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Abstract: FR-PO763

An Unusual Regional Cellular FSGS Secondary to Artery Stenosis in a Renal Allograft

Session Information

Category: Transplantation

  • 2102 Transplantation: Clinical


  • Wang, Qihua, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China
  • Xu, Zhengyuan, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China
  • Yang, Shicong, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China
  • Chen, Wenfang, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China

Focal segmental glomerulosclerosis (FSGS) in renal allograft derived from various etiology shares similar morphology regardless of recurrent or de novo onset. Here, we reported a recipient presented with moderated proteinuria whose consecutive renal biopsies showed drastic discrepancy due to different regional hemodynamics.

Case Description

A 20-year-old female with end stage IgA nephropathy received a successful renal transplantation 3 years ago. Two years later she developed hypertension and serum creatinine (Scr) increased from 60 to 177 umol/L. Computer tomography angiography (CTA) showed renal artery stenosis. After a percutaneous transluminal angioplasty, her Scr recovered and urine protein remained negative. Six months later she developed moderate proteinuria (2.5g/d) for unknown reason. Renal biopsy showed diffuse (10 out of 16 glomeruli) cellular FSGS lesion without IgA deposition. Ultrastructure change of podocytes was not available due to absence of glomeruli in EM. De novo FSGS was diagnosed with uncertain etiology. Corticosteroid impulse therapy was applied and meanwhile a second biopsy was performed because of unmatched pathology and symptoms. No FSGS among 37 glomeruli but mild ischemic change and remarkable enlarged juxtaglomerular apparatus (JGA) was found. CTA and ultrasound revealed two different hemodynamic areas, which the hypo-infused upper role was fed by the stenotic main artery and the hyper-infused lower pole by an accessary artery. The two biopsies happened to be sampled from opposite poles. Therefore the cellular FSGS was speculated as secondary to hyperperfusion. Corticosteroid impulse therapy was stopped. Her urinary protein turned negative and Scr decreased to 80umol/L 3 days after an endovascular stent angioplasty.


Adaptive FSGS caused by hyperperfusion usually shows perihilar pattern. This allograft kidney perfectly simulated unilateral renal artery stenosis of native kidneys, i.e. the hypoperfused area underwent ischemia and proliferation of JGA, while the hyperperfused developed secondary FSGS which could be reversed by improved hemodynamics.