The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

Lu, Chien Lin; Yeih, Dong Feng; Hou, Yi; Jow, Guey–Mei; Li, Zong Yu; Liu, Wen-Chih; Zheng, Cai Mei; Lin, Yuh Feng; Shyu, Jia Fwu; Chen, Remy; Huang, Chiou-Jye; Lu, Kuo Cheng

doi:10.3390/nu10121890

Cited by 25 publications

(22 citation statements)

References 130 publications

(155 reference statements)

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“…Uremic hyperparathyroidism (uHPT) is a common complication of end-stage chronic kidney disease (CKD), including secondary hyperparathyroidism (SHPT) and tertiary hyperparathyroidism (THPT) [1]. In CKD progression, both hyperphosphatemia and 1,25-dihydroxy vitamin D deficiency cause hypocalcemia and stimulate parathyroid hormone (PTH) secretion from the parathyroid gland, called SHPT [2]. SHPT patients remain in a stage of HPT 1 year after receiving a kidney transplantation, called THPT [3,4].…”

Section: Introductionmentioning

confidence: 99%

The role of 18F-FCH PET/CT in patients with uremic hyperparathyroidism compared with 99mTc-sestaMIBI SPECT/CT and ultrasonography

Xia

et al. 2019

EJNMMI Res

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Background: The aim of this study was to evaluate the diagnostic efficacy of 18 F-fluorocholine ( 18 F-FCH) PET/CT for uremic hyperparathyroidism (uHPT) compared to 99m Tc-sestaMIBI SPECT/CT and ultrasonography (US). Methods: A total of 17 uHPT patients with stage 5 chronic kidney disease (CKD) were prospectively enrolled. All patients underwent US, 99m Tc-sestaMIBI SPECT/CT, and 18 F-FCH within 2 months and received surgical treatment. Visual and quantitative methods were used for image analyses. Intraoperative localization and postoperative histological results of the reference standard as well as the sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) of the three modalities were analyzed using Pearson's χ 2 tests. In addition, the diagnostic efficacy of 18 F-FCH PET/CT for uHPT was evaluated. The relationships between PET parameters and laboratory parameters were assessed using the Spearman correlation coefficient.Results: A total of 63 parathyroid hyperplasia lesions were resected in 17 uHPT patients, and 53 lesions were detected using 18 F-FCH PET/CT with no false-positive results. The sensitivity, specificity, accuracy, PPV, and NPV were 84.13%, 100%, 86.49%, 100%, and 52.38%, respectively. In comparison, the corresponding values for 99m Tc-sestaMIBI SPECT/CT and US were 63.49%, 90.91%, 67.57%, 97.56%, and 30.30% and 61.90%, 81.82%, 64.86%, 95.12%, and 27.27%, respectively. The volume of hyper-functioning parathyroid glands was significantly different between lesions positive in 18 F-FCH PET/CT and negative in 18 F-FCH PET/CT (mean volume 1.36 ± 0.55 cm 3 vs. 0.83 ± 0.26 cm 3 ; P = 0.019). US misidentified intrathyroidal parathyroid hyperplasia as thyroid nodules in three patients, while 18 F-FCH PET correctly identified the anatomy. No significant associations were observed between PET parameters and laboratory parameters in uHPT.Conclusion: 18 F-FCH PET/CT was more sensitive and accurate for uHPT than 99m Tc-sestaMIBI SPECT/CT and US, and had better preoperative diagnostic efficacy, particularly for lesions diagnosed as a thyroid nodule by US.

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Section: Introductionmentioning

confidence: 99%

The role of 18F-FCH PET/CT in patients with uremic hyperparathyroidism compared with 99mTc-sestaMIBI SPECT/CT and ultrasonography

Xia

et al. 2019

EJNMMI Res

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“…A vitamin D deficiency is a common condition associated with kidney disease. Many clinical studies have highlighted how a vitamin D deficiency is an important risk factor for CKD patients [36, 37].…”

Section: Resultsmentioning

confidence: 99%

Inflammation-Related Patterns in the Clinical Staging and Severity Assessment of Chronic Kidney Disease

et al. 2019

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Chronic kidney disease (CKD) is an irreversible loss of kidney function, and it represents a major global public health burden due to both its prevalence and its continuously increasing incidence. Mineral bone disorders (MBDs) constitute a hallmark of CKD, and alongside cardiovascular complications, they underlie a poor prognosis for these patients. Thus, our study focused on novel CKD biomarker patterns and their impact on the clinical staging of the disease. As a first testing approach, the relative expression levels of 105 proteins were assessed by the Proteome Profiler Cytokine Array Kit for pooled CKD stage 2–4 serum samples to establish an overall view regarding the proteins involved in CKD pathogenesis. Among the molecules that displayed significant dysregulation in the CKD stages, we further explored the involvement of Dickkopf-related protein 1 (Dkk-1), a recognised inhibitor of the Wnt signalling pathway, and its crosstalk with 1,25OH2D3 (calcitriol) as new players in renal bone and vascular disease. The serum levels of these two molecules were quantified by an ELISA (76 samples), and the results reveal decreasing circulating levels of Dkk-1 and calcitriol in advanced CKD stages, with their circulating expression showing a downward trend as the CKD develops. In the next step, we analysed the inflammation and MBD biomarkers' expression in CKD (by xMAP array). Our results show that the molecules involved in orchestrating the inflammatory response, interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFα), as well as the mineral biomarkers osteoprotegerin (OPG), osteocalcin (OC), osteopontin (OPN), and fibroblast growth factor 23 (FGF-23), correlate with Dkk-1 and calcitriol, raising the possibility of them being potential useful CKD biomarkers. These results reveal the impact of different biomarker patterns in CKD staging and severity, thus opening up novel approaches to be explored in CKD clinical management.

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“…При хронічній хворобі нирок, коли частково блокується активація вітаміну D, крім альфа-форм 1,25(OH) 2 D 3 , необхідно паралельно використовувати стандартні дози вітаміну 25(OH)D 3 , тобто проводити комбіновану терапію гіперпаратиреозу для досягнення більшої ефективності. Протеїнуричні захворювання нирок призводять до гіповітамінозу D через втрату з сечею білка, який зв'язує вітамін D, а також метаболітів вітаміну D [12]. Підвищені рівні паратгормону при вторинному гіперпаратиреозі викликають швидку деградацію 25(OH)D до неактивних метаболітів за рахунок активації ферменту 24,25-дигідроксилази [12].…”

Section: рисунок 2 дозування вітаміну Dunclassified

Vitamin D dosage

Kaminskyi

2022

Mìžnarodnij endokrinologìčnij žurnal

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Despite its historical name, vitamin D is not a vitamin at all but a hormone that, when activated, is a metabolically active steroid fat-soluble hormone that acts on cellular receptors. Vitamin D hormone is synthesized endogenously and then metabolized in the body, provi-ding that there are the necessary precursors and some factors — the effects of ultraviolet light on the skin. At the same time, vitamins themselves are nutrients, co-factors of biochemical reactions that are not synthesized in the body and cannot interact with receptors, consumed with food, so the hormone D is not a vitamin. Disputes about its use and dosage continue throughout the study period of vitamin D hormone. Most reputable experts in Europe and the USA support the need to replenish and maintain a normal level of vitamin D, believing it to be completely safe and useful. In 2011, the US Endocrine Society issued clinical practice guidelines for vitamin D, indicating that the desired serum concentration of 25(OH)D is > 75 nmol/l (> 30 ng/ml) to achieve the maximum effect of this vitamin on calcium metabolism, bone, and muscle metabolism. According to them, for a consistent increase in serum 25(OH)D above 75 nmol/l (30 ng/ml), adults may require at least 1,500-2,000 IU/day of additional vitamin D, at least 1,000 IU/day in children and adolescents. The most common form of thyroid dysfunction is secondary hyperparathyroidism, which develops due to vitamin D defect/deficiency (80–90 %). Non-optimal serum concentrations of 25(OH)D lead to secondary hyperparathyroidism, potentially leading to decreased bone mineralization and, ultimately, to an increased risk of osteopenia, osteoporosis and fractures, cardiac arrhythmia, and increased blood pressure. Vitamin D is most commonly used at a star-ting dose of 5,000 IU daily for 2–3 months, then transferring patients to maintenance doses of 2,000–4,000 IU/day daily that are consi-dered safe. However, it should be noted that some patients will need constant administration of 5,000 IU of vitamin D per day for a long time (years) to maintain the target optimal level of 25(OH)D in the blood, especially in patients with normocalcemic forms of secondary hyperparathyroidism.

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The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

Cited by 25 publications

References 130 publications

The role of 18F-FCH PET/CT in patients with uremic hyperparathyroidism compared with 99mTc-sestaMIBI SPECT/CT and ultrasonography

The role of 18F-FCH PET/CT in patients with uremic hyperparathyroidism compared with 99mTc-sestaMIBI SPECT/CT and ultrasonography

Inflammation-Related Patterns in the Clinical Staging and Severity Assessment of Chronic Kidney Disease

Vitamin D dosage

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