In Vitro Analysis of Platelet Adhesion, Aggregation, and Surface GP1bα Expression in Stored Refrigerated Whole Blood: A Pilot Study.

BACKGROUND: Warm, fresh whole blood (WB) has been used by the US military to treat casualties in Iraq and Afghanistan. Based on data in that setting, cold-stored WB has been used to treat hemorrhagic shock and severe bleeding in civilian trauma patients in the United States. In an exploratory study, we performed serial measurements of WB's composition and platelet function during cold storage. Our hypothesis was that in vitro platelet adhesion and aggregation would decrease over time. METHODS: WB samples were analyzed on storage days 5, 12, and 19. Hemoglobin, platelet count, blood gas parameters (pH, Po2, Pco2, and Spo2), and lactate were measured at each timepoint. Platelet adhesion and aggregation under high shear were assessed with a platelet function analyzer. Platelet aggregation under low shear was assessed using a lumi-aggregometer. Platelet activation was assessed by measuring dense granule release in response to high-dose thrombin. Platelet GP1bα levels were measured with flow cytometry, as a surrogate for adhesive capacity. Results at the 3 study timepoints were compared using repeat measures analysis of variance and post hoc Tukey tests. RESULTS: Measurable platelet count decreased from a mean of (163 + 53) × 109 platelets per liter at timepoint 1 to (107 + 32) × 109 at timepoint 3 (P = .02). Mean closure time on the platelet function analyzer (PFA)-100 adenosine diphosphate (ADP)/collagen test increased from 208.7 + 91.5 seconds at timepoint 1 to 390.0 + 148.3 at timepoint 3 (P = .04). Mean peak granule release in response to thrombin decreased significantly from 0.7 + 0.3 nmol at timepoint 1 to 0.4 + 0.3 at timepoint 3 (P = .05). Mean GP1bα surface expression decreased from 232,552.8 + 32,887.0 relative fluorescence units at timepoint 1 to 95,133.3 + 20,759.2 at timepoint 3 (P < .001). CONCLUSIONS: Our study demonstrated significant decreases in measurable platelet count, platelet adhesion, and aggregation under high shear, platelet activation, and surface GP1bα expression between cold-storage days 5 and 19. Further studies are needed to understand the significance of our findings and to what degree in vivo platelet function recovers after WB transfusion.

Unexpected Fabry disease in a renal allograft kidney: an underrecognized cause of poor allograft function.

Fabry disease is an X-linked recessive lysosomal storage disease caused by a deficiency of α-galactosidase A, with characteristic ultrastructural cytoplasmic myelin-like inclusions. Renal lesions are seen in male and variably in heterozygous female patients. One previous report has described Fabry disease involving a renal allograft from a deceased female donor with no history of Fabry disease. The authors describe another case, in which suspicion for Fabry disease was raised ultrastructurally. This serves as a reminder that proteinuria after renal transplantation may be due to donor-derived disease. Fabry disease is probably an underrecognized cause of graft dysfunction. This case provides further justification for ultrastructural examination of renal allograft biopsies.