Donor thrombotic microangiopathy

Determining the etiology of a thrombotic microangiopathy (TMA) in a transplanted kidney biopsy may not be an easy task, the causes include: antibody-mediated rejection, infections, drug toxicity, ischemia and other systemic causes of TMA (HUS, TTP, etc.). In our case, the presence of a delayed graft function, the short post-transplantation time at the time of the biopsy, and the presence of similar characteristics in the other recipient from the same donor, in addition to ruling out other possible alterations and knowing that the microthrombi were limited to the transplanted kidney, leading us to conclude that the TMA originated from the donor.

The etiology of TMA in this donor was possibly related to final pre-mortem events, since he was a patient with sustained hypotension who required high doses of vasoconstrictors. In a series by Gao G et al, they report that diffuse glomerular thrombi only occurred in donors who suffered severe head trauma, which may be a predisposing factor (Gao G, et al. Donor Characteristics, Recipient Outcomes, and Histologic Findings of Kidney Allografts With Diffuse Donor-derived Glomerular Fibrin Thrombi. Transplantation. 2019;103(9):1921-1927. [PubMed link]).

An intact fibrinolytic system in the recipient usually dissolves the microthrombi and, in general, the prognosis is good, as in our patient and the other recipient, who two weeks after the transplant improved kidney function to normalize creatinine.

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