Acute renal failure, gastrointestinal bleeding, and cardiac

arrhythmia
By Yashar Najiaghdam, M.D

PURPOSE: The case of a patient who developed acute renal failure, gastrointestinal bleeding, and cardiac
arrhythmia after receiving arsenic trioxide for the treatment of acute promyelocytic leukemia (APL) is
described. SUMMARY: An 84-year-old Caucasian woman with a history of osteoarthritis sought medical
attention for relapse of her APL, which had initially been diagnosed approximately 30 months earlier.
Complete remission was accomplished with three cycles of i.v. daunorubicin for 3 days and oral tretinoin
for 28 days. After 19 months in remission, she was noted to have increased bruising and blood test values
consistent with APL relapse. Two additional trials of oral tretinoin were unsuccessful, and arsenic trioxide
was initiated at a daily dosage of 0.15 mg/kg of actual body weight. Less than 24 hours after receiving
arsenic trioxide, the patient had "bile-like emesis" and her hemoglobin level decreased. Upper
gastrointestinal bleeding was suspected and managed aggressively with transfusions of platelets and fresh
frozen plasma and i.v. desmopressin. She became anuric, and her serum creatinine level more than
doubled. Hemodialysis was started due to a sudden increase in potassium and fluid overload that did not
respond to i.v. furosemide. One hour after hemodialysis, the patient was found pulseless and
unresponsive by nursing staff. The cardiac arrest team rapidly responded and noted atrial fibrillation with
a fast ventricular rate. Postresuscitation, the patient was transferred to the intensive care unit. Despite
aggressive life-support therapy, the patient remained unresponsive. CONCLUSION: An 84-year-old woman
developed acute renal failure, gastrointestinal bleeding, and cardiac arrhythmia after receiving arsenic
trioxide for the treatment of APL.Anemia is a frequent complication during the later stages of chronic
kidney disease. When present, it may cause symptoms such as fatigue and shortness of breath. The
pathogenesis of anemia in chronic kidney disease is complex, but a central feature is a relative deficit of
erythropoietin. New information has elucidated the critical role of the hypoxia-sensing system in mediating
erythropoietin synthesis and release. Iron deficiency is a second important factor in the anemia of chronic
kidney disease. New insights into the dynamics of iron metabolism have clarified the role of chronic
inflammation and hepcidin as key mediators of impaired iron utilization. In this article, we review the
epidemiology, pathobiology, clinical evaluation, and treatment of anemia in chronic kidney disease.

Index Words

anemiachronic kidney disease (CKD)erythropoietin deficiencyironhemoglobinerythropoiesiserythropoiesis-

stimulating agent (ESA)epoetin alfadarbepoeitin alfacardiovascular diseasequality of
lifefatiguereviewKidney failure produces numerous changes that destabilize homeostasis.