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A 33-year-old mestizo woman was evaluated following a deceased-donor kidney transplant.
Case ReportShe was diagnosed with chronic kidney disease and nephrotic-range proteinuria at age 12, initially suspected to be seronegative lupus (alopecia, malar rash). She received corticosteroids with transient improvement; a renal biopsy was declined by the family.
Four years later, she progressed to end-stage renal disease (ESRD) and underwent two years of hemodialysis followed by two years of peritoneal dialysis.
At age 20, she received a deceased-donor kidney transplant. Two years post-transplant, she developed proteinuria of 1.2 g/day with serum creatinine 0.8 mg/dL. The first biopsy was performed, and she received methylprednisolone pulses and plasma exchange (PLEX), reducing proteinuria to 500 mg/day.
Four years post-transplant, proteinuria increased to 4.7 g/day with negative autoimmune serologies (ADES). A second biopsy was performed, followed by rituximab and PLEX, resulting in a reduction of proteinuria to 1 g/day.
Six years post-transplant, serum creatinine rose from 0.8 to 2.4 mg/dL. Infection was ruled out, and rituximab was proposed but postponed due to COVID-19 infection. A third biopsy was obtained.
Seven years post-transplant, she presented with oliguria, volume overload, and required renal replacement therapy; a fourth biopsy was performed.
Pathology FindingsThe first biopsy showed mild mesangial expansion; the second, mesangial hypercellularity; the third, a mesangioproliferative pattern; and the fourth, mesangial nodules. Immunofluorescence was negative, and immunohistochemistry was positive for fibronectin.
Final Diagnosis: Recurrent fibronectin glomerulopathy (FGN) in a kidney allograft.
FGN is a rare hereditary cause of glomerular disease, most commonly reported in Caucasian and Asian populations. Only a few cases of recurrence in kidney transplants have been described (two Asian patients and three of unspecified ethnicity).
Morphologically, FGN should be suspected in patients showing mesangial expansion without immune complex deposits, accompanied by PAS-positive mesangial material.
We describe the morphological progression of fibronectin deposits: initial mesangial expansion, followed by mesangial hypercellularity, mesangioproliferative pattern, and finally mesangial nodules.
FGN should be considered in young patients presenting with nephrotic-range proteinuria, slowly progressive renal dysfunction, and a mesangioproliferative pattern with negative immunofluorescence findings.
