Glomerulopathy characterized by deposits of fibrillary material was first reported in 1977 [1]. Fibrillary immunotactoid glomerulopathy is a clinicopathological entity characterized by extracellular deposition of non‐branching microfibrils or microtubules (Congo‐red and thioflavin T negative) within the mesangium and capillary walls of renal glomeruli. It is clinically characterized by the presence of glomerular proteinuria (often in the nephrotic range), microscopic haematuria, and often hypertension. It can lead to chronic renal failure. Based on the size and the arrangement of the microfibrils or microtubules in intraglomerular deposit, fibrillary immunotactoid glomerulopathies have been divided into two distinct entities: fibrillary glomerulopathy (FG) is characterized by small, randomly organized fibrils (≤30 nm in diameter), whereas immunotactoid glomerulopathy (ITG) is typified by larger fibrils and often organized in parallel arrays (≥30 nm in diameter) [2,3]. Patients with FG are less likely than those with ITG to have associated haematopoietic disease, i.e. monoclonal gammopathies; they also have poorer renal survival [2]. The two above‐mentioned entities are primarily renal in most cases. Despite the fact that there is limited information about kidney transplantation in the context of end‐stage renal failure related to fibrillar immunotactoid glomerulopathies, the few reports available indicated that fibril deposition recurred in more than 50% of patients, although the allograft functioned satisfactorily for a few years [4–6]. We report the case of a patient with ITG who had an early recurrence of this disease after renal transplantation but who responded favourably to an increase in immunosuppressive therapy.
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Carles et al. (2000) studied this question.
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