Nephrology · Medical Literature
Eight weeks of MitoQ supplementation does not alter kidney function or urinary kidney injury biomarkers in middle-aged and older adults.
Abstract
Several human trials have used the mitochondrial antioxidant mitoquinol mesylate (MitoQ). There are no apparent negative consequences on the kidneys following an acute high dose of MitoQ in young adults; however, it remains unclear whether chronic MitoQ influences kidney function. Therefore, we examined whether 8 wk MitoQ supplementation (20 mg/day) impacts kidney function and kidney injury biomarkers using a randomized, placebo-controlled, crossover study in middle-aged and older adults (n = 30, 8 males/22 females, 57 ± 8 yr). Participants completed four visits (pre- and postplacebo; pre- and post-MitoQ) where we collected serum samples (creatinine and cystatin c) and 24-h urine samples to assess general kidney function [estimated glomerular filtration rate (eGFR) and creatinine clearance], and kidney injury markers [neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), nephrin, tissue inhibitor of metalloproteinase-2 (TIMP-2), and insulin-like growth factor binding protein-7 (IGFBP7)]. We used mixed-effects models to examine time, condition, and interaction effects. We observed no alterations in glomerular filtration measures (Ps ≥ 0.309) or kidney injury markers when indexed to flow rate, osmolality, or creatinine (Ps ≥ 0.198). For example, TIMP-2 × IGFBP7 was not different between groups (preplacebo: 114 ± 162, postplacebo: 138 ± 161; pre-MitoQ: 162 ± 238, post-MitoQ: 127 ± 137 ng2/min; interaction P = 0.754). Eight weeks of MitoQ supplementation does not appear to benefit or harm kidney function or kidney injury markers in middle-aged and older adults.NEW & NOTEWORTHY To our knowledge, this is the first study to examine extended mitoquinol mesylate (MitoQ) supplementation on kidney health in humans. Eight weeks of MitoQ (20 mg/day) produced no meaningful changes in kidney function or urinary biomarkers of tubular injury in middle-aged and older adults. Although no benefit was observed, the absence of harm is reassuring given existing evidence that MitoQ improves peripheral vascular endothelial function, a primary antecedent to cardiovascular disease, in multiple human studies.
Clinical relevance
Does 8 weeks of oral mitoquinol mesylate (MitoQ) supplementation at 20 mg/day alter kidney function or urinary kidney injury biomarkers in middle-aged and older adults compared to placebo? __SNAPSHOT__ {"studyDesign":"Randomized, placebo-controlled, crossover trial","setting":"Multi-institutional, United States (Auburn University, Indiana University, LaGrange College, Texas A&M University-Kingsville, Virginia Commonwealth University, University of Alabama at Birmingham); clinical setting not further specified","sampleSize":"n = 30 (8 males, 22 females); crossover design — all participants received both MitoQ and placebo","population":"Middle-aged and older adults; mean age 57 ± 8 years; sex distribution skewed female (73%); baseline kidney health status and CKD exclusion/inclusion criteria not reported in abstract","intervention":"Oral MitoQ (mitoquinol mesylate) 20 mg/day for 8 weeks","comparator":"Placebo for 8 weeks (crossover design; washout duration not reported in abstract)","primaryOutcome":"Kidney function (eGFR estimated from serum creatinine and cystatin C; 24-hour creatinine clearance) and urinary kidney injury biomarkers (NGAL, KIM-1, nephrin, TIMP-2, IGFBP7), assessed pre- and post-intervention for each condition","followUp":"8 weeks per condition (crossover); total study duration not reported in abstract","fundingSource":"Not reported in abstract"}
Key findings
Across all glomerular filtration metrics (eGFR by creatinine and cystatin C; creatinine clearance), no statistically significant time, condition, or interaction effects were detected following 8 weeks of MitoQ 20 mg/day versus placebo (all p-values ≥ 0.309). Similarly, none of the five urinary kidney injury biomarkers — NGAL, KIM-1, nephrin, TIMP-2, and IGFBP7 — differed significantly between MitoQ and placebo conditions when indexed to urine flow rate, osmolality, or creatinine (all p-values ≥ 0.198). The TIMP-2 × IGFBP7 product, a validated composite marker of cell-cycle arrest and tubular stress, was specifically reported: pre-placebo 114 ± 162, post-placebo 138 ± 161; pre-MitoQ 162 ± 238, post-MitoQ 127 ± 137 ng²/min (interaction p = 0.754). No clinically meaningful adverse renal signals or nephrotoxic events were reported. Absolute and relative effect sizes, confidence intervals, and NNT/NNH are not reported in the abstract and therefore cannot be cited or calculated.
Practice implications
This study established that 8 weeks of MitoQ at the standard human supplementation dose of 20 mg/day does not measurably impair or improve kidney function or subclinical tubular injury markers in apparently healthy middle-aged and older adults. The absence of harm is clinically reassuring, particularly given that prior in vitro data had raised concerns about potential nephrotoxicity at supraphysiologic MitoQ concentrations, and given that prior evidence supports vascular endothelial benefits of MitoQ in humans. Critically, the study does NOT establish whether MitoQ benefits kidney function in individuals with pre-existing chronic kidney disease, significant oxidative stress burden, or mitochondrial dysfunction — populations where a therapeutic signal might be more detectable. The cohort is predominantly female (73%) and was presumably drawn from a relatively healthy community sample, limiting generalizability to populations with comorbid CKD, diabetes, or hypertension. The study also does not establish safety beyond 8 weeks, at higher doses, or in persons with reduced renal reserve. Only the abstract is available for review; full methods, baseline characteristics, washout period, adherence monitoring, and power calculations are not accessible and represent important interpretive limitations. __LIMITATIONS__ Small sample size (n = 30) substantially limits statistical power to detect modest but clinically meaningful changes in kidney function or injury biomarkers; underpowering may have produced false-negative results.,Crossover design requires an adequate washout period between conditions; washout duration is not reported in the abstract, raising concern for carryover effects.,Predominantly female cohort (73%) limits generalizability across sexes.,Participants appear to be relatively healthy community-dwelling adults; applicability to patients with CKD, diabetes, hypertension, or known mitochondrial dysfunction is unknown and explicitly unestablished.,Only an 8-week supplementation window was studied; longer-duration effects on kidney structure or function remain unknown.,Dose tested (20 mg/day) is the standard commercial dose; safety and efficacy at higher clinically used doses are not evaluated.,Absence of benefit may reflect a floor/ceiling effect in a healthy population without significant baseline oxidative stress or mitochondrial dysfunction.,Funding source not reported in the abstract; potential conflicts of interest cannot be assessed.,Full statistical outputs (confidence intervals, effect sizes, power calculations) are not available from the abstract alone; conclusions are based on reported p-values only.,This is described as the first human study of extended MitoQ supplementation on kidney health; findings have not yet been independently replicated. __BOTTOM_LINE_CATEGORY__ confirmatory __BOTTOM_LINE__ Eight weeks of MitoQ 20 mg/day does not appear to harm or benefit kidney function or tubular injury biomarkers in healthy middle-aged and older adults, providing initial reassurance regarding renal safety at standard supplementation doses in this population. However, the small, predominantly healthy, female-skewed sample means these findings cannot yet be extrapolated to patients with CKD, diabetes, or significant comorbidities. No change in clinical practice is warranted; this study supports continued safe use of MitoQ in ongoing cardiovascular and metabolic trials while underscoring the need for dedicated renal safety and efficacy studies in at-risk populations.