Sclerostin Blood Levels Before and After Kidney Transplantation

Abstract

Background/Aims: Sclerostin is secreted by osteocytes. As a circulating inhibitor of the Wnt-signaling pathway it inhibits bone formation and contributes to the development of osteoporosis. Sclerostin levels are elevated in patients with chronic kidney disease and end-stage renal disease. Since data for patients after kidney transplantation are scarce, we have prospectively measured sclerostin levels before and during the first year after renal transplantation and have examined the association of sclerostin with parameters of bone mineral metabolism and with bone mineral density. Methods: Sclerostin levels were measured by ELISA in 42 consecutive renal transplant recipients before and at defined intervals in the first year after transplantation. Bone mineral density was measured by dual energy X-ray absorptiometry. Results: Pre-transplant serum sclerostin levels were elevated in all patients (61.8 ± 32.3 pmol/l, normal range 20-30 pmol/l). Within 15 days after transplantation and correlating with the improvement of renal function, sclerostin levels dropped to 21.0 ± 14.7 pmol/l and subsequently increased to 23.8 ± 14.9 and 28.0 ± 16.8 pmol/l after 6 and 12 months, respectively (P<0.001). A linear mixed model indicated that pre-transplant sclerostin levels (P<0.001) and time after transplantation (P<0.001) were the most important predictors for the rise of post-transplant sclerostin levels. No correlation was found between post-transplant sclerostin levels and bone mineral density. Conclusions: The rapid reduction of elevated serum sclerostin levels shortly after kidney transplantation parallels the improvement of renal function, but contrasts with the more delayed improvement of hyperparathyroidism. The normalization of both hormones could contribute to improved bone health after renal transplantation.

Osteoporosis and Impaired Trabecular Bone Score in Hemodialysis Patients

“…At the same time he showed that these markers reflected bone turnover in dialysis patients so that they still had information value in its assessment [28]. Another relatively new marker, sclerostin, studied in progressed CKD or transplanted population [9,29] would be of interest, unfortunately we did not include it into the analyses.…”

From skeletal to cardiovascular disease in 12 steps—the evolution of sclerostin as a major player in CKD-MBD

“…As far as sclerostin is concerned, recent clinical data argue against simple renal retention, since in parallel with increasing serum concentrations, urinary sclerostin concentrations as well as fractional sclerostin excretion also increase with declining renal function (the latter from 0.45±0.26 % in patients with CKD stage 1 to 26±18 % (n=15) in CKD stage 5 (n=19) [47]. Serum levels rapidly return to the normal range following successful renal transplantation [48]. If elevated sclerostin levels are not solely consequential to renal retention, increased production comes into play.…”

Sclerostin Quo Vadis? - Is This a Useful Long-Term Mortality Parameter in Prevalent Hemodialysis Patients?

“…Also the study by Bonani et al showed a dramatic sclerostin decrease after kidney transplantation in patients with ESRD. This effect can predominantly be explained by the improved kidney function [23].…”