Case Presentation: Introduction: We report a case of acute kidney injury (AKI) secondary to heme-induced nephropathy requiring hemodialysis, following percutaneous mechanical thrombectomy using AngioJetTM.
Case Report: A 63 years-old African-American female with prior history of deep vein thrombosis (DVT) who was on treatment with apixaban, presented to the emergency room with acute-onset left leg pain and swelling starting 4 days prior to admission. Her past history was significant for recurrent DVTs, pulmonary embolism, diabetes mellitus and hypertension.

Physical examination at admission was normal except left leg swelling, erythema and tenderness of the calf muscles. Peripheral pulses were palpable. A venous duplex ultrasound revealed extensive thrombosis of the left saphenous and femoral veins. A computerized tomographic angiogram showed proximal extension of the thrombus into the inferior vena cava. Intravenous heparin was started and she underwent catheter-induced pharmacologic thrombolysis along with AngioJet thrombectomy. A post-procedure intravascular ultrasound confirmed vessel patency. Intravenous fluids (IVF) were continued postoperatively.

Between 24 to 48 hours post-thrombectomy, the patient suddenly became anuric despite a positive fluid balance. Serum creatinine increased from 0.7 to 2.5 mg/dl. Other serum chemistry showed a drop in hemoglobin from 10.7 to 9.1 g/dl, increased transaminases (AST 330 U/L, ALT 110 U/L, both previously normal), mild indirect hyperbilirubinemia, elevated lactate dehydrogenase (643 U/L) and normal creatine phosphokinase. A urinalysis showed no casts but dipstick test showed ‘3+’ blood without any red blood cells. Urine myoglobin and eosinophils were negative. Fractional excretion of sodium was 3%, consistent with tubular pathology. Renal doppler ultrasound showed no evidence of urinary tract obstruction, renal vascular compromise or parenchymal injury. No other etiology was found to explain the sudden oliguric AKI. A diagnosis of heme pigment nephropathy was made. Renal biopsy was not attempted in this anticoagulated patient.
Supportive therapy with IVF and electrolyte correction was started, however she remained oliguric and became progressively volume overloaded with a rising creatinine. Hemodialysis was started and she underwent 5 sessions. Spontaneous urine output was gradually noted. Serum creatinine improved, from a peak of 6.1 down to 2.4 mg/dl at discharge on the 16th postoperative day.

Discussion: Discussion: Heme pigment nephropathy is characterized by the abrupt loss of renal function due to nephrotoxicity of the endogenous heme-based pigments. Heme nephropathy from mechanical thrombectomy remains under-appreciated but can be associated with significant morbidity. Further research is needed to accurately risk-stratify the patients, as well as to identify interventions to reduce the risk of heme nephropathy after mechanical thrombectomy.

Conclusions: Internists should be aware of this condition as an early and aggressive approach such as maintaining the intravascular volume and favourable hemodynamics, preventing anemia and sepsis, and avoidance of other nephrotoxins will limit the progressive renal damage.