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Foodborne mycotoxins are widespread environmental exposures, but their contribution to human kidney disease remains uncertain. This critical narrative review distinguishes food contamination, human internal exposure, experimental nephrotoxicity, and human renal outcomes and proposes an evidence-atlas framework that does not equate geographic overlap with causation. Quantitative examples illustrate the differences between evidence domains: in one Kenyan survey of 200 milled-rice samples, citrinin (CIT) and ochratoxin A (OTA) were detected in 55.5% and 30%, respectively, with reported ranges of 0–9 and 0–110 µg/kg across all samples. Human biomonitoring studies report frequent internal exposure, but exposure detection alone does not establish renal injury. Human renal studies are heterogeneous: one Taiwanese analysis reported an association between 24-h OTA excretion and proteinuria (N = 85; r = 0.303; p = 0.006), whereas a Polish comparison found no significant difference in mean serum OTA between 88 dialysis patients and 16 controls (0.75 versus 0.70 ng/mL). Experimental studies support toxin-specific mechanisms involving impaired antioxidant defense, mitochondrial disturbance, lipid-peroxide injury, and endoplasmic-reticulum stress, but tested doses and durations often differ from usual dietary exposure. Reverse causation, altered renal elimination, co-exposures, assay specificity, and inconsistent endpoints limit causal inference. The proposed atlas separates food-occurrence, biomonitoring, and renal-outcome evidence, while evaluating experimental mechanisms independently. Prospective studies integrating dietary assessment, repeated biomonitoring, and renal outcomes are needed to test temporality and dose–response outcome.
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Puspitasari et al. (2026) studied this question.
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