Acute oxalate nephropathy after a massive intravenous dose of vitamin C

Wong, K.M.; Thomson, Christine D.; Bailey, Ross R.; McDiarmid, Suzanne V.; Gardner, Jacqui

doi:10.1111/j.1445-5994.1994.tb01477.x

Cited by 72 publications

(54 citation statements)

References 4 publications

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“…The patients are sometimes treated with very high oral or parenteral doses of vitamin C. How ever, this is clearly contraindicated, as has been documented in several reports showing that oxalosis due to renal failure may be severely aggravated by vitamin C. Complica tions due to oxalate deposits in several organs and other pathological conditions have been described after excessively high doses of vita min C (in 1 case 60 g i.v. ), including cuta neous oxalosis with calcifications of fingers, accelerated renal failure, and death [54][55][56][57][58][59][60].…”

Section: Patients With Renal Failure and Vitamin Cmentioning

confidence: 99%

No Contribution of Ascorbic Acid to Renal Calcium Oxalate Stones

Gerster¹

1997

Ann Nutr Metab

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Even though a certain part of oxalate in the urine derives from metabolized ascorbic acid (AA), the intake of high doses of vitamin C does not increase the risk of calcium oxalate kidney stones due to physiological regulatory factor: gastrointestinal absorption as well as renal tubular reabsorption of AA are saturable processes, and the metabolic transformation of AA to oxalate is limited as well. Older assays for urinary oxalate favored in vitro conversion of AA to oxalate during storage and processing of the samples. Recurrent stone formers and patients with renal failure who have a defect in AA or oxalate metabolism should restrict daily vitamin C intakes to -100 mg. But in the large-scale Harvard Prospective Health Professional Follow-Up Study, those groups in the highest quintile of vitamin C intake (> 1,500 mg/day) had a lower risk of kidney stones than the groups in the lowest quintiles.

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Section: Patients With Renal Failure and Vitamin Cmentioning

confidence: 99%

No Contribution of Ascorbic Acid to Renal Calcium Oxalate Stones

Gerster¹

1997

Ann Nutr Metab

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“…46,47 Ascorbic acid is metabolized to oxalate, and 2 cases of acute oxalate nephropathy were reported in patients with pre-existing renal insufficiency given massive intravenous doses of vitamin C. 48,49 Therefore, patients with renal insufficiency or renal failure, or who are undergoing dialysis, should not receive high doses of vitamin C. 46 It is controversial whether high-dose vitamin C use is associated with oxalate kidney stones, and patients with hyperoxaluria or a prior history of oxalate kidney stones have a relative contraindication to high-dose vitamin C.…”

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confidence: 99%

Intravenously administered vitamin C as cancer therapy: three cases

Padayatty

Riordan²,

Hewitt³

et al. 2006

Canadian Medical Association Journal

227

163

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“…Since then, there have been several case reports in the literature mentioning acute oxalate nephropathy in association with excessive vitamin C intake. Wong et al [19] reports a patient with metastatic carcinoma of the prostate with underlying obstructive renal insufficiency who received a 60 gm bolus of IV vitamin C an an alternative therapy and developed anuric renal failure. Two days later on renal biopsy, the patient had similar findings to our patient.…”

Section: Discussionmentioning

confidence: 99%

“…An autopsy showed extensive deposition of calcium oxalate in the kidneys and pancreas. Table 1 provides a summary of the various cases reported in the literature of biopsy proven oxalate nephropathy suspected to be secondary to ascorbic acid [10,14,[19][20][21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Vitamin C Induced Oxalate Nephropathy

2017

American Journal of Kidney Diseases

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Although a multitude of syndromes have been thoroughly described as a result of vitamin deficiencies, over consumption of such substances may also be quite dangerous. Intratubular crystallization of calcium oxalate as a result of hyperoxaluria can cause acute renal failure. This type of renal failure is known as oxalate nephropathy. Hyperoxaluria occurs as a result of inherited enzymatic deficiencies known as primary hyperoxaluria or from exogenous sources known as secondary hyperoxaluria. Extensive literature has reported and explained the mechanism of increased absorption of oxalate in malabsorptive syndromes leading to renal injury. However, other causes of secondary hyperoxaluria may also take place either via direct dietary consumption of oxalate rich products or via other substances which may metabolize into oxalate within the body. Vitamin C is metabolized to oxalate. Oral or parenteral administration of this vitamin has been used in multiple settings such as an alternative treatment of malignancy or as an immune booster. This article presents a clinical case in which ingestion of high amounts of vitamin C lead to oxalate nephropathy. This article further reviews other previously published cases in order to illustrate and highlight the potential renal harm this vitamin poses if consumed in excessive amounts.

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Acute oxalate nephropathy after a massive intravenous dose of vitamin C

Cited by 72 publications

References 4 publications

No Contribution of Ascorbic Acid to Renal Calcium Oxalate Stones

No Contribution of Ascorbic Acid to Renal Calcium Oxalate Stones

Intravenously administered vitamin C as cancer therapy: three cases

Vitamin C Induced Oxalate Nephropathy

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