ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2021 and some content may be unavailable. To unlock all content for 2021, please visit the archives.

Abstract: PO0579

Association of Metabolic Acidosis with Impaired Bone Quality

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Levy, Rebecca, Montefiore Medical Center, Bronx, New York, United States
  • Mcmahon, Donald J., Columbia University Irving Medical Center, New York, New York, United States
  • Aponte Farias, Maria A., Columbia University Irving Medical Center, New York, New York, United States
  • Melamed, Michal L., Montefiore Medical Center, Bronx, New York, United States
  • Nickolas, Thomas, Columbia University Irving Medical Center, New York, New York, United States
Background

Chronic kidney disease (CKD) is a state of impaired bone quality and strength, usually presenting as renal osteodystrophy. Metabolic acidosis (MA) is an important complication of CKD that alters bone quality and strength and is associated with increased fracture risk. Few studies have investigated bone tissue-level effects of MA in humans with CKD. We hypothesized that CKD patients with MA would have altered bone-tissue level mineral content.

Methods

This retrospective cross-sectional analysis included 22 patients with eGFR <90 mL/min/1.73m2, including those receiving kidney replacement therapy, recruited from the general nephrology clinics of Columbia University Irvine Medical Center. Patients were considered to have MA for serum bicarbonate ≤22mEq/L. Transiliac crest bone biopsy was assessed for bone formation and mineralization measures from quantitative histomorphometry of tetracycline double labels, tissue mineral density (TMD) by microCT and bone mineral density distribution (BMDD) by quantitative backscatter electron imaging (qBEI). Spearman correlations (ρ) were adjusted for eGFR. Univariate Wilcoxon tests assessed between group differences.

Results

Twelve participants had MA. There were no differences in age, sex or race/ethnicity. After eGFR adjustment, there was a correlation between serum bicarbonate and TMD (ρ=0.60, p=0.004). Bone formation and mineralization measures did not differ. TMD by microCT showed a trend. Measures of calcium content by BMDD differed between groups.

Conclusion

MA is associated with lower TMD and altered calcium content in patients with CKD. Further investigation is needed to determine whether impairments in TMD and BMDD are associated with decreased bone strength and are corrected by bicarbonate supplementation.

 Nonacidotic (HCO3 >22mEq/dL) (n=12)Acidotic (HCO3 ≤22mEq/dL) (n=10)p
microCT
  Tissue Mineral Density1011±43.3973.9±35.80.07
BMDD
 Trabecular
  Camean22.5±0.621.7±0.860.06
  Capeak23.4±0.622.6±0.890.07
  Cawidth3.8±0.354.6±0.680.002
  Calow5.5±1.57.9±3.00.02
  Cahigh12.0±7.88.4±7.00.2
 Cortical
  Camean22.4±0.5821.9±0.860.2
  Capeak23.4±0.5023.0±0.770.2
  Cawidth4.1±0.334.4±0.500.1
  Calow5.8±1.97.4±2.90.3
  Cahigh12.8±5.110.3±7.80.2

Funding

  • NIDDK Support