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Intrinsic Coagulation Pathway in End‐Stage Renal Disease Associated with Spinal Cord Injury Treated with Hemodialysis
Author(s) -
Vaziri N. D.,
Winer R. L.,
Toohey J.,
Danviriyasup K.,
Alikhani S.,
Eltorai I.,
Gordon S.,
Paule P.
Publication year - 1985
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1111/j.1525-1594.1985.tb04366.x
Subject(s) - end stage renal disease , hemodialysis , medicine , spinal cord injury , coagulation , renal injury , spinal cord , urology , surgery , kidney , psychiatry
Plasma procoagulant activities of factors XII, XI, IX, and VIII and plasma concentrations of factor XII antigen and high molecular weight kininogen (HMK) were determined in nine men with chronic renal failure (CRF) associated with long‐standing spinal cord injury (SCI) treated with hemodialysis. The results were compared with those obtained in a group of 10 ambulatory CRF patients and 8 normal volunteers (control group). Congenitally deficient plasmas were used as the substrate for the measurement of procoagulant activities in a one‐stage clotting assay. Monospecific antibodies were employed in the measurement of factor XII antigen and HMK using gradient plate immunodiffusion and rocket immunoelectrophoresis. Factor XII coagulant activity and antigen concentration were significantly increased in the SCI group. The mean values for plasma factor XI and IX activities in the SCI group were comparable with those observed in the ambulatory patients and normal control group. However, marked variations in factor XI and IX levels were noted among the SCI patients with a few instances of mild to moderate factor deficiencies and several cases of markedly elevated levels. Factor VIII activity was markedly increased, with only two of the nine patients exhibiting normal values. HMK concentration in the SCI group was comparable with values obtained for the other groups. Following dialysis, factor XII antigen concentration rose and factor XI activity fell slightly but signficantly. The results indicate that the combination of CRF and long‐standing SCI is associated with marked aberrations of intrinsic coagulation pathway. The underlying mechanisms and the clinical consequences of these abnormalities are not known and require further investigation.