There is growing interest for osteocytes’ produced proteins. After the discovery of FGF23, attention is now directed toward Sclerostin which, by inhibiting the canonical Wnt pathway, suppresses osteoblasts activity and stimulates their apoptosis. A diagnostic role can be then hypothesized in bone metabolism derangements of CKD. Serum levels of sclerostin have been reported to increase along with GFR reduction and to correlate, in hemodialysis, with bone volume (positively) and with bone turnover (negatively).

Aim of our study was to evaluate the possible diagnostic role of serum sclerostin levels in renal transplant patients (Tx) in whom almost no data are available.


We performed a cross sectional observational study in 80 Tx (55±10 y.o.; 49M/31F) with CKD stage 2-4. Thirty healthy subjects (35 ± 12 y.o.; 14M/16F) were the  control group (N). We evaluated in all: serum Calcium (Ca), Phosphate (P), Alkaline Phosphatase (AP), PTH, vitamin D, FGF23 and Sclerostin. Commercial kits for Sclerostin: ELISA Biomedica, and for FGF23: ELISA Kainos.


eGFR averaged 47±16 ml/min in Tx and 106 ± 15 ml /min in N (p<.001). Table 1 shows mean values of the evaluated parameters (Figura 1). Tx patients had higher PTH, Ca and AP with lower P and 1,25D. Levels of FGF23 were higher than N (47,3±28,8 vs 36,0±11,0 pg/ml, p<.05). Serum levels of Sclerostin were not different between Tx and N (27,6±10,3 vs 28,0±10,0 pmol/l, p: n.s) and were positively correlated with FGF23 in both N (r=.395 p<.05) and Tx (r=.236 p<.05) (Figura 2). A negative correlation with AP was evident in Tx only (r= -.375; p<.05) (Figura 3). Finally, we confirmed a negative correlation between FGF23 and 1,25D both in Tx (r= -.31 p<.05) and in N (r=-.44 p<.05) (Figura 4).


Renal function does not seem to affect serum levels of Sclerostin in Tx. The positive correlation between Sclerostin and FGF23, in both populations, indicates a coordinated osteocyte production of the two proteins. In Tx the negative correlation between Sclerostin and AP clearly points to a negative modulatory role on osteoblastic activity. Further, the negative effect of FGF23 on 1,25D synthesis in both populations is in line with expected results. Therefore, we confirm in Tx the physiologic effects on osteoblasts activity: for Sclerostin (directly through Wnt inhibition); and for FGF23 (indirectly through 1,25D inhibition) (Figura 5). We conclude that serum Sclerostin may be an additional marker of bone metabolism, useful to understand metabolic pathways in normal subjects and in CRF.