Abstract
Several commonly used chemotherapeutic agents, antibiotics, antivirals, and antiepileptic medications can cause partial or full Fanconi syndrome, disorders which can generally be described as transport defects in the proximal renal tubule, associated with non-anion gap metabolic acidosis. Fanconi syndrome is underreported and therefore often missed in the clinical setting. Herein, we present a case report that details the course of a 64-year-old female with a history of stage IV undifferentiated pleomorphic sarcoma who after her sixth chemotherapeutic cycle (adriamycin, ifosfamide, and mesna) developed severe hypokalemia, hypophosphatemia, and proteinuria without glycosuria, eventually diagnosed with partial Fanconi syndrome. The aim of this report is to highlight the importance of routine serum and urine monitoring in patients undergoing therapy with potentially nephrotoxic agents to avoid potentially fatal renal nephrotoxicity, including partial and full Fanconi syndrome.
Highlights
Several commonly used chemotherapeutic agents, antibiotics, antivirals, and anti-epileptic medications can cause partial or full Fanconi syndrome
It is characterized by dysfunction of the proximal renal tubules, leading to impaired proximal tubular reabsorption of amino acids, glucose, phosphate, urate, and bicarbonate
Toxicity arises from tubular cell organic cation transporter-mediated uptake and metabolism of ifosfamide into chloroacetaldehyde [5,9]
Summary
Several commonly used chemotherapeutic agents, antibiotics, antivirals, and anti-epileptic medications can cause partial or full Fanconi syndrome. Fanconi syndrome is a metabolic disorder, which was first described by Lignac in 1924 and later defined by Fanconi in 1936 [1,2,3] It is characterized by dysfunction of the proximal renal tubules, leading to impaired proximal tubular reabsorption of amino acids, glucose, phosphate, urate, and bicarbonate. Ifosfamide toxicity is often associated with hypokalemia and diabetes insipidus, more worrisome complications include acute renal failure and severe bone demineralization from urinary phosphate loss, either through partial or full Fanconi syndrome. Weekly laboratory studies revealed normal sodium, potassium, bicarbonate, creatinine, and phosphorus levels. Laboratory studies revealed a non-anion gap metabolic acidosis and acute kidney injury; markedly abnormal laboratory values include 152 mmol/L of sodium, 1.3 mmol/L of potassium, 16 mmol/L of bicarbonate, 1.1 mg/dL of phosphorus, 1.8 mg/dL of magnesium, and 3.3 mg/dL of creatinine.
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