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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

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High-serum phosphate and parathyroid hormone distinctly regulate bone loss and vascular calcification in experimental

Natalia Carrillo-López1, Sara Panizo1, Cristina Alonso-Montes1

  • 1Bone and Mineral Research Unit, Hospital Universitario Central de Asturias, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), REDinREN-ISCIII, Oviedo, Spain.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|September 7, 2018
PubMed

Insights

In chronic kidney disease (CKD), high parathyroid hormone (PTH) worsens vascular calcification and bone loss. Lowering PTH in hyperphosphatemic rats reduced vascular calcium and bone loss by inhibiting osteogenic differentiation.

Area of Science:

  • Nephrology
  • Endocrinology
  • Vascular Biology

Background:

  • Chronic kidney disease (CKD) is associated with elevated serum phosphate and parathyroid hormone (PTH).
  • These elevations contribute to vascular calcification (VC) and bone loss.
  • Distinguishing the specific roles of high phosphorus (HP) and PTH in these complications is crucial.

Purpose of the Study:

  • To investigate the individual contributions of high phosphorus (HP) and elevated parathyroid hormone (PTH) to vascular calcification (VC) and bone loss in a rat model of CKD.
  • To elucidate the molecular mechanisms underlying these contributions.

Main Methods:

  • Nephrectomized rats were fed a high phosphorus (HP) diet.
  • Rats underwent either sham operation or parathyroidectomy with PTH 1-34 supplementation to normalize serum PTH levels.
  • Vascular and bone tissues were analyzed for calcification and resorption markers.
  • Vascular smooth muscle cells (VSMCs) were studied in vitro.

Main Results:

  • Parathyroidectomy with PTH 1-34 supplementation significantly reduced aortic calcium by 80% in uraemic rats, attenuating osteogenic differentiation and increasing sclerostin.
  • Bone loss was prevented by attenuating bone resorption and increasing Wnt inhibitors.
  • Serum calcitriol decreased by 70% despite reduced FGF23, challenging FGF23's role in calcitriol regulation.
  • In vitro, high PTH enhanced VSMC calcification, while low PTH attenuated it via PTH1R signaling.

Conclusions:

  • In hyperphosphatemic CKD, inadequate suppression of high PTH exacerbates HP-induced osteogenic VSMC differentiation.
  • High PTH also reduces vascular sclerostin levels, a key inhibitor of calcification.
  • These findings highlight the detrimental role of excessive PTH in CKD-related vascular and bone pathology.
Abstract

Keywords:
gene expressionmineral metabolismparathyroidectomyrenal osteodystrophyvascular calcification

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