A 27-year-old female patient was admitted with complaints of hematuria and black stools for over 11 days. Eleven days before admission, the patient reported multiple blood blisters in the right buccal mucos after eating out and subsequently developed gross hematuria with foamy urine later that evening. After seven days of persistent hematuria, she sought medical attention at a local hospital. Initial laboratory results indicated normal hemoglobin (126 g/L), an elevated platelet count (420 × 109/L), impaired renal function (creatinine: 0.86 mg/dL), hematuria (urine erythrocyte 3+) and proteinuria (urine protein 3+), and abnormal coagulation function, including a prothrombin time (PT) > 180.0 s, activated partial thromboplastin time (APTT) > 180 s,, international normalized ratio (INR) > 10 and hyperfibrinogenemia (7.65 g/L). Despite the administration of antibiotics and plasma transfusions, her condition deteriorated, evidenced by a notable reduction in hemoglobin levels (90 g/L) and exacerbated kidney dysfunction (serum creatinine 4.71 mg/dL). She was then transferred to our hospital. Further lab tests showed a decline in hemoglobin (51 g/L), elevated urea (25.55 mmol/L) and creatinine (6.95 mg/dL) levels, along with gross hematuria (urine red blood cells 3298/µl), leukocyturia, and abnormal coagulation parameters (Table 1). A chest and abdominal CT scan ruled out thoracic and abdominal hemorrhage. In the emergency room, the patient was treated with anti-infection measures (levofloxacin 0.4 g per day), acid suppression, hemostasis and blood transfusion before being transferred. to our department.

Upon admission, the physical examination revealed normal body temperature, an elevated pulse rate, and normal blood pressure. The patient displayed ecchymosis on various body parts, including the chest wall, left elbow, left groin, right middle thigh, and left ankle. Obvious moist rales were heard in both lower lungs, while the heart and abdominal examination were normal. There was no lower limb edema. The patient’s medical history did not indicate any pre-existing hematological or coagulation disorders. Random urinary chemistry showed the fractional excretion of sodium of 5.8% (suggesting little possibility of pre-renal AKI), normal urinary N-acetyl-beta-D-glucosaminidase and urinary α-1 microglobulin concentration, and an obvious discrepancy between urinary protein to creatinine ratio (5866 mg/g) and urinary albumin to creatinine ratio (241 mg/g). Random urine sediment indicated gross dysmorphic red blood cells (Table 1). The kidney ultrasound indicated a horseshoe kidney without kidney stones or hydronephrosis.

Further examination of coagulation factors revealed vitamin K deficiency, with significantly reduced levels of factors II (26.9↓%), VII (16.9↓%), IX (28.2↓%), and X (26.2↓%). The levels of factor V (76.1%), factor XI (94.8%) were normal and factor VII (208.9↑%) was elevated. Given this patient’s severe coagulopathy, characterized by low activity of vitamin K1-dependent clotting factor, prolonged PT and INR, and normal liver function, we considered the possibility of exposure to a coumarin-based anticoagulant rodenticide. Therefore, a toxicological examination was performed on the first day of admission, which revealed a plasma bromadiolone concentration of 117 ng/ml by gas chromatography/mass spectrometry.

The patient received treatment, including vitamin K1 injections (two 10 mg dose intramuscularly before the confirmation of bromadiolone intoxication, and 20 mg twice daily intramuscularly after the confirmation), 1.5 units of red blood cell transfusion to correct anemia, and other symptomatic therapies. On the first day after admission, renal function tests indicated the improved levels of urea (14 mmol/L) and creatinine (1.59 mg/dL). Coagulation function remained abnormal, with prolonged PT and APTT, while the fibrinogen and platelet counts were within or above the normal range (Table 1). After three days of treatment, creatinine levels decreased further to 1.05 mg/dL (Fig. 1), INR dropped to 2.68, and urine color returned to normal. Due to bromadiolone’s long half-life, repeat measurement of its levels was not performed.

During a telephone follow-up three days after discharge, the patient exhibited normal renal function (serum creatinine of 0.71 mg/dL), with coagulation function and blood routine returning to normal. Vitamin K treatment was discontinued under the recommendation of the local physician 11 days after discharge. Six months later, the patient was re-examined in the local hospital, where routine blood and coagulation function were within normal ranges, and renal function was stable (serum creatinine of 0.51 mg/dL). Urine test showed 1 + urine glucose, 1 + urine occult blood, 2 + urine leukocyte esterase. The patient is advised to continue close monitoring kidney function, urine examination, and kidney ultrasound during follow-ups. Consent for publication of this case was obtained and provided to the journal in accordance with BMC policy.