Ascorbic acid
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Acute oxalate nephropathy due to off label use: case report A 64-year-old man developed acute oxalate nephropathy during off-label treatment with ascorbic acid for Covid-19. The man, who had a history of diabetes mellitus, stage III chronic kidney disease, hypertension and controlled HIV on unspecified highly active antiretroviral therapy (HAART), presented to the emergency department with fever and shortness of breath. He had no history of malabsorption syndromes, gastric bypass, small bowel resection, bariatric surgery, chronic pancreatitis or prior use of vitamin C. As home medications, he had been receiving various drugs, including unspecified HAART regimen. At presentation, he was treated with unspecified broad-spectrum antibiotics. Subsequently, the COVID-19 RNA polymerase chain reaction showed positive results for Covid-19 infection. His respiratory status worsened. Hence, he was placed on non-rebreather oxygen and was transferred to the ICU within 24h of admission. On hospital admission day 2, he started receiving off-label Covid-19 treatment with IV ascorbic acid [vitamin C] 3g every 6h, IV methylprednisolone sodium succinate [solumedrol] and IV zinc for 7 days. His total dose of ascorbic acid was 84g. His initial urine test on admission showed new haematuria and proteinuria. After initiation of ascorbic acid, he developed acute kidney injury (AKI) with a worsening of oliguria and azotemia. Renal ultrasound of kidneys was non-significant. On day 3 of admission, he started receiving continuous renal replacement therapy (CRRT) because of anuric AKI and metabolic acidosis. He had received CRRT with an Oxiris filter for 2 days, followed by CRRT with a standard filter for additional 4 days. Due to the worsening of respiratory status on the fourth day of admission, he required intubation with mechanical ventilation . The man’s treatment was switched to intermittent haemodialysis on day 9. On day 11, a renal biopsy was performed, which showed 6 glomeruli, of which, 3 glomeruli were globally sclerosed, and 1 glomeruli showed foam cells, epithelial hyperplasia and compression of glomerular capillaries. The remaining glomeruli revealed mesangial expansion. The flattening of tubular epithelial cells with debris and cells in the tubular lumena was also observed. Occasional tubules revealed neutrophils infiltrates in the tubular epithelial cells. Based on findings, a diagnosis of collapsing glomerulopathy caused by Covid-19 infection was made. In tubular lumens, extensively distributed polarizable material was observed. Additionally, interstitial fibrosis and tubular atrophy including 25% to 30% of the tissue was observed. Electron microscopy showed negative results for electron-dense deposits, along with 80% effacement of epithelial cell foot processes. The thickness of the basement membranes was normal. An epithelial cell retracted from basement membrane with condensed cytoplasm was also noted on an instance. He also showed signs of acute tubular injury and focal pyelonephritis. No viral inclusion was noted. Bas
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