PMC5937576_01
Zero-time biopsy of the renal graft. (a) Hematoxylin and eosin staining. (b) Periodic acid-Schiff staining. (c) Masson stain. (d) Silver methenamine stain. Renal tissue is visualized without significant vascular, tubular, and glomerular alterations. All photomicrographs are in 40x.
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The renal biopsy at time zero was without significant vascular, glomerular, and interstitial tubule alterations (Figures 1(a)-1(d)).
Doppler ultrasound. (a) Graft of the patient shows the absence of blood flow at the level of the renal cortex, arcuate arteries, interlobular arteries, and arterial anastomosis. (b) Duplex mode shows an arterial biphasic waveform with delayed acceleration, decreased systolic peak, and increased flow in diastole, which is a suggestive pattern of ischemia.
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Meanwhile, the renal vein could not be identified at the time of the study (Figures 2(a) and 2(b)).
Micrographs of graft nephrectomy (40x). Stained, respectively, with Jones' Methenamine (a), PAS (b), Hematoxylin and Eosin (c), and indirect peroxidase immunostaining for C4d (d). In all sections, fibrin thrombi adhered to the endothelium of the glomeruli ((a) and (c)) and the arteriolar walls (b) can be observed. C4d (d) was negative. All photomicrographs are in 40x.
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Due to the damage, graft transplantectomy was performed and the graft was sent for revision by a pathologist who reported diffuse medullary cortical infarction and acute thrombotic microangiopathy with negative immunohistochemistry for C4d (Figures 3(a)-3(d)).
Results of two platelet aggregometry tests: patient (blue line) and control (black line). (a) From left to right, the percentage of platelet aggregation with decreasing doses of ADE is shown. At 1 mumol, the patient presents platelet aggregation of almost 90% at 10 min. At lower concentrations of ADE, the pattern of aggregation is similar to that of the control (0.5 and 0.25 mumol). (b) From left to right, the percentage of platelet aggregation with decreasing doses of EPI is shown. At 11 mumol, the patient and control present platelet aggregation that reaches more than 80% at 10 min. In contrast to lower concentrations of EPI, while the control stops having platelet aggregation, the patient maintains a pattern of aggregation above 80% at concentrations of 0.25 and 0.125 mumol.
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In search of other pathologies, we requested studies of platelet aggregation, which showed platelet hyperaggregability at decreasing doses of epinephrine and normal aggregability associated with the exposure of adenosine diphosphate, compatible with sticky platelet syndrome type II (Figures 4(a) and 4(b)).