Hyperchloraemic metabolic acidosis induced by the iron chelator deferasirox: a case report and review of the literature

Dell’Orto, V.; Bianchetti, Mario G.; Brazzola, Pierluigi

doi:10.1111/jcpt.12095

Cited by 15 publications

(14 citation statements)

References 12 publications

(26 reference statements)

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“…Also, during dose reduction but not total withdrawal, there was no resolution of renal tubular dysfunction. This finding was consistent with other case reports . Therefore this adverse effect of deferasirox may be idiosyncratic rather than dose‐dependent.…”

Section: Discussionsupporting

confidence: 93%

“…They all had metabolic acidosis and hypophosphataemia. Similarly, all the other case reports did not document complete FS. Most of these patients also had hypophosphataemia and/or normal anion gap metabolic acidosis.…”

Section: Discussionmentioning

confidence: 88%

“…Renal side‐effects of deferasirox are also major concerns of this drug and most of them are mild elevations of serum creatinine level . In recent years, several case reports demonstrated the association between Fanconi syndrome (FS) or proximal renal tubular acidosis and long‐term use of deferasirox, indicating the possible adverse effect of deferasirox on proximal tubule. The mechanism is not clear but may be associated with chelation of mitochondrial iron in tubular cells, which interferes with the production of adenosine triphosphate (ATP) and thus causes tubular dysfunction …”

mentioning

confidence: 99%

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Transfusion‐dependent thalassaemic patients with renalFanconi syndrome due to deferasirox use

et al. 2015

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

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Transfusion‐dependent thalassaemic patients with renalFanconi syndrome due to deferasirox use

et al. 2015

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“…Acute kidney injury has been reported in the post-marketing surveillance of DFX [24,25]. Hyperchloraemic metabolic acidosis induced by DFX -that resolved after withdrawing -has also been reported previously [26]. In a multicentre randomized phase 3 trial, mild, dose dependent increases in serum creatinine were observed in 38% of patients receiving DFX at doses of 20-30 mg/kg/day.…”

Section: Discussionmentioning

confidence: 61%

Insidious Renal Damage in Patients with Thalassemia Major: Is it More Serious than Appreciated?

Gökçe¹

2014

J Hematol Thrombo Dis

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Aim: To investigate early renal injury in thalassemia major patients by using novel serum markers and demonstrate the factors leading to renal injury. Material and Methods: Seventy-one thalassemia major patients (37 males) who were on regular transfusion and chelation programme with deferasirox have been enrolled in this study. Thirty-five healthy children of the same age served as a control group. Serum urea-creatinine, electrolytes, cystatin C and glomerular filtration rate were all noted in our cohort and compared with the control group. Proteinuria was also investigated by calculating UPr/UCr ratio. Results: The median serum creatinine level was 0.4 mg/dL (range; 0.2-0.76 mg/dL) and the median glomerular filtration rate level was 192 mL/min/1.73 m 2 (range; 106-308 mL/min/1.73 m 2) in patients. More than half of the patients had glomerular hyperfiltration (n=48, 67.6%). Hyperfiltration was prominent in thalassemia group (66.2% vs. 19.4%) (p=0.0001). Mean serum cystatin C levels were found to be statistically elevated in patient group comparing with controls (p=0.0001). Serum cystatin C level was above >1 mg/L in 46 patients (64.7%) whereas only three in controls (p=0.0001). Sex, age, hemoglobin level and cardiac T2* MRI results were not related to the elevated cystatin C levels. On the other hand, liver iron burden and serum ferritin levels were noted to be statistically correlated to elevated cystatin C level (p=0.024 and p=0.04). Deferasirox dose below 25 mg/kg/day was also found in relation with elevated cystatin C levels. Conclusion: Renal injury is multifactorial, insidious but progressive in thalassemia patients. High index of suspicion and routine use of novel markers are required for detection of renal injury during the follow up of thalassemia patients.

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“… 5. Deferasirox 139 – 143 increases hemodynamic iron removal, causes vacuolization of proximal tubular epithelial cells 142 , and elevates iron absorption in various organs. All could lead to acidosis.…”

Section: Drugs Causing Decreased Renal Acid Excretionmentioning

confidence: 99%

Drug-Induced Metabolic Acidosis

Pham

Moe

2015

F1000Res

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Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs’ characteristics.

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Hyperchloraemic metabolic acidosis induced by the iron chelator deferasirox: a case report and review of the literature

Abstract: We describe herein a case of metabolic acidosis in the setting of treatment with the deferasirox. Our case and the literature indicate a potential risk of kidney toxicity on this agent.

Cited by 15 publications

References 12 publications

Transfusion‐dependent thalassaemic patients with renalFanconi syndrome due to deferasirox use

Transfusion‐dependent thalassaemic patients with renalFanconi syndrome due to deferasirox use

Insidious Renal Damage in Patients with Thalassemia Major: Is it More Serious than Appreciated?

Drug-Induced Metabolic Acidosis

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