Systemic Oxalosis with Retinopathy Secondary to Vitamin C in a Patient on Peritoneal Dialysis
November 02, 2017 | 10:00 AM - 10:00 AM
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Abstract: TH-PO433
Systemic Oxalosis with Retinopathy Secondary to Vitamin C in a Patient on Peritoneal Dialysis
Session Information
Category: Nutrition, Inflammation, and Metabolism
- 1401 Nutrition, Inflammation, Metabolism
Authors
- D'Costa, Matthew R., Mayo Clinic, Rochester, Minnesota, United States
- Winkler, Nelson S, Mayo Clinic, Rochester, Minnesota, United States
- Milliner, Dawn S., Mayo Clinic, Rochester, Minnesota, United States
- Norby, Suzanne M., Mayo Clinic, Rochester, Minnesota, United States
- Hickson, LaTonya J., Mayo Clinic, Rochester, Minnesota, United States
- Lieske, John C., Mayo Clinic, Rochester, Minnesota, United States
Background
We report a case of systemic oxalosis involving the eyes and joints due to long-term use of high-dose vitamin C in a peritoneal dialysis (PD) patient.
Methods
A 76-year-old female presented to the hospital with a 1-month history of decreasing vision and polyarthralgias. She had developed ESRD secondary to autosomal dominant polycystic kidney disease and underwent living unrelated kidney transplant 10 years earlier. Due to declining allograft function, biopsy was performed 1 year prior to admission revealing severe arteriosclerosis, focal segmental glomerulosclerosis, and early transplant glomerulopathy but no calcium oxalate (CaOx) crystals. She initiated hemodialysis (HD) 6 months later and transitioned to PD 2 months prior to admission. At presentation, ophthalmologic exam revealed crystalline retinopathy consistent with CaOx deposition. Fluorescein angiography demonstrated significant retinal non-perfusion, and optical coherence tomography showed hyperreflective deposits throughout the inner and outer retina. Plasma oxalate (POx) was markedly elevated at 187 μmol/L (normal < 1.7 μmol/L). Urine oxalate/creatinine ratio was high (0.18 mg/mg) while urine glycolate, glycerate and 4-hydroxy-2-oxoglutarate were normal. Genetic testing confirmed absence of pathogenic changes in AGXT, GR/HPR and HOGA1. Stool analysis did not suggest significant fat malabsorption and she had no previous gastrointestinal surgery, diarrhea, or other gastrointestinal symptoms. While excessive intake of high oxalate foods was not identified, she reported chronic use of high-dose vitamin C of up to 4 grams per day for many years. With discontinuation of vitamin C and nearly daily HD for 2 weeks, predialysis POx fell markedly to 30-50 μmol/L. Serial funduscopic examinations remained stable in the setting of mild improvement in visual acuity and marked improvement in joint pain. She was discharged on standard thrice weekly HD. Three months later, her most recent predialysis POx was 35.2 μmol/L.
Conclusion
This case demonstrates that in vitro conversion of vitamin C to oxalate can occur in patients with significant renal impairment producing significant hyperoxalemia. Therefore, high-dose vitamin C should be avoided in later stage CKD patients, especially those on PD which does not clear oxalate effectively.