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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Among patients with chronic kidney disease (CKD) at predialysis stage, secondary hyperparathyroidism is highly prevalent. Metabolic alterations related to secondary hyperparathyroidism contribute to the development of renal osteodystrophy, characterized by osteitis fibrosa, ectopic calcification, cardiovascular complications, and increased mortality risk. Serum parathyroid hormone levels are influenced by various nutritional factors. Non-dialyzed CKD patients are particularly susceptible to vitamin C deficiency due to dietary restrictions and malnutrition. Vitamin C, an essential antioxidant, plays a key role in bone development and maintenance. However, the relationship between vitamin C deficiency and parathyroid hormone secretion remains unclear. In this study, we conducted a single-center cross-sectional analysis to investigate the association between serum vitamin C levels and parathyroid hormone concentrations in non-dialyzed CKD patients.
From January 2013 to November 2017, a total of 280 consecutive patients underwent serum vitamin C and intact parathyroid hormone (iPTH) measurements for screening purposes. After excluding 152 patients due to vitamin C or vitamin D supplementation, age under 20 years, dialysis treatment, positive serostatus for HIV, hepatitis B or C, chronic infection, or malignancy, 128 patients (mean age 71 ± 12 years; 80 males) with an estimated glomerular filtration rate (eGFR) consistently below 60 mL/min/1.73 m² were included in the analysis.
Vitamin C levels were below 2.0 μg/mL (a range indicative of severe deficiency) in 23% of patients (n=29), between 2.0 and 5.5 μg/mL in 53% (n=68), and above 5.5 μg/mL (the upper limit of normal in healthy individuals) in 24% (n=31). Log(iPTH) showed significant correlations with age (r=-0.238, p=0.00672), log(eGFR) (r=-0.625, p<0.0001), serum calcium (r=-0.609, p<0.0001), and serum phosphate (r=0.41, p<0.0001), and exhibited a trend toward correlation with serum albumin (r=-0.146, p=0.101). Patients with low serum vitamin C levels had significantly higher serum iPTH concentrations (p=0.0005, one-way ANOVA). In a multiple linear regression model with log(iPTH) as the dependent variable and age, sex, log(eGFR), serum calcium, phosphate, albumin, and vitamin C as independent variables, the inverse association between log(iPTH) and serum vitamin C was confirmed (R²=0.568, adjusted R²=0.543, p<0.0001), along with other significant predictors including age, log(eGFR), serum calcium, and phosphate. Low vitamin C levels were also associated with increased serum alkaline phosphatase (r=-0.209, p=0.0179), a further indicator of the impact of vitamin C status on bone metabolism.
Vitamin C deficiency is common among non-dialyzed patients with CKD. Beyond minerals, reduced vitamin C levels may contribute to the development of secondary hyperparathyroidism, thereby promoting increased bone turnover. This novel finding may be attributable to the effects of vitamin C on vitamin D metabolism, vitamin D binding within target tissues, and cyclic AMP-mediated signaling pathways in bone and the parathyroid gland. Future research may reveal a critical interplay between vitamin C and parathyroid hormone–associated signaling pathways, potentially uncovering mechanisms of clinical and therapeutic significance.
