Ascorbic acid
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Acute tubular injury and oxalate nephropathy: 2 case reports A 50-year-old man (Patient 1) and a 70-year-old man (Patient 2) developed acute tubular injury (ATI) and oxalate nephropathy during treatment with ascorbic acid for sepsis [durations of treatments to reactions onsets not stated]. Patient 1: The man was admitted for persistent fever, cough and dyspnoea. Five days before admission, he was found positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. His medical history was significant for arterial hypertension and Brugada syndrome. He did not have history of kidney disease or kidney stones. On admission, a chest x-ray showed bilateral interstitial pneumonia, moderate respiratory insufficiency and his kidney function was normal (serum creatinine 1 mg/dL). Due to rapid deterioration of respiratory function, he was transferred to the ICU on the same day of admission where he was intubated and put on lung-protective mechanical ventilation. According to the protocol for COVID-19, he was initiated on offlabel treatment with hydroxychloroquine 400mg twice a day, lopinavir/ritonavir 200/50 mg/day and azithromycin 500 mg/day. Lopinavir/ritonavir was rapidly switched to cobicistat/darunavir 150/800 mg/day. A single dose of SC tocilizumab was used to counteract cytokine storm. Considering his septic status, he received IV steroids and broad-spectrum antibiotics [specific drug not stated] therapy. He received a high-dose of IV ascorbic acid [vitamin C] 50 mg/kg four times a day for his septic status. He was put on enteral nutrition. His clinical course was complicated immediately by septic shock, requiring inotropes. He developed multi-organ failure with hepatic dysfunction as well as acute kidney injury (AKI) with anuria. Anuria was noted for 10 days. He was started on continuous venovenous haemodiafiltration on hospital day 2. He was treated with meropenem for Klebsiella pneumoniae bacteraemia. His respiratory status improved, and he was extubated by day 15 from admission. From day 18, swabs for SARS-CoV-2 were found to be negative. Despite an increase in urine output, his kidney function did not show any improvement and he was transferred to the nephrology unit. At day 36, a biopsy of the kidney was performed. At that time, his serum creatinine was 5.85 mg/dL and the urine output was 2000 mL/day. His kidney biopsy specimen showed extensive ATI and focal acute tubular necrosis, with degenerative and reactive aspects of tubular cells (epithelial attenuation and focal detachment with presence of cellular debris in tubular lumen). Additionally, calcium oxalate crystals (fan-shaped radially arranged translucent crystals on hematoxylin and eosin stain, birefringent when examined with polarised light) were identified in several tubular lumina. Few degenerated tubules contained periodic acid–Schiff–positive casts. There was mild focal interstitial inflammation; glomeruli showed no relevant alterations, apart from focal and segmental presence of inflammatory cells in capillary lumina; arteri
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