Background: Various pathogenic factors were blamed for the neurologic deficits in renal patients. Fumonosin (FB1) is an occasional mycotoxin that was shown to be responsible for neurologic disturbances in horses by disturbing the sphingolipid metabolism. It was detected as a contaminant among several foodstuffs in Egypt, but was not studied as a risk factor in humans. Objectives: To study the cross-sectional associations between serum FB1, sphinganine and sphingonsine and the prevalence of neurologic deficits among other related factors including serum aluminium (Al), serum parathyroid hormone (PTH) levels and other hematological and chemical parameters in a group of children and adult renal patients. Methods: Visual evoked potential (VEP) was tested in 40 end stage renal disease patients (20 children and 20 adults) on regular dialysis treatment (RDT), 40 patients with different glomerulonephritis (GN) (20 children and 20 adults) and 10 healthy controls. They were studied for serum FB1, sphinganine, sphingosine, calcium, phosphorus, PTH levels, Al, albumin, blood urea, serum creatinine, blood gases and hemoglobin percentage. Results: FB1 with elevation of sphinganine/sphingosine ratio was found in 12/40 of ESRD patients and 12/40 GN patients but in none of controls (p ˂ 0.05). Of the GN group, 9/40 had delayed VEP and 3 of these 9 had positive FB1, but showed no significant correlation with neither FB1 nor PTH (p ˃ 0.05). Of the ESRD group, 13/40had delayed VEP. This delay was detected in 8/12 cases with positive FB1 and in 10/19 cases with more than double the high serum PTH and in 13/34 cases with Al more than 20 ug/dl. Al was a sole risk factor in 2/13 ESRD patients with delayed VEP, but neither high PTH nor positive FB1 was encountered solely in any of these cases. In adults ESRD group, VEP abnormalities showed significant correlation with PTH (p ˂ 0.05) but not with Al or FB1. Yet, in children it was significantly correlation with the serum PTH, Al and FB1 (p ˂ 0.004, 0.03, 0.0001 respectively). Conclusions: We conclude that long duration of hyperparathyroidism is a risk factor causing neurologic deficits in ESRD patients and may be aggravated by high serum Al and/or a positive FB1, particularly in children.