questions.Regarding the open-label noted in Clin-icalTrials.gov, this was probably a mislabeling since the trial was in fact blinded only to the investigators but not the subjectsdie, the trial was a singleblinded trial. 1 The assertion that our end point introduces potential bias since it uses systemic inflammatory response syndrome is somewhat misleading since the primary outcome is actually sepsis. Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection. 2 And for this trial, the probable or documented infection is the kidney stone. Therefore, there was no soft end point.Ishikawa highlighted that 4 subjects from the 7-day cohort were excluded (incomplete follow-up) and this may have biased the results toward significance. He performed a brief sensitivity analysis: by including these 4 subjects and assuming that all had sepsis, the 95% CI crosses 1 and therefore no significance is seen. We agree this loss to follow-up potentially introduced bias.Lastly, Ishikawa alludes to a potential bias caused by imbalance in staghorn calculi distributed between the 2 cohorts. We did state in the discussion that "in a post hoc subanalysis of just staghorn subjects, the 2-day cohort did not have an increased risk of sepsis compared to the 7-day cohort (univariate 26.7% vs 9.1%, P [ .11)." However, we also admit that the study is underpowered to detect a difference in this subanalysis (potential type 2 error). As to whether the study is confounded and underpowered for the primary outcome (sepsis)die, type 2 error for the primary outcomedwe discussed this possibility with our statistician. The statistician inferred from our analysis that staghorn was not a confounder given our subanalysis, and our multivariate analysis therefore accounts for this and other potential confounding.