Acute kidney injury aggravated by treatment initiation with apixaban: Another twist of anticoagulant-related nephropathy.

Anticoagulant-related nephropathy (ARN) was initially described in patients on warfarin (as warfarin-related nephropathy) and recently in those using dabigatran. Herein, we report clinical history and kidney biopsy findings in a patient on apixaban (Eliquis). Initiation of treatment with apixaban resulted in aggravation of preexisting mild acute kidney injury (AKI). A few days after apixaban therapy, the patient became oligoanuric, and kidney biopsy showed severe acute tubular necrosis with numerous occlusive red blood cell casts. Only one out of 68 glomeruli with open capillary loops had small segmental cellular crescent. Therefore, there was major discrepancy between the degree of glomerular injury and the glomerular hematuria. Considering that the onset of this AKI was associated with apixaban treatment initiation, we propose that this patient had ARN associated with factor Xa inhibitor (apixaban), which has not previously been described. Monitoring of kidney function is recommended after initiation of anticoagulant therapy.

Evaluating proteinuria and nephrotic syndrome in patients with venous thromboembolism.

INTRODUCTION: Venous thromboembolism (VTE) is a well-known complication of nephrotic syndrome (NS). Proteinuria, a marker of chronic kidney disease, discovered at the time of VTE, may be the first presentation in patients with occult chronic kidney disease and/or NS. METHODS: Electronic medical records at a community teaching hospital were retrospectively reviewed to measure the percentage of patients with acute VTE who had a urinalysis (UA) and/or an evaluation of 24-hour urine protein collection or urine protein to creatinine ratio. Thromboembolic events were defined as acute deep vein thrombosis and/or pulmonary embolism. NS was defined as ≥3.5 g proteinuria in 24 hours or by urine protein to creatinine ratio exceeding 3.5. RESULTS: UA was done in 198 patients (63%) on the same admission for VTE and in 83 patients (26%) at a later date. Proteinuria, on routine UA, was identified in 154 (54%) patients. However, only 29 of 154 patients (19%) with proteinuria on UA had a formal evaluation of urine protein excretion, either by 24-hour collection or by spot protein to creatinine ratio. Eight of these 29 patients (28%) had NS. CONCLUSIONS: Patients suffering from VTE may have proteinuria if not frank NS. The UA should be part of the routine evaluation of a patient with VTE given the unexpectedly high prevalence of proteinuria and even NS in this cohort.