TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Fanconi syndrome is a generalized dysfunction of the renal proximal tubules without primary glomerular involvement, characterized by wasting of phosphate, amino acids, or glucose by the proximal tubules. In addition, hypokalemia, hypouricemia, metabolic acidosis and proteinuria can be found (1, 2, 3). Acquired forms of Fanconi syndrome are caused by paraproteinemia, Sjogren syndrome, Primary Biliary Cirrhosis, and medications like cisplatin. Infectious diseases have not been reported as a common cause of Fanconi Syndrome (2). In this case report, we present an extremely rare case of Legionella pneumonia complicated by Fanconi syndrome. CASE PRESENTATION: A 42 year old woman with no past medical history was admitted to the hospital with fever, myalgias, diarrhea, and dyspnea. Vital signs on admission were; temperature 38.4 °C, blood pressure 114/57 mmHg, pulse 102 beats/min, respiration rate 20. Labs showed a white blood cell count of 10.9 x 10^3/ul, sedimentation rate of 126 mm/hr, procalcitonin 0.17 ng/ml, and C-reactive protein of 22.9 mg/dL. A CXR revealed a mild left lower lobe opacity compatible with pneumonia (figure 1). The patient tested positive for the Legionella urine antigen and was diagnosed with Legionella pneumonia. Multiple electrolyte abnormalities coexisted with the pneumonia including hypokalemia of 2.8mm/l, hypouricemia of 1.9mg/dl, hypophosphatemia of 1.8mg/dl and hypocalcemia of 8mg/dl. The patient's renal function was normal with no indication of metabolic acidosis. The urinalysis showed 4+ proteinuria, glucosuria and bilirubin with no WBCs. The patient was diagnosed with Fanconi Syndrome based on these findings. The patient was treated for Legionella pneumonia with Levaquin and improved clinically and serum electrolytes normalized. The repeat urinalysis after treatment revealed trace amounts of protein, negative glucose, decreased urobilinogen, and negative bilirubin. DISCUSSION: In this case because the electrolyte abnormalities disappeared after treatment for Legionella pneumonia and there was no evidence of other causes of Fanconi syndrome, it is most likely that Fanconi syndrome was associated with Legionella pneumonia. However, we are uncertain; (1) if Legionella pneumophila entered from basolateral/apical side of the renal proximal tubular cells and (2) why it specifically targeted the proximal tubular cells, developing reabsorption defects but not distal tubular cells. To our knowledge, only two cases (2, 3) have been reported in the literature linking Fanconi syndrome to Legionella pneumonia which makes our case exceedingly rare. CONCLUSIONS: This is an extremely rare case of Fanconi syndrome associated with Legionella pneumonia. Further studies are needed to understand the mechanisms responsible for electrolyte imbalances, which is important for the management of this potentially fatal infection. REFERENCE #1: Klootwijk ED, Reichold M, Unwin RJ, Kleta R, Warth R, Bockenhauer D. Renal Fanconi syndrome: taking a proximal look at the nephron. Nephrol Dial Transplant 30: 1456-1460, 2015. REFERENCE #2: Kinoshita-Katahashi, N., Fukasawa, H., Ishigaki, S., Isobe, S., Imokawa, S., Fujigaki, Y., & Furuya, R. (2013). Acquired Fanconi syndrome in patients with Legionella pneumonia. BMC nephrology, 14, 171. REFERENCE #3: Ryuge, A., Ito, Y., Yamakawa, T., Tanaka, H., Yasui, H., Mashimo, S., Watanabe, K., Nomura, R., Suganuma, N., & Maruyama, S. (2016). Fanconi Syndrome Associated with Hyponatremia in Two Patients with Legionella Pneumonia. Internal medicine (Tokyo, Japan), 55(23), 3479–3484. DISCLOSURES: No relevant relationships by Dilesha Kumanayaka, source=Web Response No relevant relationships by Richard Miller, source=Web Response No relevant relationships by Rutwik Patel, source=Web Response No relevant relationships by Bhavik Patel, source=Web Response
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