Aims: Klotho is a co-receptor for FGF-23 and key regulator of phosphate excretion. Soluble klotho modulates ion-channel expression and growth factor sensitivity. In chronic kidney disease (CKD), impaired klotho expression has been demonstrated. Likewise, reduced soluble klotho levels in serum and urine have been established in rodents in experimental acute kidney injury (AKI). In contrast, no data on soluble serum klotho levels in human AKI has been presented to date.
Material and methods: A cross-sectional case-control study of klotho serum levels in 30 subjects with AKI and 126 control subjects with kidney functions ranging from normal to end-stage renal disease (ESRD).
Results: Klotho levels were higher in AKI patients (567.6 ± 294.4 pg/mL, vs. 403.5 ± 152.5 pg/mL, p < 0.01) and females (463.0 ± 202.6 pg/mL vs. 387.6 ± 132.0 pg/mL, p < 0.01) and lower in ESRD patients than in healthy adults and patients with moderate CKD (368.3 ± 99.0 pg/mL vs. 468.1 ± 205.8, p < 0.01 and 368.3 ± 99.0 pg/mL vs. 498.7 ± 221.9, p < 0.01). There was a correlation with estimated glomerular filtration rate (eGFR) in CKD (p < 0.0001, r = 0.34).
Conclusions: In AKI, serum klotho levels are not associated with kidney function whereas in CKD, impaired klotho levels may be observed and are significantly correlated to eGFR. .