Chronic renal failure (CRF) promotes endothelial cells and neutrophils damage in the severe stages of disease [1]. Disturbances in nitric oxide (NO) bioavailability are involved in the pathogenesis of CRF. [2]. NO is a potent vasodilator, inhibitor of platelet activation and aggregation. Recent studies have demonstrated that activated neutrophils promotes an inhibitory effect on platelet aggregation, contributing to vascular homeostasis [3] . The aim of this study was to evaluate the transport of L-arginine, the activity of the enzyme nitric oxide synthase (NOS) and the platelet-neutrophil relationship in CRF. Six CRF patients under haemodialysis and six healthy controls matched for sex and age were included in this study. The Pedro Ernesto Hospital Ethical Committee approved this study (451- CEP/HUPE), and informed consent was obtained from each participant. Basal NOS activity was measured by the conversion of L-[3H]-arginine into L-[3H]-citrulline. L-arginine transport into neutrophils was analysed in these patients. Saturable influx of L-arginine into neutrophils was mediated by systems y+ and y+L. Platelet aggregation was induced by ADP 5 μM, incubated by neutrophils at different times (5 and 30 minutes) and monitored for 8 min in a four-channel aggregometer. Student’s t and Mann Whitney tests were used for statistical analysis and values were considered significant when p<0.05. Values were expressed as means ± SEM. Results: Total L-[3H]-arginine transport (controls: 1.56 ± 0.46 vs. CRF: 0.50 ± 0.12 pmol/106cells/min), transport by y+ system (controls: 0.5 ± 0.18 vs. CRF: 0.25 ± 0.05 pmol/106cells/min) and transport by y+L system (controls: 1.06 ± 0.4 vs. CRF: 0.24 ± 0.08 pmol/106cells/min) were reduced in CRF patients. There was a significant decrease in NOS activity (pmol/106 cells/min) in neutrophils from CRF patients (0.18 ± 0.03) compared to controls (0.62 ± 0.02).There was no change in platelet aggregation induced by ADP in CRF patients compared to controls. In the presence of neutrophils, there was a reduction-time dependent in platelet aggregation in both groups with no difference between them. Conclusion: This study demonstrated a lower L-[3H]-arginine influx associated with a reduction in NOS activity in neutrophils from CRF patients compared with controls. These data suggest alterations in the L-arginine-NO pathway that may lead to a decrease in NO bioavailability in patients under haemodialysis. Financial Support: FAPERJ, CNPq, CAPES.