Vitamin C-induced hyperoxaluria causing reversible tubulointerstitial nephritis and chronic renal failure: a case report

Abstract

Vitamin C is a precursor of oxalate and promoter of its absorption, potentially causing hyperoxaluria. Malabsorption causes Calcium (Ca) chelation with fatty acids, producing enteric hyperoxaluria.CaseA 73-year-old man with both risk factors was hospitalized with serum creatinine of 8.4 mg/dL (versus 1.2 mg/dL four months earlier) (normal 0.6–1.3 mg/dL). Given his oxalate-rich diet, chronic diarrhea, and daily 680 mg vitamin C and furosemide, we postulated Ca oxalate-induced nephropathy, a diagnosis confirmed by documenting hyperoxaluria, and finding of diffuse intraluminal crystals and extensive interstitial fibrosis on biopsy. He was hemodialysed 6 times to remove excess oxalate. Two weeks off vitamin C, his creatinine spontaneously fell to 3.1 mg/dL. Three months later, on low oxalate diet and 100 mg vitamin B6, urine oxalate to creatinine ratio decreased from 0.084 to 0.02 (normal < 0.035), while creatinine fell and stayed at 1.8 mg/dL.Conclusion1) High-dose vitamin C can induce hyperoxaluric nephropathy and progressive renal failure, especially if aggravated by diarrhea, oxalate-rich diet, metabolic acidosis, and dehydration. 2) The diagnosis should be suspected in unexplained renal insufficiency when associated with these risk factors. 3) Since prompt treatment could avert end-stage renal disease, we recommend monitoring urinary oxalate in patients on high-dose vitamin C and renal biopsy if necessary.

Acute Kidney Disease Due to Excessive Vitamin C Ingestion and Remote Roux-en-Y Gastric Bypass Surgery Superimposed on CKD

“…34 The mechanism in this setting is thought to relate to the availability of calcium in the intestine. 17 The inability to absorb fatty acid in the small intestine results in increased calcium saponification. A decrease in free intestinal calcium leads to higher levels of unbound oxalate in the large bowel that are ultimately absorbed, filtered by the kidney, and deposited into the tissue.…”

“…A decrease in free intestinal calcium leads to higher levels of unbound oxalate in the large bowel that are ultimately absorbed, filtered by the kidney, and deposited into the tissue. 17,36 CKD is the third mechanism. This impairs circulating oxalate excretion and increases the risk for oxalate nephropathy.…”

“…1,15 In particular, vitamin C or ascorbic acid is readily converted to oxalate and is believed to result in a hyperoxaluric state. 4,[16][17][18][19][20][21][22][23] For women and men, the recommended daily intakes of vitamin C are 75 and 90 mg/d, respectively. 24,25 Although there is some controversy about its relation to oxalate stone formation, cases of oxalate nephropathy have been reported with vitamin C intake , 2 g/d, 4,15,17 although that 2 g/d has been regarded as a safe upper limit.…”

Esophageal mucosa exfoliation induced by oxalic acid poisoning: A case report

“…The renal biopsy results of patients with OA poisoning suggest the occurrence of acute tubulointerstitial nephritis (1). Chronic hyperoxaluria cases exhibit pathological changes associated with interstitial nephritis (12,13). In such cases, the results may be attributable to oxalate itself, although the patients were typically treated with omeprazole, a proton pump inhibitor, simultaneously due to gastrointestinal symptoms.…”

Vitamin C Induced Oxalate Nephropathy

“…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].…”