Tranexamic Acid-Induced Acute Renal Cortical Necrosis in Post-Endoscopic Papillectomy Bleeding

Acute renal failure can be the result of acute renal cortical necrosis (RCN), which commonly occurs from complications occurring during pregnancy. RCN is rarely caused by medications, although tranexamic acid, which is used in patients with acute bleeding for its antifibrinolytic effects, reportedly causes acute RCN in rare cases. An 82-year-old woman experienced gastrointestinal bleeding after endoscopic papillectomy of an ampullary adenoma. The bleeding was controlled with tranexamic acid administration; however, 4 days later, her urine volume decreased and she developed pulmonary edema and dyspnea. Serum creatinine levels increased from 0.8 to 3.9 mg/dL and dialysis was performed. Abdominal pelvic computed tomography with contrast enhancement revealed bilateral RCN with no renal cortex enhancement. Renal dysfunction and oliguria persisted and hemodialysis was continued. Clinicians must be aware that acute RCN can occur after tranexamic acid administration to control bleeding.

Effect of panax notoginseng saponins on renal cortical tubule cell Bax in early stage after renal trauma in rats / 中华创伤杂志

Objective To measure the effect of panax notoginseng saponins (PNS) on renal cortical tubule cell apoptosis and apoptosis-related genes in early stage after renal trauma and to investigate the protective mechanism of PNS for renal trauma.Methods Seventy-eight Wistar rats were divided into trauma group (n =36),trauma + treatment group (treatment group,n =36),normal control group (control group,n =6) according to the random number table.In treatment group,rats received intraperitoneal administration of PNS (70 mg/kg).Instead,substitute of an equal dose of isotonic saline was used for the rats in trauma and normal control groups.Trauma and treatment groups were subdivided at 1,6,12,24,36 and 48 hours posttrauma,with 6 rats per group.The kidney specimens were extracted at each time point to detect Bax expression in the cortex with immunohistochemistry and in situ hybridization histochemistry.Moreover,the positive expression of Bax was compared among groups and its variation regularity with time were detected.Results In trauma group,mRNA transcription of pro-apoptosis gene Bax increased at 12 hours in the superficial cortex,but increased at 1 hour in deep cortex; protein expression of pro-apoptosis factor Bax showed no apparent reduction within 36 hours in the superficial cortex,but evident decrease within 12 hours in the deep cortex.In treatment group,mRNA transcription of pro-apoptosis gene Bax decreased immediately after treatment in the renal cortex and lasted until 48 h; protein expression of pro-apoptosis factor Bax showed unidirectional reduction until 48 h in the renal cortex.Conclusion PNS inhibits cell apoptosis by down-regulating the mRNA and protein expression of Bax.

A Case of Acute Kidney Cortex Necrosis Caused by Tranexamic-Acid / 대한내과학회지

Kidney cortex necrosis is a relatively rare cause of acute kidney injury and is characterized by complete or partial destruction of the renal cortex, but sparing of the medulla. Tranexamic acid has antifibrinolytic activity and is used to reduce bleeding. We report a rare case of kidney cortex necrosis caused by tranexamic acid. A 49-year-old woman complained of coughing up blood-tinged sputum. She had a history of bronchiectasis and was treated with tranexamic acid for 3 days. Four days after admission, she developed anuria and azotemia. Computerized tomography showed enhancement of the renal medulla, but not the bilateral renal cortex. The patient was treated with hemodialysis, and has since been maintained on hemodialysis for 6 months. Due to the development of kidney cortex necrosis in patients treated with tranexamic acid, all its potential complications should be considered.

A Case of Acute Kidney Cortex Necrosis Caused by Tranexamic-Acid / 대한내과학회지

Kidney cortex necrosis is a relatively rare cause of acute kidney injury and is characterized by complete or partial destruction of the renal cortex, but sparing of the medulla. Tranexamic acid has antifibrinolytic activity and is used to reduce bleeding. We report a rare case of kidney cortex necrosis caused by tranexamic acid. A 49-year-old woman complained of coughing up blood-tinged sputum. She had a history of bronchiectasis and was treated with tranexamic acid for 3 days. Four days after admission, she developed anuria and azotemia. Computerized tomography showed enhancement of the renal medulla, but not the bilateral renal cortex. The patient was treated with hemodialysis, and has since been maintained on hemodialysis for 6 months. Due to the development of kidney cortex necrosis in patients treated with tranexamic acid, all its potential complications should be considered.

A Case of Bilateral Acute Renal Cortical Necrosis Complicated by Tranexamic Acid Administration / 대한내과학회지

Acute renal cortical necrosis is an anuric form of acute renal failure. We experienced a case of renal cortical necrosis complicated by tranexamic acid administration. To our knowledge, only three cases of renal cortical necrosis have been reported worldwide. A 49-year-old man was referred with hemothorax and multiple bone fractures following a traffic accident. Tranexamic acid, and hemocoagulase were injected three times a day. After the 4th dose of hemostatics, anuria developed abruptly, the platelet count decreased to 84,000 /microL, and the serum creatinine was increased to 2.56 from 1.06 mg/dL. On the 4th Intensive Care Unit (ICU) day, computed tomography (CT) showed bilateral renal cortical necrosis with normal renal arteries and aorta. The oliguria persisted for 14 days and temporary hemodialysis was performed. The serum creatinine had decreased to 2.12 mg/dL 8 months after discharge.

Disección espontánea de la arteria renal e infarto renal: dos casos clínicos / Spontaneous dissection of the renal artery ano kidney infarction: report of two cases

We report two previously healthy males aged 33 and 37 years, presenting with severe pain in the right and left part of the abdomen, respectively. An abdominal CT sean showed in both a kidney infarction. An angio-CAT sean showed changes compatible with a fibromuscular dysplasia in the renal arterial wall. An angiography showed an intimal tear or complex dissection flap in both cases. Both had a satisfactory evolution with conservative treatment. The relationship between fibromuscular dysplasia and spontaneous dissection of the renal artery is discussed.