Tranexamic acid increases peritoneal ultrafiltration volume in patients on CAPD.
OBJECTIVE
The preservation of ultrafiltration (UF) capacity is crucial to maintaining long-term continuous ambulatory peritoneal dialysis (CAPD).The aim of the present study was to investigate whether the antiplasmin agent tranexamic acid (TNA) increases UF volume in CAPD patients.


METHODS
Fifteen patients on CAPD, 5 with UF loss and 10 without UF loss, were recruited for the study. The effect of TNA was evaluated with respect to changes in UF volume, peritoneal permeability, peritoneal clearance, bradykinin (BK), and tissue plasminogen activator (tPA) concentration.


METHODS
Dialysis unit of the Saiseikai Central Hospital.


RESULTS
In patients with UF loss, 2 weeks of treatment with oral TNA produced a significant increase in UF volume in all subjects (5/5).TNA also produced a significant increase in peritoneal clearances of urea and creatinine (Cr). However, the peritoneal equilibration test (PET) revealed that TNA had no effect on dialysate/plasma (D/P) Cr, Kt/V, or the protein catabolic rate (PCR).TNA also had no effect on net glucose reabsorption. In contrast, significant decreases in BK and blood tPA concentrations in response to TNA treatment were noted. BK concentration in drainage fluid was also reduced. In the case of patients without UF loss,TNA produced an increase in UF volume in 70% (7/10). However, no differences were found in blood and drainage BK and tPA concentrations between theTNA treatment and nontreatment periods in these patients. A comparison of basal BK and tPA concentration showed that there were no differences in these parameters between patients with UF loss and those without loss of UF. Furthermore,TNA given intraperitoneally to a patient also produced a marked increase in UF volume.


CONCLUSIONS
The present study suggests thatTNA enhances UF volume in patients both with and without UF loss. SinceTNA did not affect peritoneal permeability and glucose reabsorption, the mechanism by which TNA exerts an enhancing action on UF is largely unknown. We speculate that it may be associated with suppression of the BK and/or tPA system, at least in patients with UF loss.
Kuriyama
S
S
Division of Nephrology, Saiseikai Central Hospital, Tokyo, Japan.
Nakayama
M
M
Tomonari
H
H
Kawaguchi
Y
Y
Hosoya
T
T
D000042:Absorption; D000284:Administration, Oral; D000328:Adult; D000368:Aged; D000933:Antifibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001798:Blood Proteins / Q000378:metabolism; D001920:Bradykinin / Q000032:analysis / Q000097:blood; D003404:Creatinine / Q000032:analysis / Q000097:blood; D015314:Dialysis Solutions / Q000032:analysis; D005260:Female; D005947:Glucose / Q000493:pharmacokinetics; D006801:Humans; D007274:Injections, Intraperitoneal; D008297:Male; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory; D010537:Peritoneum / Q000187:drug effects* / Q000378:metabolism; D010539:Permeability / Q000187:drug effects; D010959:Tissue Plasminogen Activator / Q000032:analysis / Q000097:blood; D014148:Tranexamic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D014462:Ultrafiltration; D014508:Urea / Q000032:analysis / Q000097:blood
D000933:Antifibrinolytic Agents; D001798:Blood Proteins; D015314:Dialysis Solutions; D014148:Tranexamic Acid; D014508:Urea; D003404:Creatinine; D010959:Tissue Plasminogen Activator; D005947:Glucose; D001920:Bradykinin