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An event is serious (based on the ICH definition) when the patient outcome is:

  • * death

  • * life-threatening

  • * hospitalisation

  • * disability

  • * congenital anomaly

  • * other medically important event

A 28-year-old woman developed ischaemic renal cortical necrosis during treatment with tranexamic acid for peripartal uterine bleeding.

The woman delivered a healthy female neonate by caesarean section at gestational week 41. During the caesarean section, she developed uterine bleeding leading to haemorrhagic shock secondary to uterine atony, and her BP dropped to 80/40mm Hg. Immediately, the bleeding was stopped, and uterine tamponade was performed. She was transfused erythrocyte concentrates. Additionally, she was administered 2g of tranexamic acid [route not stated], prothrombin complex concentrate [PPSB], plasma [lyoplasmas; free-dried plasma], fibrinogen, sulprostone and oxytocin. Subsequently, she developed anuric kidney failure. In view of anuria/oliguria, the woman was initiated on haemodialysis with a continuous kidney replacement for volume therapy. She developed pronounced hydropic decompensation and pleural effusions due to the anuria. Significant volume depletion was achieved by means of generalised volume overloading. Initially, a repeated drop in haemoglobin was observed, and additional erythrocyte concentrates were transfused. After the caesarean section, on the same day, her BP elevated to 180/100mm Hg with a tendency to reach beyond 200mm Hg systolic. She started receiving anti-hypertensive therapy with amlodipine and magnesium. She appeared increasingly disoriented and developed an acute, generalised seizure. MRI findings were suggestive of hypertensive encephalopathy or posterior reversible encephalopathy syndrome. Her BP lowered after continued antihypertensive treatment and volume withdrawal. She was then transferred to another hospital. On post-partum day 1, laboratory investigations revealed elevated levels of creatinine, urea, LDH, AST and ALT, decease in thrombocyte count, abnormal levels of haptoglobin and coagulation factors, and evidence of fragmentocytes. The findings were suggestive of thrombotic microangiopathy. The laboratory test constellation was in line with HELLP syndrome or disseminated intravascular coagulation with severe blood loss. Four weeks after the delivery, following improvement in the neurological symptoms, a renal biopsy was performed. During the biopsy, 12 glomeruli were found, of which 9 were completely necrotic or scarred. The tubular apparatus of the cortex was rarefied, atrophic and nodular, with loss of the core ability to stain (approximately 50-60 %). This finding was consistent with ischaemic renal cortical necrosis [duration of treatment to reaction onset not stated]. Additionally, a fibrin clot was observed in the pre-arteriole. She received treatment with furosemide; however, the excretory renal function did not recover completely. On post-partum day 7, laboratory investigations revealed improvement in her levels of creatinine, urea and thrombocyte count, and no fragmentocytes were observed. After sufficient volume withdrawal, was switched on intermittent haemodialysis from continuous haemodialysis. Demers catheter was installed, and she was discharged from the inpatient treatment. One year later, she underwent living donor kidney transplantation.

Author comment: "[T]he application of tranexamic acid with its pro-thrombotic effect seems to be responsible for the major renal cortical necrosis." "[T]he administration of tranexamic acid can lead to acute renal cortical necrosis due to the prothrombogenic effect."