Kidney Week

Abstract: SA-PO699

Association of Secondary Hyperparathyroidism with Thymic Atrophy in Patients with CKD

Session Information

• Bone and Mineral Metabolism: Clinical - 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

• Iio, Kenichiro, National Hospital Organization, Osaka Minami Medical Center, Kawachinagano, Japan

Kenichiro Iio,

• Iio, Rei, Osaka General Medical Center, Osaka, Japan

Rei Iio,

• Hamano, Takayuki, Osaka University Graduate School of Medicine, Suita, Japan

Takayuki Hamano,

• Isaka, Yoshitaka, Osaka University Graduate School of Medicine, Suita, Japan

Yoshitaka Isaka,

• Ando, Yutaka, National Hospital Organization, Osaka Minami Medical Center, Kawachinagano, Japan

Yutaka Ando,

Background

Immune aging, including thymic atrophy, is accelerated in patients with chronic kidney disease (CKD) and can lead to cardiovascular and infectious diseases. However, the mechanism of thymic atrophy is not well understood. Mineral and bone disorders (MBD) affect mortality through bone-related factors and blood vessel calcification; parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) also affect immune cells and possibly thymic atrophy.

Methods

We examined the cross-sectional association between thymic atrophy, evaluated as the number of CD3⁺CD4⁺CD45RA⁺CD31⁺ cells [recent thymic emigrants (RTE)/μL], and MBD-related factors (PTH, FGF23, and alkaline phosphatase) in patients with non-dialysis-dependent CKD.

Results

This study enrolled 125 patients with CKD (median eGFR, 17 mL/min/1.73 m²). Age (r = −0.46) and male sex (r = −0.34) correlated negatively and eGFR (r = 0.27) correlated positively with RTE. In terms of MBD-related factors, corrected calcium (r = 0.27) correlated positively whereas PTH (r = −0.36) and alkaline phosphatase (r = −0.20) correlated negatively with RTE. In contrast, FGF23 and phosphorus were not correlated with RTE. Multivariate non-linear regression analysis adjusted for age, sex, eGFR, diabetes, corrected calcium, phosphorus, vitamin D supplementation, and use of phosphate binder indicated a negative association between PTH and log-transformed RTE (P = 0.030, P for non-linearity = 0.124). However, FGF23 and alkaline phosphatase were not associated with RTE.

Conclusion

Secondary hyperparathyroidism appears to be related to thymic atrophy, contributing to immune abnormalities in patients with CKD. Our findings may partially explain the mechanism through which PTH is associated with mortality.