Abstract
There are numerous causes of acute and chronic kidney disease following HSCT. Excluding nephrotoxic drugs and infections, the role of GVHD in the genesis of several glomerulopathies is a controversial or incompletely understood subject. Transplant-associated thrombotic microangiopathy (TA-TMA) has been associated with exposure to calcineurin inhibitors (CNIs) in earlier studies, and more recent studies have demonstrated associations with GVHD. Many of these processes can coexist, making etiologic determination difficult. The development of TA-TMA has not been conclusively linked with the use of high-dose conditioning regimens nor has a clear or consistent response to anticomplement treatment (e.g., eculizumab) been observed. Other post-HSCT glomerulopathies associated with nephrotic syndrome include membranous nephropathy, minimal change disease, and focal segmental glomerulosclerosis (FSGS). The potential mechanisms of GVHD’s role in kidney injury, e.g., the contributions of T cells, macrophages, cytokines, and immune responses against kidney proteins, require further investigation.
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Bauer, A.R., Finn, L.S., Hingorani, S.R. (2019). Kidney Involvement in GVHD. In: Yeung, C., Shulman, H. (eds) Pathology of Graft vs. Host Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-42099-8_19
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