A renal transplant patient on long-term calcineurin inhibitor therapy develops vacuolar changes in proximal tubular cells without necrosis, progressive tubulointerstitial fibrosis, and arteriolar hyalinosis. This pattern of injury is best classified as:
- A Acute tubular necrosis from ischemia
- B Chronic antibody-mediated rejection
- C Cyclosporine/tacrolimus nephrotoxicity — chronic CNI nephropathy ✓
- D BK virus nephropathy
Explanation
Chronic calcineurin inhibitor (CNI) nephropathy is a well-recognized pattern of injury from cyclosporine and tacrolimus characterized by tubular vacuolization, striped interstitial fibrosis following vascular distribution, and afferent arteriolar hyalinosis (with periodic acid-Schiff positive nodular deposits — 'beads on a string' pattern). It is dose-dependent and results from renal vasoconstriction, TGF-beta mediated fibrogenesis, and direct tubular toxicity. BK virus nephropathy shows nuclear viral inclusions in tubular cells.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.