Abstract
The theory that platelets once activated to secrete their granule constituents may continue to circulate in an "exhausted" state has found basis in experimental research, and has led clinical investigators to utilize the measurement of platelet serotonin content as an indirect reflection of in vivo platelet activation. In a patient with clinical and laboratory evidence of glomerulopathy, but without evident disease activity elsewhere, a low level of intraplatelet serotonin indicates that platelet activation is occuring within the glomerulus. To test the hypothesis that intraglomerular platelet activation is integral to the evolution and maintenance of glomerular injury in FSGS we have measured platelet serotonin content in 15 patients with biopsy-proven FSGS, 11 patients with treatment responsive N.S., and 20 normal controls. Expressed as nanograms 5-HT per 109 platelets, the following results were obtained:
Nine of fifteen FSGS patients and all patients in the treatment-responsive N.S. group were nephrotic at the time of study. We feel that these results indicate that, as a group, patients with the histopathology of FSGS have a statistically significant reduction in platelet serotonin content, that the nephrotic state per se does not influence the level of platelet serotonin and that platelet activation is involved in the sclerosing glomerulopathy.
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Leone, M., Hitzemann, R. & Strife, C. INDIRECT EVIDENCE OF INTRAGLOMERULAR PLATELET ACTIVATION IN A SUBTYPE OF CHILDHOOD NEPHROTIC SYNDROME, FOCAL SEGMENTAL GLOMERULOSCLEROSIS. Pediatr Res 18 (Suppl 4), 365 (1984). https://doi.org/10.1203/00006450-198404001-01631
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DOI: https://doi.org/10.1203/00006450-198404001-01631