Abstract
Fanconi syndrome is described as a defect in the proximal tubular reabsorption of glucose, amino acids, uric acid, phosphate, and bicarbonate, falling under type 2 renal tubular acidosis (RTA). Some common causes include drugs, heavy metals, infections, and genetics (particularly mitochondrial disorders). We present a case of a 33-year-old Caucasian female with chronic alcohol use disorder. She was treated for acute kidney injury (AKI) but had persistent hypophosphatemia, hypokalemia, hypouricemia, low bicarbonate, along with glycosuria consistent with Fanconi syndrome. An exhaustive workup ruled out the most common causes. Alcohol abstinence proved to correct the underlying abnormality. Alcohol is a mitochondrial toxin, and its role in the pathophysiology of Fanconi syndrome is under investigation. Early diagnosis of Fanconi is imperative to avoid complications such as rickets and osteomalacia. Therefore, testing for markers of alcohol abuse should be considered when determining the etiology of Fanconi syndrome. Alcohol use disorder is a common disorder, with more than 3 million cases annually in the US alone. Clinicians should have a high index of suspicion for Fanconi syndrome in a patient with similar anomalous labs considering the high prevalence of alcohol use disorder. More research regarding this topic is warranted.