Warfarin related acute kidney injury: A case report
The present case has been reported in the Indian Journal of Nephrology.

A 33-year-old male, recently de-inducted from a high altitude area with no known prior comorbidities, was admitted for center with breathlessness, dry cough, hemoptysis, and left-sided pleuritic chest pain of sudden onset. Physical examination revealed tachypnea, tachycardia, and normal blood pressure.

On systemic examination, the chest was clear and there were no cardiovascular localizing signs. His initial evaluation revealed normal hematological and biochemical parameters. The serum creatinine at admission was 0.9 mg/dl (normal range - 0.8–1.1 mg/dl), blood urea was 20 mg/dl (normal range - 20–40 mg/dl), and urine examination was normal. Chest X-ray, 2D echocardiography, and Doppler scan of lower limbs and pelvic vessels were normal.

Electrocardiogram revealed sinus tachycardia. Renal ultrasound demonstrated normal-sized kidneys with preserved cortical thickness and no obstruction. A computed tomography pulmonary angiogram revealed acute pulmonary thromboembolism in the descending branch of the left pulmonary artery and the 2nd order branch medial basal and superior segment of the right descending pulmonary artery (modified Well's score - 4).

A serological workup including antineutrophil antibody, ds DNA, complement C3/C4 levels, antineutrophil cytoplasmic antibody, and procoagulant studies was essentially normal. He was thrombolyzed with recombinant tissue plasminogen activator and thereafter started on low molecular weight heparin and bridged onto warfarin.

On day 22 of the warfarin therapy, he again developed increasing left-sided chest pain and hematuria. Repeat imaging revealed no fresh embolism. His INR was 5.3 and his serum creatinine had also progressively risen to 2.6 mg/dl. His urine routine examination revealed albumin of 2+, with numerous red blood cells (RBCs) and a 24 h urinary protein of 2292 mg/day. He however was nonoliguric.

A pre- and post-renal cause for acute kidney injury (AKI) was excluded, and a thorough drug history was also not contributory toward a cause for suspicion of acute interstitial nephritis. A provisional diagnosis of WRN was made.

His warfarin was withheld and the coagulation parameters corrected with adequate blood component support. Over the next few days, his azotemia showed a settling trend. As the INR normalized, a renal biopsy was done which revealed the modest matrix expansion associated with vascular hyalinosis, glomerular congestion with RBCs, and diffuse tubular damage with large and occlusive RBC casts in the tubules associated with interstitial hemosiderin-laden macrophages suggestive of interstitial haemorrhage. Immunofluorescence studies were negative.

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