Case Reports in Nephrology · Published 2025-01-01 · DOI 10.1155/crin/7613213
Transplant kidneys face increased functional demands in comparison to physiological conditions, and glomerular hypertrophy (GH) appears to be a common compensatory mechanism. Adaptive GH could contribute to improved graft function, but a so-called “maladaptive” response may lead to shortened graft survival. We assessed in three patients the mean glomerular diameter in donor preimplantation wedge biopsies and in subsequent posttransplant biopsies and correlated the glomerular size with Banff scores and clinical course. Mean glomerular size increased from 192.09 ± 28.65, 188.98 ± 19.86, and 168.96 ± 18.5 in preimplantation biopsies to 279.43 ± 50.6 (p < 0.0001), 275.23 ± 68.17 (p < 0.0001), and 266.23 ± 40.5 (p < 0.00001) in the last biopsies, respectively. The proportion of enlarged glomeruli (> 200 µ) increased from 42.86%, 31%, and 5% in the donor biopsies to 93.3% (p0.008), 95.7% (p < 0.0001), and 95.1% (p < 0.00001) in the last biopsy, respectively. Although GH was initially associated with the achievement of good graft function, secondary FSGS and proteinuria developed at 3, 7, and > 17 years posttransplant, respectively. GH (glomerulomegaly) can be easily appreciated by light microscopy, but is not routinely recorded in transplant biopsy reports. Recognition and documentation of GH could help identify factors associated with the “maladaptive” phase of this adaptive response and find interventions that can potentially prolong graft survival.
Abstract from DOAJ. Public domain (CC0 1.0).
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