Kidney Week

Abstract: PUB640

Severe AKI in a Sickle Cell Patient Taking Deferasirox

Session Information

• Publication Only

Category: Nephrology Education

• 1302 Fellows and Residents Case Reports

Authors

• Cadet, Bair, SUNY- Downstate School of Medicine , Brooklyn, New York, United States

Bair Cadet,

• Brar, Amarpali, SUNY- Downstate School of Medicine , Brooklyn, New York, United States

Amarpali Brar,

• Nnaji, Okwudili, SUNY downstatemedicsl center, Brooklyn, New York, United States

Okwudili Nnaji,

• Mallappallil, Mary C., SUNY- Downstate School of Medicine , Brooklyn, New York, United States

Mary C. Mallappallil,

• Tawadrous, Hanan K., SUNY- Downstate School of Medicine , Brooklyn, New York, United States

Hanan K. Tawadrous,

• Salifu, Moro O., SUNY Downstate Medical Center, Valley stream, New York, United States

Moro O. Salifu,

Background

Introduction
Acute kidney injury (AKI) occurs in five to seven percent of hospitalized patients. Deferasirox is an iron chelating agent used in treatment of chronic iron overload. Here we report a case of severe AKI associated with use of Deferasirox in a patient with sickle cell disease and iron overload.

Methods

Case description
A 24-year-old man with Moya Moya disease, sickle cell disease who was dependent on chronic blood transfusions, stroke associated with bilateral extremities weakness presented with 3 days of non-bloody diarrhea and vomiting. He was found to have AKI on admission. His medications at home included lisinopril, deferasirox, levetiracetam, carbamazepine and folic acid.

Laboratory investigation revealed calculated fractional excretion of sodium to be 1.7 %, creatinine on the day of admission was 7.18 mg/dl with baseline creatinine of 0.83 mg/dl recorded 2 weeks prior. Urinalysis was noted for a pH 6.0, RBCs <1, WBCs 3 and negative for protein. Renal ultrasound showed normal echogenicity without any acute renal pathology.

Conclusion

Discussion
In this case, the patient who was treated with deferasirox for iron overload developed AKI. Recognized mechanism of renal injury include decrease prostaglandin synthesis, inhibition of tubular reabsorption of solute and direct mitochondrial injury. The discontinuation of the deferasirox and lisinopril resulted in the serum creatinine decreasing to 0.88 mg/dl.

Deferasirox should be used with caution in patient on ACE inhibitor with rapid discontinuation in the setting of dehydration.