ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: SA-PO471

Bone and Circulating Sclerostin and Histomorphometry in Pediatric Patients with CKD

Session Information

  • Pediatric Nephrology - II
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Laster, Marciana, University of California Los Angeles, Los Angeles, California, United States
  • Pereira, Renata C., University of California, Los Angeles, California, United States
  • Gales, Barbara, University of California Los Angeles, Los Angeles, California, United States
  • Salusky, Isidro B., Mattel Children's Hospital, Los Angeles, California, United States
Background

Serum sclerostin, a bone formation inhibitor, increases in CKD but little is known of its role in predicting turnover and mineralization states in pediatric renal osteodystrophy.

Methods

Serum sclerostin was measured in a group of 58 dialysis and 35 pre-dialysis CKD patients at the time of iliac crest bone biopsy. Sclerostin expression in bone biopsy specimens was quantified using immunohistochemistry (IHC). Spearman correlations and multivariable linear regression analyses were performed to determine the relationship between serum and bone sclerostin levels and parameters of the TMV bone classification system. Models were controlled for gender and PTH-two well-known confounders of serum sclerostin.

Results

Cohort characteristics are presented in Table 1. Median serum sclerostin levels were higher in the dialysis vs. CKD patients; although IHC expression was no different (Table 2). In dialysis patients, significant correlations (p<0.05) included sclerostin with osteoid thickness (OTH, r=-0.27), osteoid volume (OV/BV, r=-0.26) and osteoid surface (OS/BS, r=-0.26). These relationships were lost after adjustment for gender and PTH. In CKD patients, significant correlations included serum sclerostin with bone formation rate (BFR/BS, r=-0.37) and eroded surface (ES/BS, r=-0.48). Both relationships persisted after adjustment resulting in sclerostin predicting 3% lower BFR/BS and 2% lower ES/BS for every unit increase in sclerostin (p=0.03 and p=0.01, respectively). Bone expression of sclerostin predominated in cortical areas and likely for this reason failed to correlate with trabecular TMV parameters.

Conclusion

The association of serum sclerostin with bone histomorphometry varies across the spectrum of GFR. The association of sclerostin with bone turnover in CKD patients is consistent with descriptions of Wnt antagonism as an early determinant of bone turnover in CKD. Such findings may have potential therapeutic implications in CKD-MBD.

Funding

  • NIDDK Support