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International Journal of Endocrinology
Volume 2015, Article ID 872193, 8 pages
Research Article

Soluble α-Klotho Serum Levels in Chronic Kidney Disease

1Department of Cardiovascular, Respiratory, Nephrology, Geriatric, and Anesthetic Sciences, “Sapienza” University, 5 Piazzale Aldo Moro, 00185 Rome, Italy
2Department of Public Health and Infectious Diseases, Section of Statistics, “Sapienza” University, 5 Piazzale Aldo Moro, 00185 Rome, Italy

Received 8 August 2014; Accepted 17 November 2014

Academic Editor: Andrea Del Fattore

Copyright © 2015 Silverio Rotondi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Transmembrane α-Klotho (TM-Klotho), expressed in renal tubules, is a cofactor for FGF23-receptor. Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport. Decreased TM-Klotho, described in experimental chronic kidney disease (CKD), prevents actions of FGF23 and lessens circulating s-Klotho. Thus, levels of s-Klotho could represent a marker of CKD-MBD. To evaluate the clinical significance of s-Klotho in CKD we assayed serum s-Klotho and serum FGF23 in 68 patients (age ; eGFR  mL/min). s-Klotho was lower than normal ( versus  pg/mL, ) in renal patients and its reduction was detectable since CKD stage 2 (). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal ( versus , ) with significantly increased levels since CKD stage 2 (). Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD. Assuming that s-Klotho mirrors TM-Klotho synthesis, low circulating s-Klotho seems to reflect the ensuing of tubular resistance to FGF23, which, accordingly, is increased. We endorse s-Klotho as an early marker of CKD-MBD.