Acute oxalate nephropathy after massive ascorbic acid administration.
Level 4 - case-series / case-control
Single clinical case report
What was done
A single patient with primary amyloidosis and nephrotic syndrome received a single 45-g intravenous dose of ascorbic acid as adjuvant therapy. Following the onset of acute oliguric renal failure, postmortem histopathologic examination of renal tissue was performed using a microincineration technique, and plasma oxalate and ascorbic acid concentrations were measured.
What was found
The patient developed acute oliguric renal failure following the infusion. Postmortem examination demonstrated extensive intratubular calcium oxalate crystalline deposits with no extrarenal deposits. Plasma oxalate and ascorbic acid concentrations were increased; specific numerical values and time intervals are not reported in the abstract.
Why it matters
This report indicates that massive intravenous ascorbic acid administration can rapidly lead to fatal acute oxalate nephropathy through extensive intratubular crystal deposition.
Limits
Findings are derived from a single patient (n = 1) with pre-existing primary amyloidosis and nephrotic syndrome, which limits generalizability to individuals with normal baseline kidney function. No numerical values for plasma concentrations or renal function tests are provided in the abstract.
Cited by
- supports High doses of intravenous vitamin C have been observed to cause oxalate nephropathy in patients with preexisting kidney impairment.