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Purpose <p>Parathyroid hormone controls calcium and phosphate metabolism. The latter is also regulated by both FGF23 and 1–25(OH)<sub>2</sub>VitaminD. The polymorphic variant c.716 C &gt; T of the <i>FGF23</i> gene was previously found to be associated with renal phosphate leak/nephrolithiasis. The aim of our research is to study the metabolism of phosphate in a cohort of patients with primary hyperparathyroidism (PHPT) and its impact on bone and kidney.</p> Methods <p>We have retrospectively compared a large sample of sporadic PHPT patients (339) with historical comparison cohort (HCC 503: Olivetti Study Group and Siena Osteoporosis Study). Moreover, in 51 PHPT patients, phosphate metabolism indexes were also revaluated at least 2 years after surgical cure. The variant c.716 C &gt; T of the <i>FGF23</i> gene was genotyped in patients and in a small sample of the control group.</p> Results <p>In PHPT patients we found higher levels of serum calcium, PTH, alkaline phosphatase, beta-C-terminal telopeptide (CTx), urinary calcium, while serum phosphate, 25OH-VitaminD, maximal tubular renal phosphate reabsorption adjusted for glomerular filtration rate (TmPO4/GFR) were lower than what was found in HCC. In PHPT patients fibroblast growth factor 23 (FGF23) levels were higher than in controls. Patients with kidney stones carried the 716 T allele more frequently than patients without it (χ<sup>2</sup> 7.20, p = 0.027). In PHPT patients revaluated at least 2 years after surgery, we observed a significant reduction of 1–25(OH)<sub>2</sub>VitaminD and FGF23. According to the median of serum phosphate levels, PHPT patients were subdivided into two subgroups: ≤2.8 mg/dL and &gt; 2.8 mg/dL. The lowest phosphate group had a significantly higher serum calcium, PTH, 1–25(OH)<sub>2</sub>VitaminD, urinary calcium and a higher prevalence of kidney stones than in the highest phosphate group. The rate of males in the lowest phosphate group was significantly higher than in the highest phosphate group.</p> Conclusion <p>Our study shows that the regulators of phosphate metabolism in PHPT patients are higher than controls and they significantly reduce after surgical cure. PHPT patients with low serum phosphate have a worse biochemical and clinical phenotype.</p>

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Phosphate metabolism in primary hyperparathyroidism: a real-life long-term study

  • 期刊论文

  • 发表日期：

    2025年2月11日

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  • Carla Columbu,
  • Domenico Rendina,
  • Luigi Gennari,
  • Flavia Pugliese,
  • Vincenzo Carnevale,
  • Antonio Stefano Salcuni,
  • Iacopo Chiodini,
  • Claudia Battista,
  • Patrizia Tabacco,
  • Vito Guarnieri,
  • Giuseppe Guglielmi,
  • Cristina Eller-Vainicher,
  • Cristiana Cipriani,
  • Antonello Cuttitta,
  • Gianpaolo De Filippo,
  • Fernanda Velluzzi,
  • Alberto Falchetti,
  • Salvatore Minisola,
  • Afredo Scillitani,
  • Fabio Vescini

摘要

Purpose

Parathyroid hormone controls calcium and phosphate metabolism. The latter is also regulated by both FGF23 and 1–25(OH)2VitaminD. The polymorphic variant c.716 C > T of the FGF23 gene was previously found to be associated with renal phosphate leak/nephrolithiasis. The aim of our research is to study the metabolism of phosphate in a cohort of patients with primary hyperparathyroidism (PHPT) and its impact on bone and kidney.

Methods

We have retrospectively compared a large sample of sporadic PHPT patients (339) with historical comparison cohort (HCC 503: Olivetti Study Group and Siena Osteoporosis Study). Moreover, in 51 PHPT patients, phosphate metabolism indexes were also revaluated at least 2 years after surgical cure. The variant c.716 C > T of the FGF23 gene was genotyped in patients and in a small sample of the control group.

Results

In PHPT patients we found higher levels of serum calcium, PTH, alkaline phosphatase, beta-C-terminal telopeptide (CTx), urinary calcium, while serum phosphate, 25OH-VitaminD, maximal tubular renal phosphate reabsorption adjusted for glomerular filtration rate (TmPO4/GFR) were lower than what was found in HCC. In PHPT patients fibroblast growth factor 23 (FGF23) levels were higher than in controls. Patients with kidney stones carried the 716 T allele more frequently than patients without it (χ2 7.20, p = 0.027). In PHPT patients revaluated at least 2 years after surgery, we observed a significant reduction of 1–25(OH)2VitaminD and FGF23. According to the median of serum phosphate levels, PHPT patients were subdivided into two subgroups: ≤2.8 mg/dL and > 2.8 mg/dL. The lowest phosphate group had a significantly higher serum calcium, PTH, 1–25(OH)2VitaminD, urinary calcium and a higher prevalence of kidney stones than in the highest phosphate group. The rate of males in the lowest phosphate group was significantly higher than in the highest phosphate group.

Conclusion

Our study shows that the regulators of phosphate metabolism in PHPT patients are higher than controls and they significantly reduce after surgical cure. PHPT patients with low serum phosphate have a worse biochemical and clinical phenotype.