Abstract Background and Aims Warfarin-related nephropathy (WRN) is defined as acute kidney injury subsequent to excessive anticoagulation with warfarin. Patients with mechanical valves required long-term anticoagulant therapy, and warfarin remains the sole available option for anticoagulant therapy. Consequently, patients with mechanical valves constitute a special group among the entire anticoagulant population. Method The present study recorded two patients receiving warfarin therapy for mechanical valve presented to the hospital with gross hematuria and progressive creatinine levels. Results The first patient was a 56-year-old female, who had previously undergone mechanical aortic valve replacement surgery nine months ago and was prescribed warfarin, was admitted to the hospital due to the occurrence of gross hematuria six days before hospitalization. Additionally, her creatinine levels exhibited a rapid increase from 120.5umol/L to 207.5 μmol/L within three days. Laboratory analysis revealed a creatinine level of 167.8 μmol/L, albumin level of 39.6 g/L, and an INR value of 2.08. The urinary test results indicated the presence of urinary protein (+) and urinary occult blood (3+). The quantification of urinary protein over a 24-hour period was measured at 0.69 g. The immunoglobulin, complements, ANA, ANCA, anti-GBM antibody, serum protein electrophoresis, serum light chains and PLAR2 were within normal range. The second patient was a 63-year-old male, who has been diagnosed with hypertension for the twenty years, underwent Bentall+Sun's surgery for type A aortic dissection five years ago. Following the surgery, the patient was prescribed warfarin. The patient was admitted to the hospital due to persistent gross hematuria for a duration of twenty days and an increase in creatinine levels. Upon admission, laboratory analysis revealed a creatinine level of 169.9μmol/L (which was within the normal range one year ago), and an INR of 2.69. The urinary test indicated the presence of urinary protein (2+) and urinary occult blood (3+). Urinary protein quantification was 3.06 g/24 hours. The serum IgA level was measured at 4.55 g/L (normal range: 1.0-4.2 g/L). The complements, ANA, ANCA, anti-GBM antibody, serum protein electrophoresis, serum light chains and PLAR2 were within normal range. Pathology of two patients all showed red blood casts and tubular injury consistent with ARN and underlying IgA nephropathy (Fig. 1). The two patients was administered a daily dosage of 20 mg of prednisolone and an oral dosage of 50 mg of cyclophosphamide every other day. During a subsequent follow-up after a two-month period, the first patient's creatinine had decreased to 109.2μmol/L, and the urine protein quantification was recorded as 119.7 mg/24 hours. The second patient's creatinine had decreased to 159.2 μmol/L, and the quantification of urine protein was recorded at 310 mg/24 hours. Conclusion Clinicians should maintain a state of increased alertness with regards to the potential occurrence of WRN who exhibit hematuria and elevated creatinine levels while on warfarin therapy, even if their INR remains within the normal range. Considering most patents of WRN have an underlying glomerular disease (mostly IgA nephropathy), the use of steroids and immunosuppressive drugs may appear to be an attractive option, particularly in patients who are unable to replace warfarin with direct oral anticoagulants (NOACs).
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