min/1.73 m and the proteinuria/creatininuria ratio was 145 mg/mmol. Six weeks after transplantation, the serum creatinine level increased by 20% compared with baseline, and a kidney biopsy was performed (proteinuria 0 g/L). Histopathologic analysis showed mild tubulitis and mild interstitial inflammation (i1, t1, g0, v0, cpt0, ci0, ct0, cg0, mm0, cv0, and ah0), and an immunofluorescence study was negative for C4d, IgM, and C3 deposits, leading to the diagnosis of borderline rejection. None of the nine glomeruli had lesions of membranoproliferative glomerulonephritis. The patient received three pulses of methylprednisolone (500 mg/day). Three months posttransplantation, a protocol kidney biopsy was performed. It contained 14 glomeruli and showed mild interstitial fibrosis and tubular atrophy (i0, t0, g0, v0, cpt0, ci1, ct1, cg0, mm0, cv0, and ah0). An immunofluorescence study was negative for C4d, IgM, and C3 deposits. Six months posttransplantation, the eGFR was 62 mL/min/1.73 m and the proteinuria/ creatininuria ratio was 17 mg/mmol. This is the first reported case of kidney transplantation from a donor with shunt nephritis. As we had hypothesized, the glomerular lesions were reversible and the graft outcome was good, likely because the kidney was extracted from a deleterious immunologic environment of the donor (3). We cannot rule out the potential role of immunosuppressive treatment on this outcome (4). In conclusion, kidneys with diseases induced by immune-mediated extrarenal mechanisms may be considered for transplantation, after histological evaluation in emergency. This strategy could increase the pool of donors.

Late subcapsular lymphocele in a kidney graft.

Late onset-lymphocele after renal transplantation

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Late onset-lymphocele after renal transplantation