From cross-section to prognosis: risk factors for renal function deterioration in primary hyperparathyroidism
Abstract
Renal dysfunction is an important complication of primary hyperparathyroidism (pHPT). However, the factors associated with a decline in estimated glomerular filtration rate (eGFR) in patients with pHPT have not been fully investigated. This study aimed to identify the factors associated with reduced eGFR at diagnosis in patients with pHPT, and the determinants of longitudinal eGFR decline among those with follow-up data. Eighty-nine patients with pHPT were categorized by renal function at diagnosis. In addition, the annual eGFR decline rate was assessed in 47 patients with more than one year of follow-up. Clinical and biochemical variables were analyzed to determine their association with renal function. Compared with the normal renal function group, the reduced renal function group (eGFR <60 mL/min/1.73 m2) had higher age, and uric acid levels, lower diastolic blood pressure, daily urinary calcium (Ca) excretion, and % tubular reabsorption of phosphate (%TRP). In the multivariable logistic regression analysis, a low %TRP remained significantly associated with reduced renal function at diagnosis. Patients with an eGFR decline faster than –3 mL/min/1.73 m2 per year had significantly higher serum chloride and 25-hydroxyvitamin D levels, and lower HbA1c levels than those with a slower decline. Logistic regression analysis showed, that higher serum chloride levels were associated with a faster annual decline in eGFR. In conclusion, reduced eGFR at pHPT diagnosis was associated with lower %TRP, whereas a faster annual eGFR decline was associated with higher serum chloride levels.
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BibTeX
@article{yamoto2026from,
title = {{From cross-section to prognosis: risk factors for renal function deterioration in primary hyperparathyroidism}},
author = {Takuma Yamoto and Masakazu Notsu and Keizo Kanasaki},
journal = {Endocrine Journal},
year = {2026},
month = aug,
doi = {10.1507/endocrj.ej25-0616},
url = {https://www.jstage.jst.go.jp/article/endocrj/73/8/73_EJ25-0616/_article},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - From cross-section to prognosis: risk factors for renal function deterioration in primary hyperparathyroidism
AU - Takuma Yamoto
AU - Masakazu Notsu
AU - Keizo Kanasaki
PY - 2026
DA - 2026/08/03
JO - Endocrine Journal
DO - 10.1507/endocrj.ej25-0616
UR - https://www.jstage.jst.go.jp/article/endocrj/73/8/73_EJ25-0616/_article
AB - Renal dysfunction is an important complication of primary hyperparathyroidism (pHPT). However, the factors associated with a decline in estimated glomerular filtration rate (eGFR) in patients with pHPT have not been fully investigated. This study aimed to identify the factors associated with reduced eGFR at diagnosis in patients with pHPT, and the determinants of longitudinal eGFR decline among those with follow-up data. Eighty-nine patients with pHPT were categorized by renal function at diagnosis. In addition, the annual eGFR decline rate was assessed in 47 patients with more than one year of follow-up. Clinical and biochemical variables were analyzed to determine their association with renal function. Compared with the normal renal function group, the reduced renal function group (eGFR <60 mL/min/1.73 m2) had higher age, and uric acid levels, lower diastolic blood pressure, daily urinary calcium (Ca) excretion, and % tubular reabsorption of phosphate (%TRP). In the multivariable logistic regression analysis, a low %TRP remained significantly associated with reduced renal function at diagnosis. Patients with an eGFR decline faster than –3 mL/min/1.73 m2 per year had significantly higher serum chloride and 25-hydroxyvitamin D levels, and lower HbA1c levels than those with a slower decline. Logistic regression analysis showed, that higher serum chloride levels were associated with a faster annual decline in eGFR. In conclusion, reduced eGFR at pHPT diagnosis was associated with lower %TRP, whereas a faster annual eGFR decline was associated with higher serum chloride levels.
SN - 1348-4540
SN - 0918-8959
ER -