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Nephrol Dial Transplant (1993) 8: 631-636
© 1993 European Renal Association-European Dialysis and Transplant Association

research-article

In vivo prostanoid formation during acute renal allograft rejection

B. Tönshoff1,, C. Busch1, H. Schweer2, K. Schärer1 and H. W. Seyberth2

1Division of Pediatric Nephrology, University Children's Hospital D-6900 Heidelberg, Germany 2University Children's Hospital D-3550 Marburg, Germany

Correspondence and offprint requests to: Correspondence and offprint requests to: Dr B. Tönshoff, University Children's Hospital, Division of Pediatric Nephrology, Im Neuenheimer Feld 150, D-6900 Heidelberg, Germany

Vasoconstriction during acute renal allograft rejection may be regulated by increased formation of vasoactive prostanoids. To address this hypothesis we investigated the biosynthesis of thromboxane (Tx)A2, a potent vasoconstrictor and platelet agonist, of prosta-cyclin (PGI2), a vasodilator and platelet antagonist, and of prostaglandin (PG)E2, a mediator of salt and water excretion, in nine children with 12 acute rejection episodes, prospectively during the first 7 weeks after renal transplantation. We used physicochemical analysis of stable urinary prostanoid index metabolites. Rejection crises were associated with an increase in TxB2 excretion from baseline median 9.2 (range 1.9–18.6) ng/h/1.73m2 to 21.2 (range 10.0–133.0) ng/h/1.73m2 (P<0.005) during acute rejection episodes. Methylprednisolone pulse therapy resulted in a partial reduction, but not normalization of TxB2 excretion. Urinary 2,3-dinor-TxB2 was slightly stimulated during allograft rejection, urinary 1 l-dehydro-TxB2 did not change significantly. Renal PGI2 and PGE2 biosynthesis remained essentially unchanged. In contrast to acute graft rejection, patients with chronic graft rejection and those with stable graft function on different immunosuppressive regimens with or without cyclosporin A did not present stimulated renal TxA2 formation. Increased renal TxA2 formation in acute renal allograft rejection is likely to mediate vasoconstriction and potentiate the loss of renal blood flow and glomerular filtration rate, in the absence of an adequate response of the renoprotective prostanoids PGI2 and PGE2.

Keywords: acute renal allograft rejection; renal vasoconstriction; thromboxane A2; prostacyclin; prostaglandin E2


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