Background <p>Tranexamic acid is an anti-fibrinolytic drug recommended in the setting of post-partum hemorrhage and non-obstetrical massive bleeding. Its putative role in the pathogenesis of renal cortical necrosis is unclear and has been rarely reported.</p> Case presentation <p>We report the case of a young woman who developed anuric acute kidney injury upon administration of tranexamic acid in the setting of mild traumatic hemorrhage. Early contrast-enhanced computed tomography revealed diffuse defects of cortical enhancement in both kidneys, consistent with the diagnosis of acute bilateral renal cortical necrosis. Biological tests did not detect hallmarks of thrombotic microangiopathy or disseminated intravascular coagulation and testing for acquired thrombophilic disorders were negative. The patient remained dialysis-dependent for two months and then partially recovered renal function to an estimated glomerular filtration rate of 40&#xa0;ml/min/1.73 m<sup>2</sup>.</p> Conclusions <p>This case illustrates the potential prothrombotic effect of tranexamic acid administered in the context of non-obstetric acute bleeding and the importance of re-considering its prescription in the presence of concomitant estrogenic impregnation in order to alleviate the risk of occurrence of renal cortical necrosis. It also addresses the predictive value of kidney imaging for the severity of renal cortical necrosis and subsequent renal recovery.</p>

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Tranexamic acid-induced acute bilateral renal cortical necrosis in a young trauma patient: a case report and literature review

  • Jérémy Berri,
  • Moglie Le Quintrec Donnette,
  • Ingrid Millet,
  • Leila Chenine,
  • Jean-Emmanuel Serre,
  • Manal Mazloum

摘要

Background

Tranexamic acid is an anti-fibrinolytic drug recommended in the setting of post-partum hemorrhage and non-obstetrical massive bleeding. Its putative role in the pathogenesis of renal cortical necrosis is unclear and has been rarely reported.

Case presentation

We report the case of a young woman who developed anuric acute kidney injury upon administration of tranexamic acid in the setting of mild traumatic hemorrhage. Early contrast-enhanced computed tomography revealed diffuse defects of cortical enhancement in both kidneys, consistent with the diagnosis of acute bilateral renal cortical necrosis. Biological tests did not detect hallmarks of thrombotic microangiopathy or disseminated intravascular coagulation and testing for acquired thrombophilic disorders were negative. The patient remained dialysis-dependent for two months and then partially recovered renal function to an estimated glomerular filtration rate of 40 ml/min/1.73 m2.

Conclusions

This case illustrates the potential prothrombotic effect of tranexamic acid administered in the context of non-obstetric acute bleeding and the importance of re-considering its prescription in the presence of concomitant estrogenic impregnation in order to alleviate the risk of occurrence of renal cortical necrosis. It also addresses the predictive value of kidney imaging for the severity of renal cortical necrosis and subsequent renal recovery.