiotensin system blockade, however DN remains the commonest cause of end-stage renal disease. Thus, novel targets for antagonism are urgently needed. The P2X receptors (P2XRs) potentially provide such targets. P2XRs (P2X1-7R) are ligand-gated ion channels activated by extracellular ATP. They are present within the kidney and increased expression of subtypes P2X4R and P2X7R may predispose it to vascular injury(1). Upregulated glomerular P2X7R expression also occurs in rats with established DN(2). Therefore, we have explored whether the expression of these P2XR subtypes changes in early Type 1 Diabetes Mellitus (T1DM). T1DM was induced in male Sprague Dawley rats (n=6) via intraperitoneal (IP) injection of streptozotocin (35mg/kg). Blood glucose concentration was measured at 48h and all rats were confirmed diabetic (27.5-30.7mmol/L). Control rats received a citrate vehicle IP injection (n=3) or were untouched (n=3). All rats were culled after 3 weeks by IP anaesthetic overdose (50mg/kg Sagatal). The kidneys were excised and stored at -80°C for Western and qRT-PCR analysis on whole extracts or fixed in 4% paraformaldehyde for staining. Western blots were performed on 18μg of protein for P2X1R, P2X4R and P2X7R. qRT-PCR detected Havcr1 (KIM1) and Col1a1 (collagen 1) gene expression and results were log-transformed. Picrosirius red (PSR) staining was quantified via densitometry to identify collagen levels indicative of fibrosis. The values presented are means±SEM and statistical comparisons were made using Mann-Whitney U-tests and unpaired t-tests, with significance stated at P value<0.05. Renal collagen expression was low and no distinct differences were noted between the T1DM (PSR 0.35±0.12 n=6, Col1a1 0.08±0.17 n=5) and control kidneys (PSR 0.56±0.13 n=6, Col1a1 0.07±0.21 n=5). Furthermore, there was no change in Havcr1 expression (T1DM -0.02±0.19 n=5, control -0.11±0.13 n=5), illustrating the absence of fibrosis and overall renal injury. Whole kidney levels of P2X1R (T1DM 0.17±0.01 n=6, control 0.20±0.03 n=6) and P2X4R (T1DM 0.05±0.01 n=6, control 0.07±0.02 n=6) were similar between the two groups. P2X7R expression was significantly reduced after 3 weeks of T1DM compared to the controls (T1DM 0.08±0.02 n=6, control 0.12±0.02 n=6, P value = 0.04). This suggests 3 weeks of T1DM is associated with P2X7R downregulation at the whole kidney level. It is unknown whether this is limited to a specific cell type, as P2X7R is expressed on resident immune cells, podocytes and the vascular endothelium. Prolonged duration of T1DM was shown to increase glomerular P2X7R expression(2) and our data indicate this is likely in response to cell injury. It is possible P2X1R and P2X4R expression changes accompany renal injury as well, and so this time-point is too early to observe any differences.