SAN DIEGO—Moderate ascorbic acid (AA) supplementation increases plasma AA levels in hemodialysis (HD) patients without affecting their oxalate levels, according to study findings presented at Kidney Week.

Oxalate is an AA metabolite that at higher concentrations may deposit pathologically in organs, researchers noted.

The study, led by William D. Sirover, MD, of Cooper Medical School of Rowan University, Camden, N.J., included 186 HD patients, of whom 132 took up to 100 mg of oral AA per day (treatment group) and 54 who did not (control group). The median pre-HD plasma concentration was 47.2 µM in the treatment group compared with 15.8 µM in the control group, a significant difference between the groups. The treatment and control groups showed no significant difference in mean pre-HD plasma oxalate levels (21.9 vs. 20.6 µM, respectively).

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AA supplementation may prevent depletion of this important water-soluble vitamin in HD patients, and may help to treat anemia, Dr. Sirover told Renal & Urology News.

“Because AA is metabolized to oxalate, AA supplementation poses a risk of oxalosis,” Dr. Sirover explained. “Oxalate is removed by HD.  Nonetheless, early studies showed that patients on HD could develop high plasma oxalate levels when taking moderate doses of AA —up to 100 mg/day.”

Despite this evidence, contemporary HD patients often ingest this amount of AA. “We hypothesized that current high-flux HD prevents an increase in plasma oxalate levels in patients who take moderate dose AA supplementation. By measuring plasma AA and oxalate levels, we now demonstrate that with contemporary, high-flux HD, moderate AA supplementation is associated with increases in plasma AA levels and not linked with increases in plasma oxalate levels.”

Although a controlled study is needed to validate the findings, the current findings are important for 2 reasons, Dr. Sirover said. “Moderate AA supplementation may become the standard of care for HD patients, and, while the optimal plasma AA level that may be needed to improve anemia in HD patients is not known, our results provide a better understanding of the achieved plasma AA levels when HD patients take moderate AA supplementation.”

In a separate presentation at Kidney Week, researchers reported that oral AA supplementation may be effective at decreasing erythropoietin requirements in HD patients with functional iron deficiency.

AA acts as a reducing agent and enhances mobilization of the ferrous form of iron to transferrin, thereby increasing its bioavailability, Tanjim Sultana, MD, and colleagues at Lenox Hill Hospital in New York explained.

Dr. Sultana’s group prospectively studied 22 stable HD patients with functional iron deficiency, defined as a transferrin saturation (TSAT) less than 30% and ferritin levels greater than 100 mcg/L with EPO requirement of 4,000 units/HD session. Patients received 250 mg of oral AA daily for 3 months.

The mean EPO dose declined by a significant 867 units/HD session in 15 subjects. In 7 responders, the EPO dose declined by 33% from baseline. Despite adjustment of EPO dose, the mean hemoglobin level increased significantly from 10.1 to 10.7 mg/dL. The researchers observed no significant change in TSAT and ferritin levels.