The International Tinnitus Journal

Laboratory Biomarkers of Auditory Dysfunction in Chronic Kidney Disease: From Uremic Burden and Anemia to Iron Status, Mineral Metabolism, Inflammation, and Dialysis Adequacy

D. M. Nabiyeva, N. E. Makhkamova

Background: Hearing impairment is increasingly recognized as an extra-renal complication of chronic kidney disease (CKD). Although pure-tone audiometry remains the conventional method for documenting hearing loss, a laboratorycentered approach may provide earlier and more mechanistically relevant information. Uremic burden, anemia, iron deficiency, disordered mineral metabolism, inflammation, malnutrition, electrolyte abnormalities, and dialysis-related factors can alter cochlear perfusion, outer-hair-cell function, endocochlear ion homeostasis, and neural conduction. Objective: To synthesize current evidence on the relationship between laboratory biomarkers and auditory dysfunction in CKD, with particular emphasis on serum urea, creatinine, estimated glomerular filtration rate (eGFR), hemoglobin, ferritin and iron status, albumin, C-reactive protein (CRP), electrolytes, calcium-phosphate metabolism, fibroblast growth factor 23 (FGF23), parathyroid hormone (PTH), and hemodialysis adequacy. Methods: A targeted narrative review of contemporary and foundational clinical studies was performed, prioritizing studies that combined laboratory measurements with pure-tone audiometry, high-frequency audiometry, otoacoustic emissions (OAE), speech audiometry, or auditory evoked potentials. Particular attention was paid to studies published from 2020 through 2026, supplemented by earlier mechanistic and clinical reports when needed to interpret conflicting findings. Results: The most reproducible laboratory pattern is an association between greater renal dysfunction and poorer high-frequency hearing. Higher urea and creatinine frequently accompany hearing loss, although their independent predictive value is inconsistent across studies. Lower eGFR is associated with progressively worse high-frequency thresholds in several cohorts. Anemia represents a biologically plausible and clinically modifiable risk factor: lower hemoglobin is associated with worse hearing or speech performance, while iron deficiency anemia is linked to increased odds of sensorineural hearing loss in population data. Ferritin requires cautious interpretation in CKD because it reflects both iron stores and inflammation; recent population data suggest higher ferritin may be associated with a lower risk of high-frequency hearing loss, but these results cannot be directly extrapolated to inflamed or dialysis populations without concurrent transferrin saturation. Emerging data identify FGF23 and D-serine as potential biomarkers of hearing impairment in maintenance hemodialysis. CRP, albumin, calcium-phosphate balance, electrolyte shifts, Kt/V, ultrafiltration volume, and intradialytic hypotension may further define high-risk auditory phenotypes. Conclusions: Auditory dysfunction in CKD is better conceptualized as the clinical expression of a laboratory-defined metabolic, hematological, inflammatory, and dialysis-related milieu than as an isolated otological complication. A practical laboratory-audiological panel should combine renal function (creatinine, urea, eGFR), anemia and iron indices (hemoglobin, ferritin, transferrin saturation), inflammatory/nutritional markers (CRP, albumin), mineral metabolism (calcium, phosphate, PTH, FGF23 when available), and dialysis metrics (Kt/V, ultrafiltration, blood-pressure stability) with high-frequency audiometry and OAE.