Case Presentation: A 50-year-old man with a pmh of CKD stage 2 was admitted to our hospital for nausea, vomiting and acute kidney injury (AKI).2 months prior to presentation, he had been diagnosed with metastatic synovial sarcoma and had completed his first cycle of doxorubicin, ifosfamide, and mesna that was complicated by a mild AKI that resolved with fluids (creatinine peak 1.7, baseline 1.4). He proceeded with cycle 2 five days prior to presentation. Despite scheduled antiemetics, he suffered from intractable nausea and vomiting and so he presented to the ED. His exam was notable for tachycardia, cachexia, dry mucous membranes, and decreased skin turgor. Labs were remarkable for potassium 3.1, chloride 112, CO2 12, BUN 43, creatinine 3.1, calcium 11.6, glucose 157, magnesium 2.2, lactate 1.2. UA showed 3+ protein, 4+ glucose, 2+ blood, 0-5 WBC, 0-2 RBC, +mucous, no imaging obtained. The patient was treated with scheduled parenteral antiemetics and olanzapine with resolution of his nausea and vomiting. He was treated with a mixture of normal saline and bicarbonate infusion with slower than expected improvement in creatinine. First-year medical students rotate with hospitalists to learn how to take histories, perform physical exams, and write clinical documentation. For this patient, I reviewed with my student the general framework of diagnosing and treating AKI. As he was writing his note, he questioned the patient’s hypokalemia, severe acidosis, and glucosuria which didn’t fit within the framework. After ensuring that he wasn’t on an SLGT-2 inhibitor and that he didn’t have a history of diabetes or hyperglycemia, we broadened our differential diagnosis and sent off a phosphorous (0.6) and uric acid (1.4). The diagnosis of Fanconi Syndrome was made and confirmed by nephrology. He required aggressive repletion of his electrolytes and discharged with a creatinine of 2.4. After discontinuation of ifosfamide, his creatinine has since down trended to 1.6.
Discussion: Fanconi Syndrome is an acquired or inherited proximal tubular defect that causes problems with reabsorption of bicarbonate, phosphorous, potassium, glucose, and uric acid1. Our patient developed acquired Fanconi Syndrome secondary to ifosfamide. The only true treatment is supportive care and removing the offending drug. He is now being treated with single doxorubicin for his synovial sarcoma. Cognitive biases are recognized as contributing factors to medical errors in medicine2. This can be seen in my availability bias that a patient with post-chemotherapy induced nausea and vomiting would present with a pre-renal etiology of AKI. Despite labs that are obvious in retrospect for Fanconi Syndrome, the simple question of “why?” contributed to additional testing for a diagnosis, early consultation with nephrology and oncology, and expedited interdisciplinary discussion on renal prognosis and next steps for chemotherapy.
Conclusions: Oncology-hospitalists see many presumed pre-renal AKI’s from post-chemotherapy nausea and vomiting. A first-year medical student asked, “Why?” in the context of unexpected labs (hypokalemia, severe acidosis, glucosuria) which allowed us to perform a diagnostic pause and re-evaluate the differential diagnosis. Ifosfamide-induced Fanconi Syndrome is a rare but known complication and causes severe electrolyte abnormalities through proximal tubular injury. While hospitalists may be experienced clinicians, learners on the team may allow for time for diagnostic pauses, where in this case resulted in earlier diagnosis.