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

Abstract

Background phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters IIa and IIc. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal control population(P <0.001, r = 0.79). Conclusions Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

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

“…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.…”

“…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.…”

“…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.…”