A case of de novo focal segmental glomerulosclerosis occurred one and half years after kidney transplantation supposed to be caused by calcineurin inhibitor.

A 64-yr-old man with end-stage kidney disease caused by hypertensive nephrosclerosis underwent living-unrelated ABO-identical kidney transplantation (KTx) at the age of 60 yr from his 60-yr-old wife. Maintenance trough concentration of cyclosporine A (CsA) was 100 ± 30 ng/mL. Five months after KTx, proteinuria gradually increased to around 1 g/d. TRBx at eight months after KTx revealed the new-onset alteration of mild arteriolosclerosis with intimal hyalinosis, which might reflect calcineurin inhibitor (CNI)-associated arteriopathy (CAA). Nearly one and half years after KTx, urinary protein excretion became nearly 2 g/d. TRBx revealed the advanced CAA and findings of focal segmental glomerulosclerosis (FSGS). Then, CNI was switched from CsA to tacrolimus (TAC). TRBx at two and half years after KTx revealed progressed arteriolar transmural thickening and striped fibrosis, which were supposed to be induced by an increase in serum TAC concentration because of acute enterocolitis. Then, TAC dose was reduced to serum trough concentration 5-8 ng/mL, but urinary protein excretion was increased up to 10 g/d. Reduction of TAC to trough concentration 2.0 ± 0.5 ng/mL reduced urinary protein excretion. Attempts to elevate TAC trough concentration within normal range (4-8 ng/mL) reproducibly induced the recurrence of an increase in sCr or urinary protein excretion. All these findings supported the etiology of graft dysfunction, and proteinuria of this case was FSGS.