Brain-specific biomarkers in urine as a non-invasive approach to monitor neuronal and glial damage

Ninety-three urine–serum pairs in the target group and 10 urine–serum pairs in the control group were measured. The mean absolute concentration ± standard deviation in urine of the target and control groups were 184.7 ± 362.4 pg/ml and 27.3 ± 24.1 pg/ml for GFAP (r =0.3 [Wilcoxon effect size], p =0.007), 17.5 ±38.6 pg/ml and 0.9 ±0.3 pg/ml for NfL (r =0.4, p <0.005), 320.2 ±443.3 pg/ml and 109.6 ±116.8 pg/ml for UCH-L1 (r =0.26, p =0.014), and 219.5 ± 255.8 pg/ml and 21.1 ± 27.1 pg/ml for t-tau (r =0.37, p <0.005), respectively, whereas biomarker–creatinine ratio was significantly different only for NfL (r =0.29, p =0.015) and t-tau (r =0.32, p <0.01). In patients with intact glomerular barrier (ACR < 30mg/g), only NfL in urine was significantly different between the target and control group and showed a significant correlation with the respective serum concentrations (r =0.58 [Pearson’s correlation-coefficient], p <0.005).
All four investigated biomarkers could be measured in urine, with NfL and t-tau showing the strongest effect size after correction for urine dilution. NfL revealed the most accurate relation between serum and urine concentrations in patients with intact kidney function.

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