Abstract
The first concern identified by the authors is the lack of environmental standardization for our cohort; notably dietary intake. This was a major concern for many of the reviewers for this article. Our goal was to see if a measurable difference in urinary characteristics could be achieved in a real-world setting. For the purist, this study design is flawed with potential confounding factors that could affect 24-hour urinary characteristics. However, patients, especially those afflicted with metabolic syndrome, would be hard pressed to re-create the controlled dietary environments they are held to during trials in control centers. Instead, we asked our volunteers to try to be consistent with their dietary intake during trial weeks and complete dietary journal that were assessed for consistency. There will always be a concern that other factors contributed to the alkalinization of urine, especially without consistency in findings such as significant increases in citrate and urinary potassium; but this may simply be a limitation with what we can and do measure in the urine. Our research suggests that urinary pH can be increased in healthy volunteers who consume a liter of low-calorie orange juice daily for 7 days. The mechanism for urine alkalinization is healthy debate to hold, but it may simply be that not all unprotonated anions are measured in a standard 24-hour metabolic panel. For example, malate is another potential source of alkali therapy and even though citrate did not reach statistical significance, low-calorie orange juice (OJ) showed a 30% reduction in ammonium excretion. The need for alternative therapies to prescription-based potassium citrate is critical for stone prevention and although we do not feel a dietary monotherapy is likely, a multimodal approach with beverages such as low-calorie OJ is a great option. To achieve a measurable difference in urinary characteristics, we took orange juice consumption to the extreme. Instead, based on prior studies by Wabner and Pak (1993) 1 and Odvina (2006) 2 using standard OJ and now our study using low-calorie OJ, providers can recommend a dietary source for alkali therapy.
Second, the authors identify a valid risk factor in the increase of urinary oxalate from the metabolism of ascorbic acid that is rich in orange juice. Assigning absolute stone risk is a challenge based on urinary derangements that are exceedingly difficult—thus, the need for supersaturation indexes to help guide the clinician. Although this is a valid concern, the only way to answer the question would be to perform a prospective control trial and evaluate for CaOx stone events in patients consuming potassium citrate vs low-calorie OJ. I think the greater issue with this would be patient compliance with the ingestion of 1000 mL of low-calorie OJ every day for long enough to crystalize a new stone.