Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki, Forough; Kassaee, Seyed Reza; Salehifar, Azita

doi:10.1186/s12882-020-01826-5

Cited by 16 publications

(9 citation statements)

References 66 publications

(67 reference statements)

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“…All patients with hypoparathyroidism had routine follow-up by one proficient endocrinologist and treated by appropriate doses of calcium carbonate (500 mg tablet, Toliddaru pharmaceutical, Tehran, Iran), plus calcitriol (0.25 μg capsule, Zahravi Pharmaceuticals, Tehran, Iran). The range of daily dose of calcitriol was 0.5-2.5 μg/day to correct serum calcium [5,28]. The majority of transfusion-dependent thalassemia patients received routine blood transfusion therapy every 3-4 weeks to maintain their hemoglobin levels at 9-10.5 g/dL.…”

Section: Methodsmentioning

confidence: 99%

“…Serum intact FGF23 (pg/mL) and 1,25(OH)2D3 (pg/mL) was analyzed by ELISA method using an ELISA kit, (Bioassay Technology, Spain). Sensitivity, intra-and inter-assay CVs of all kits was the same as our previous published article [28]. Serum ferritin levels were recorded on an E 170 analyzer (Roche Diagnostics, Germany) by Electrochemiluminescence's Immunoassay (ECLIA) method.…”

Section: Methodsmentioning

confidence: 99%

“…In our previous case-control study, we evaluated FGF23 function in hypoparathyroid patients compared to a healthy population, and we find that although the FGF23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF23 [28]. The aim of this study was to evaluate the association of ferritin, intact PTH, FGF23, and l,25(OH)2D3 in patients with major thalassemia having normal parathyroid function and hypoparathyroidism.…”

Section: Introductionmentioning

confidence: 99%

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Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

et al. 2020

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Background FGF23 controls serum l,25(OH)2D3 levels and phosphate homeostasis. This study evaluates the effects of ferritin on intact PTH, FGF23, and l,25(OH)2D3 in patients with major thalassemia. It also evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH functioning in human. Methods In this case-control study, 25 major-beta thalassemia patients with hypoparathyroidism were age- and gender-matched with major-beta thalassemia patients having normal parathyroid function. Biochemical studies assessed the serum calcium, albumin, phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH) D, 1,25(OH)2D3, ferritin, and the fractional excretion of phosphorous. Results FGF23 was higher in the patients with hypoparathyroidism than the controls (P = 0.002). The fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of FGF23 (P = 0.001). There was a correlation between serum 1,25(OH)2D3 and FGF23 with ferritin in the controls (P = < 0.001and P = < 0.001, respectively). Conclusions The present study showed a strong positive correlation between serum ferritin and levels of FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have a stimulatory effect on the production of 1,25(OH)2D3. Moreover, a rise in FGF23 in patients with thalassemia, might be either associated with the stimulating effect of PTH and 1,25(OH)2D3, or directly related to the stimulating effect of ferritin.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

et al. 2020

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“…Meanwhile, klotho production is downregulated, so that less FGF-23 binds to its receptor in the kidney, 16,17 less 1 alpha-hydroxylase and active vitamin D are produced, and more phosphate is reabsorbed in the proximal convoluted tubule. 18,19 As chronic kidney disease progresses to its end stage, FGF-23 levels keep getting higher, and the elevation is accompanied by other calcium-phosphate axis derangements such as excess PTH release, decreased 1,25-dihydroxycholecalciferol, and increased sclerostin (an inhibitor of bone formation). 20,21 Together, these derangements lead to the clinical manifestations described below.…”

Section: ■ Calcium-phosphate Axis Derangementsmentioning

confidence: 99%

Extraosseous calcification in kidney disease

Bartolomeo

Tan

Fatica

2022

CCJM

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A consequence of chronic and end-stage kidney disease is a higher risk of calcium deposition in sites other than the bones. The authors of this review outline current understanding of the pathogenesis, presentation, diagnosis, and treatment of this group of disorders. KEY POINTSExtraosseous calcifi cation is a broad term that encompasses vascular calcifi cation, soft tissue calcifi cation, and calciphylaxis, all of which are seen in patients with end-stage kidney disease.The pathogenesis of extraosseous calcifi cation is an active process involving a complex interplay of abnormal electrolyte levels, cell differentiation, and dysregulation of many biochemical pathways.Vascular calcifi cation is predominantly diagnosed incidentally, while soft tissue calcifi cation and calciphylaxis are diagnosed on the basis of radiographic and clinical presentation, sometimes requiring biopsy.Management is based on low-quality evidence and includes maintaining a neutral calcium balance, correcting hyperphosphatemia, and controlling comorbidities. Surgical and other nonmedical therapies may help somewhat in managing calciphylaxis and soft tissue manifestations.

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“…Increasing serum levels of 1,25(OH)2D3 and calcium decrease PTH secretion, while increasing serum phosphate levels increase PTH secretion [ 25 ]. In addition to PTH, phosphate levels are mainly regulated by FGF-23, 1,25(OH)2D3, Klotho, and dietary phosphate [ 3 , 22 , 26 , 27 ], while calcitonin also affects phosphate levels [ 4 , 5 ]. PTH, FGF-23, and Klotho decrease serum phosphate levels (by inhibiting renal phosphate reabsorption), while 1,25(OH)2D3 increases serum phosphate levels (by increasing renal phosphate reabsorption, phosphate absorption from the intestine, and phosphate release from the bones) [ 2 , 22 ].…”

Section: Involvement Of Pth and Calcitonin In The Regulation Of Calcium And Phosphate Levelsmentioning

confidence: 99%

Environmental Factors That Affect Parathyroid Hormone and Calcitonin Levels

Leko

Pleić

Gunjača

et al. 2021

IJMS

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Calciotropic hormones, parathyroid hormone (PTH) and calcitonin are involved in the regulation of bone mineral metabolism and maintenance of calcium and phosphate homeostasis in the body. Therefore, an understanding of environmental and genetic factors influencing PTH and calcitonin levels is crucial. Genetic factors are estimated to account for 60% of variations in PTH levels, while the genetic background of interindividual calcitonin variations has not yet been studied. In this review, we analyzed the literature discussing the influence of environmental factors (lifestyle factors and pollutants) on PTH and calcitonin levels. Among lifestyle factors, smoking, body mass index (BMI), diet, alcohol, and exercise were analyzed; among pollutants, heavy metals and chemicals were analyzed. Lifestyle factors that showed the clearest association with PTH levels were smoking, BMI, exercise, and micronutrients taken from the diet (vitamin D and calcium). Smoking, vitamin D, and calcium intake led to a decrease in PTH levels, while higher BMI and exercise led to an increase in PTH levels. In terms of pollutants, exposure to cadmium led to a decrease in PTH levels, while exposure to lead increased PTH levels. Several studies have investigated the effect of chemicals on PTH levels in humans. Compared to PTH studies, a smaller number of studies analyzed the influence of environmental factors on calcitonin levels, which gives great variability in results. Only a few studies have analyzed the influence of pollutants on calcitonin levels in humans. The lifestyle factor with the clearest relationship with calcitonin was smoking (smokers had increased calcitonin levels). Given the importance of PTH and calcitonin in maintaining calcium and phosphate homeostasis and bone mineral metabolism, additional studies on the influence of environmental factors that could affect PTH and calcitonin levels are crucial.

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Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Cited by 16 publications

References 66 publications

Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

Extraosseous calcification in kidney disease

Environmental Factors That Affect Parathyroid Hormone and Calcitonin Levels

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