At the age of three yr, a male patient had surgical treatment for bilateral vesicoureteral reflux (VUR), and at the age of 19 yr, he developed nephrotic syndrome because of focal segmental glomerulosclerosis (FSGS). His renal function deteriorated despite treatment with temocapril and aspirin, and dialysis treatment was started when he was 19. After nine yr of dialysis, he received a living kidney transplantation from his 58-yr-old father, who had a long history of hypertension. A graft biopsy before perfusion showed moderate arteriolosclerosis. As urine protein increased to 2.15 g/d at 16 months after kidney transplantation, the graft biopsy was performed again. FSGS lesion with severe arteriosclerosis was recognized under light microscope, while the effacement of podocyte foot processes was seldom observed. The alteration of calcineurin inhibitor from cyclosporine to tacrolimus, combined with the new administration of angiotensin receptor antagonist (valsartan) and aldosterone receptor blocker, successfully decreased the amount of urine protein to 0.8 g/d within two wk. We considered that the present case showed two distinct types of FSGS lesions--one because of VUR and the other because of cyclosporine arteriolopathy--in each native kidney and transplanted kidney.