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Soluble α -Klotho Serum Levels in Chronic Kidney Disease.

Rotondi S, Pasquali M, Tartaglione L, Muci ML, Mandanici G, Leonangeli C, Sales S, Farcomeni A, Mazzaferro S - Int J Endocrinol (2015)

Bottom Line: Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport.Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD.We endorse s-Klotho as an early marker of CKD-MBD.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular, Respiratory, Nephrology, Geriatric, and Anesthetic Sciences, "Sapienza" University, 5 Piazzale Aldo Moro, 00185 Rome, Italy.

ABSTRACT
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 58 ± 15; eGFR 45 ± 21 mL/min). s-Klotho was lower than normal (519 ± 183 versus 845 ± 330 pg/mL, P < .0001) in renal patients and its reduction was detectable since CKD stage 2 (P < .01). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal (73 ± 51 versus 36 ± 11, P < .0002) with significantly increased levels since CKD stage 2 (P < .001). 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.

No MeSH data available.


Related in: MedlinePlus

Correlation tests of eGFR with s-Klotho levels (a) and FGF23 (b).
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Related In: Results  -  Collection


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fig2: Correlation tests of eGFR with s-Klotho levels (a) and FGF23 (b).

Mentions: In patients s-Klotho and FGF23 were negatively correlated (ρ = −0.33,  P < .01, Figure 1). In addition, there was a positive correlation between eGFR and s-Klotho (ρ = 0.43,  P < .001, Figure 2(a)) and a negative correlation between eGFR and FGF23 (ρ = −0.66,  P < .0001, Figure 2(b)).


Soluble α -Klotho Serum Levels in Chronic Kidney Disease.

Rotondi S, Pasquali M, Tartaglione L, Muci ML, Mandanici G, Leonangeli C, Sales S, Farcomeni A, Mazzaferro S - Int J Endocrinol (2015)

Correlation tests of eGFR with s-Klotho levels (a) and FGF23 (b).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4383388&req=5

fig2: Correlation tests of eGFR with s-Klotho levels (a) and FGF23 (b).
Mentions: In patients s-Klotho and FGF23 were negatively correlated (ρ = −0.33,  P < .01, Figure 1). In addition, there was a positive correlation between eGFR and s-Klotho (ρ = 0.43,  P < .001, Figure 2(a)) and a negative correlation between eGFR and FGF23 (ρ = −0.66,  P < .0001, Figure 2(b)).

Bottom Line: Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport.Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD.We endorse s-Klotho as an early marker of CKD-MBD.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular, Respiratory, Nephrology, Geriatric, and Anesthetic Sciences, "Sapienza" University, 5 Piazzale Aldo Moro, 00185 Rome, Italy.

ABSTRACT
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 58 ± 15; eGFR 45 ± 21 mL/min). s-Klotho was lower than normal (519 ± 183 versus 845 ± 330 pg/mL, P < .0001) in renal patients and its reduction was detectable since CKD stage 2 (P < .01). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal (73 ± 51 versus 36 ± 11, P < .0002) with significantly increased levels since CKD stage 2 (P < .001). 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.

No MeSH data available.


Related in: MedlinePlus