Clinical nephrology · 2017
Oxalate nephropathy following vitamin C intake within intensive care unit .
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Colliou Eloïse, Mari Arnaud, Delas Audrey, Delarche Antoine, Faguer Stanislas
Аннотация
OBJECTIVE: To report a case of acute oxalate nephropathy related to vitamin C intake within the intensive care unit (ICU).
DESIGN: Case report.
SETTING: ICU and nephrology department of a French university hospital.
PATIENT: A 57-year-old woman with septic shock related to <italic>Legionella pneumophila</italic> pneumonia complicated by acute respiratory distress syndrome and acute kidney injury who required renal replacement therapy for 75 days.
MEASUREMENTS AND MAIN RESULTS: A renal biopsy was performed on day 72 because of persistent anuria and because the patient showed characteristic features of severe acute oxalate nephropathy. The only cause identified was vitamin C intake received during hospitalization within the ICU (~ 30 g over 2.5 months). At month 6 after ICU admission, estimated glomerular filtration rate was 24 mL/min/1.73m2.
CONCLUSION: Compelling evidence obtained from in-vitro and animal studies suggest that vitamin C, a circulating antioxidant, may be a valuable adjunctive therapy in critically-ill patients. Data from humans are more conflicting. Oxalate, a well-known metabolite of vitamin C, is excreted by the kidneys and can exert a toxic effect on epithelial cells and causes direct tubular damage, and/or it can crystallize within the tubular lumen. This case highlights an under-recognized secondary adverse event from vitamin C given to critically-ill patients. The use of high-dose vitamin C should be prescribed with caution in this population. .
DESIGN: Case report.
SETTING: ICU and nephrology department of a French university hospital.
PATIENT: A 57-year-old woman with septic shock related to <italic>Legionella pneumophila</italic> pneumonia complicated by acute respiratory distress syndrome and acute kidney injury who required renal replacement therapy for 75 days.
MEASUREMENTS AND MAIN RESULTS: A renal biopsy was performed on day 72 because of persistent anuria and because the patient showed characteristic features of severe acute oxalate nephropathy. The only cause identified was vitamin C intake received during hospitalization within the ICU (~ 30 g over 2.5 months). At month 6 after ICU admission, estimated glomerular filtration rate was 24 mL/min/1.73m2.
CONCLUSION: Compelling evidence obtained from in-vitro and animal studies suggest that vitamin C, a circulating antioxidant, may be a valuable adjunctive therapy in critically-ill patients. Data from humans are more conflicting. Oxalate, a well-known metabolite of vitamin C, is excreted by the kidneys and can exert a toxic effect on epithelial cells and causes direct tubular damage, and/or it can crystallize within the tubular lumen. This case highlights an under-recognized secondary adverse event from vitamin C given to critically-ill patients. The use of high-dose vitamin C should be prescribed with caution in this population. .