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Excessive myocardial calcinosis in a chronic hemodialyzed patient
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High-dose intravenous ascorbic acid can lead to severe hyperoxalemia in patients with chronic kidney disease undergoing hemodialysis. This increases the risk of calcium oxalate deposition in soft tissues, necessitating avoidance of such treatments.
Area of Science:
- Nephrology
- Biochemistry
- Clinical Medicine
Background:
- Secondary oxalosis is a complication in chronic hemodialysis patients due to impaired renal excretion of oxalic acid.
- Ascorbic acid is a known precursor to oxalic acid, posing a potential risk in patients with compromised kidney function.
Abstract:
Secondary oxalosis in chronic hemodialyzed patients is caused by impaired renal excretion and inadequate removal of oxalic acid during hemodialysis. Ascorbic acid is a precursor of oxalic acid. We report a parathyroidectomized patient with chronic renal failure, on hemodialysis, who received over a period of several months a total dose of 91.0 g ascorbic acid i.v. The plasma oxalic acid level in this patient was 14-fold higher than in healthy persons. Increased oxalic acid synthesis from its precursor ascorbic acid may be responsible for hyperoxalemia, high content of oxalic acid in myocardium, aorta and lung, and calcium oxalate deposition in soft tissues. Application of high doses of ascorbic acid should be avoided in hemodialysed patients with chronic renal failure.