The present results are in agreement with other investigations that have demonstrated the safety of creatine supplementation on kidney function in distinct populations [4–9]. However, most of these studies estimated glomerular filtration rate by using serum endogenous markers, which are widely used in clinical practice but potentially susceptible to methodological errors. For instance, serum creatinine and its derivative equations are influenced by dietary intake, particularly by creatine-containing foods or supplements. Upon the ingestion of creatine, one may expect an increase in serum creatinine, since creatine is spontaneously and irreversibly converted into creatinine. As such, a false positive diagnosis of a decreased kidney function may occur in creatine-supplemented individual when only serum creatinine data are taken into consideration. Although serum creatinine was not significantly elevated in the current study, previous observations from our group  and others  support the inaccuracy of creatinine-based markers in the evaluation of kidney function in creatine-supplemented individuals. To circumvent this potential bias, we measured glomerular filtration rate using the gold-standard technique 51Cr-EDTA clearance, which allowed us to properly conclude that creatine supplementation did not affect kidney function in this study.
Applying the above mentioned technique, we previously showed that 35 days of creatine supplementation did not alter kidney function in a 20-year-old man with a single kidney . Moreover, we reported that 3 months of creatine supplementation had no deleterious effect on kidney function in post-menopausal women  and in type-2 diabetic patients , corroborating the safety of this supplement. The present data extend this notion to typical creatine consumers, suggesting that healthy resistance-trained individuals can “deal” with creatine supplementation even in combination with a higher level of protein intake (considering the Recommended Dietary Intake (RDI) of 0.8 g/Kg/d). In consonance with our findings, a few cross-sectional studies have shown no significant differences in kidney function between higher and lower protein consumers [18, 19]. In fact, given the human habituation to the high-nitrogenous diet throughout the span of evolution, these findings might not be considered unexpected. Yet, further prospective studies must explore the impact of chronic nitrogenous-rich diets upon kidney function in healthy individuals.
This study is not without limitations. First, the follow-up of this study is too short, precluding any definitive conclusions. Originally, this trial was designed to cover a 12-month period. However, a drastic withdrawal rate forced us to reduce the follow-up period. Therefore, trials of longer treatment duration are warranted. Second, we selected recreationally trained participants to increase the ecological validity of this study, since this population is thought to be the largest consumer of creatine supplements. However, it is possible that highly-trained athletes taking anabolic steroids and under exhaustive resistance training regimens may experience a differential response to creatine supplementation. Finally, it is worth noting that all of the individuals were apparently healthy, so that these data cannot be extrapolated to individuals with, or at risk of, chronic kidney diseases. In such conditions, creatine users must be systematically monitored for kidney function.