Abstract
Deferasirox is a first-line therapy for iron overload that can sometimes cause kidney damage. To better define the pattern of tubular damage, a systematic literature review was conducted on the United States National Library of Medicine, Excerpta Medica, and Web of Science databases. Twenty-three reports describing 57 individual cases could be included. The majority (n = 35) of the 57 patients were ≤18 years of age and affected by thalassemia (n = 46). Abnormal urinary findings were noted in 54, electrolyte or acid–base abnormalities in 46, and acute kidney injury in 9 patients. Latent tubular damage was diagnosed in 11 (19%), overt kidney tubular damage in 37 (65%), and an acute kidney injury in the remaining nine (16%) patients. Out of the 117 acid–base and electrolyte disorders reported in 48 patients, normal-gap metabolic acidosis and hypophosphatemia were the most frequent. Further abnormalities were, in decreasing order of frequency, hypokalemia, hypouricemia, hypocalcemia, and hyponatremia. Out of the 81 abnormal urinary findings, renal glucosuria was the most frequent, followed by tubular proteinuria, total proteinuria, and aminoaciduria. In conclusion, a proximal tubulopathy pattern may be observed on treatment with deferasirox. Since deferasirox-associated kidney damage is dose-dependent, physicians should prescribe the lowest efficacious dose.
Highlights
Iron overload secondary to regular blood transfusions may result in injury and dysfunction of the heart, liver, anterior pituitary, pancreas, and joints
Due to its efficacy and ease of use, deferasirox 20–30 mg/kg once-daily is currently the first-line therapy for iron overload secondary to blood transfusions [1,2]. It has been known for about 10 years that an increase in circulating creatinine occurs in about one out of ten cases [3]. This tendency is most likely to occur in well-chelated patients with circulating ferritin 1000 μg/L or less [4]
We performed a systematic review of the individually reported cases of kidney tubular damage that have been associated with deferasirox
Summary
Iron overload secondary to regular blood transfusions may result in injury and dysfunction of the heart, liver, anterior pituitary, pancreas, and joints. Both parenteral iron chelation with deferoxamine and oral chelation with deferiprone or deferasirox have been shown to reduce iron overload and organ damage [1,2]. Due to its efficacy and ease of use, deferasirox 20–30 mg/kg once-daily is currently the first-line therapy for iron overload secondary to blood transfusions [1,2] It has been known for about 10 years that an increase in circulating creatinine occurs in about one out of ten cases [3].
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