Klotho is highly expressed in the kidney, where it modulates renal solute transport and protects the kidney from a variety of insults in experimental models.
We found that AKI and CKD animals have low levels of renal, blood, and urine Klotho. We also showed these changes precede the rise of serum creatinine and NGAL. In addition we have shown human urinary Klotho dramatically declines with elevation of plasma creatinine in AKI patients.
Experimental results from our lab and others have clearly revealed that renal and circulating Klotho are severely reduced in chronic kidney disease (CKD) in both human patients and experimental animals.
Our research focuses on exploring the potential diagnostic and prognostic implication of Klotho in AKI and CKD.
To test Klotho's usefulness as a biomarker, we are analyzing Klotho levels in plasma and urine, and measuring Klotho mRNA and protein in the kidney when possible. We are also comparing Klotho with other AKI biomarkers, such as urine or/and plasma interleukin-18, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1).
Ideally, combining these biomarkers would amplify the sensitivity for early detection of AKI.