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Research Article Free access | 10.1172/JCI105782

Platelet factor 3 in normal subjects and patients with renal failure

S. Frederick Rabiner and Otto Hrodek

Division of Clinical Hematology, Department of Medicine, Michael Reese Hospital and Medical Center, Chicago, Illinois 60616

Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60616

Find articles by Rabiner, S. in: PubMed | Google Scholar

Division of Clinical Hematology, Department of Medicine, Michael Reese Hospital and Medical Center, Chicago, Illinois 60616

Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60616

Find articles by Hrodek, O. in: PubMed | Google Scholar

Published April 1, 1968 - More info

Published in Volume 47, Issue 4 on April 1, 1968
J Clin Invest. 1968;47(4):901–912. https://doi.org/10.1172/JCI105782.
© 1968 The American Society for Clinical Investigation
Published April 1, 1968 - Version history
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Abstract

Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's platelet-rich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1:8). The second test was similar but used “frozen and thawed” platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the non-bleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material.

The mean plasma clot retraction of uremic patients was also significantly different from the mean plasma clot retraction or normal controls. However, unlike the PF3-A time, the abnormality of plasma clot retraction was not immediately affected by dialysis. Correction of plasma clot retraction did occur after repeated dialyses.

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