In vivo mesna and amifostine do not prevent chloroacetaldehyde nephrotoxicity in vitro

Yaseen, Zeinab; Michoudet, Christian; Baverel, Gabriel; Dubourg, Laurence

doi:10.1007/s00467-007-0689-6

Cited by 12 publications

(5 citation statements)

References 32 publications

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“…The introduction of sodium 2-mercaptoethanesulphonate (mesna) has virtually eliminated haemorrhagic cystitis. However, mesna has no preventive effect on the tubular toxicity of ifosfamide [ 9 , 10 ]. Ifosfamide-induced tubular toxicity can be associated with metabolic acidosis with a normal anion gap (hyperchloremic acidosis) due to Type 1 (distal) or, less frequently, Type 2 (proximal) RTA.…”

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confidence: 99%

The growing pains of ifosfamide

Sprangers

Lapman

2020

Clinical Kidney Journal

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Ifosfamide is a commonly used chemotherapeutic known to have numerous adverse kidney manifestations. In this issue of Clinical Kidney Journal, Ensergueix et al. report a multicentric observational retrospective French study on 34 adult patients with tubular dysfunction and /or kidney dysfunction following ifosfamide treatment. Of these patients, 18% had isolated proximal tubular dysfunction, 14% had isolated acute kidney injury (AKI), 18% had isolated chronic kidney disease (CKD) and 50% had a combination of proximal tubular dysfunction and AKI. Concomitant treatment with cisplatin was identified as a risk factor for the development of AKI, and cisplatin and age were associated with estimated glomerular filtration rate at last follow-up. Interestingly, the cumulative dose of ifosfamide was not associated with renal outcomes. This report highlights the need for additional studies on the prevalence, spectrum and management of ifosfamide-associated nephrotoxicity and clearly demonstrates that patients who received ifosfamide should be followed long term to detect proximal tubular dysfunction and CKD early.

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confidence: 99%

The growing pains of ifosfamide

Sprangers

Lapman

2020

Clinical Kidney Journal

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“…14 , 30 In the in‐vitro study, Yaseen et.al demonstrated that chloroacetaldehyde altered lactate metabolism in isolated proximal tubules, and treatment with mesna, did not alter glutathione levels in renal cells. 31 …”

Section: Discussionmentioning

confidence: 99%

“…Chloroacetaldehyde directly reacts with thiols groups, leading to a decrease in the levels of glutathione (GSH) in the tubular cells, and mediates its nephrotoxicity 14,30 . In the in‐vitro study, Yaseen et.al demonstrated that chloroacetaldehyde altered lactate metabolism in isolated proximal tubules, and treatment with mesna, did not alter glutathione levels in renal cells 31 …”

Section: Discussionmentioning

confidence: 99%

“…14,30 In the in-vitro study, Yaseen et.al demonstrated that chloroacetaldehyde altered lactate metabolism in isolated proximal tubules, and treatment with mesna, did not alter glutathione levels in renal cells. 31 According to the mentioned mechanisms, the use of antioxidant drugs can be effective in preventing the toxicity of ifosfamide. Nacetylcysteine (NAC) has been effective in animal models and in vitro studies for the prevention of ifosfamide nephrotoxicity.…”

Section: T a B L E 2 Laboratory Data In The Oncology Wardmentioning

confidence: 99%

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Ifosfamide‐induced acute kidney injury in a patient with leiomyosarcoma: A case report

2022

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Background Leiomyosarcoma (LMS) is an aggressive soft tissue sarcoma that is derived from smooth muscles. Ifosfamide is in use for advanced metastatic LMS. Case A‐44‐years old woman with a chief complaint of pain in the epigastric area, itching, coughing, nausea, and vomiting was referred to the emergency department. Her medical history was LMS. She had taken Ifosfamide and mesna in her last chemotherapy. Seventy percent of her liver and her left kidney were removed 4 years ago to prevent the progress of the disease. Because of the increase in the level of creatinine and urea in the initial laboratory report, a Shaldon catheter was inserted for the patient, and she was under emergency dialysis for 3 h. In addition, during the six‐day hospitalization period, dialysis was done two times. Finally, the patient was discharged with improved clinical tests accompanied by a twice‐weekly dialysis order. Conclusion Ifosfamide is metabolized into chloroacetaldehyde, which can cause acute kidney injury. Recovery from acute kidney injury may not always be perfect and can lead to some degree of chronic kidney disease. Opposite to hemorrhagic cystitis, mesna is not effective in preventing ifosfamide's nephrotoxicity and N‐acetylcysteine may be effective in the prevention of this nephrotoxicity.

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“…The introduction of the uro-protective thiol compound “Mesna” (sodium 2-mercaptoethanesulfonate) has virtually eliminated urotoxicity associated with both cyclophosphamide and ifosfamide and allowed the use of higher and more frequent dosing. However, mesna has shown no preventive effect on the tubular toxicity of ifosfamide, which manifests in Fanconi syndrome [67,68]. This is likely due to insufficient delivery of mesna to the renal tubule, leading to failure to provide adequate protection of tubular glutathione from depletion by the metabolite(s) [69].…”

Section: Fanconi Syndromementioning

confidence: 99%

Proximal renal tubular acidosis with and without Fanconi syndrome

Kashoor

Batlle

2019

Kidney Res Clin Pract.

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Proximal renal tubular acidosis (RTA) is caused by a defect in bicarbonate (HCO 3 − ) reabsorption in the kidney proximal convoluted tubule. It usually manifests as normal anion-gap metabolic acidosis due to HCO 3 − wastage. In a normal kidney, the thick ascending limb of Henle’s loop and more distal nephron segments reclaim all of the HCO 3 − not absorbed by the proximal tubule. Bicarbonate wastage seen in type II RTA indicates that the proximal tubular defect is severe enough to overwhelm the capacity for HCO 3 − reabsorption beyond the proximal tubule. Proximal RTA can occur as an isolated syndrome or with other impairments in proximal tubular functions under the spectrum of Fanconi syndrome. Fanconi syndrome, which is characterized by a defect in proximal tubular reabsorption of glucose, amino acids, uric acid, phosphate, and HCO 3 − , can occur due to inherited or acquired causes. Primary inherited Fanconi syndrome is caused by a mutation in the sodium-phosphate cotransporter (NaP i -II) in the proximal tubule. Recent studies have identified new causes of Fanconi syndrome due to mutations in the EHHADH and the HNF4A genes. Fanconi syndrome can also be one of many manifestations of various inherited systemic diseases, such as cystinosis. Many of the acquired causes of Fanconi syndrome with or without proximal RTA are drug-induced, with the list of causative agents increasing as newer drugs are introduced for clinical use, mainly in the oncology field.

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In vivo mesna and amifostine do not prevent chloroacetaldehyde nephrotoxicity in vitro

Cited by 12 publications

References 32 publications

The growing pains of ifosfamide

The growing pains of ifosfamide

Ifosfamide‐induced acute kidney injury in a patient with leiomyosarcoma: A case report

Proximal renal tubular acidosis with and without Fanconi syndrome

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