Role of FGF23 in patients with transfusion-dependent [beta]-thalassemia and hypercalciuria

Alberto Gobbo; Fatima Chamekh; Camilla Alice Cattaneo; Martina Verrienti; Stefano Pizzicotti; Filomena Longo; Zatelli Maria Chiara; Maria Rosaria Ambrosio

doi:10.1530/endoabs.99.RC2.6

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Endocrine Abstracts (2024) 99 RC2.6 | DOI: 10.1530/endoabs.99.RC2.6

ECE2024 Rapid Communications Rapid Communications 2: Calcium and Bone | Part I (6 abstracts)

Role of FGF23 in patients with transfusion-dependent β-thalassemia and hypercalciuria

Alberto Gobbo ¹ , Fatima Chamekh ² , Camilla Alice Cattaneo ¹ , Martina Verrienti ¹ , Stefano Pizzicotti ³ , Filomena Longo ⁴ , Maria Chiara Zatelli ¹ & Maria Rosaria Ambrosio ¹

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¹University of Ferrara, Section of Endocrinology and Internal Medicine, Department of Medical Sciences, Ferrara, Italy; ²University of Ferrara, Ferrara, Italy; ³University Hospital of Ferrara, Laboratorio Unico Provinciale, Ferrara, Italy; ⁴University Hospital of Ferrara, Regional HUB Centre for Thalassaemia and Haemoglobinopathies, Department of Medicine, Ferrara, Italy

Introduction: Patients with transfusion-dependent β-thalassemia (TDT) frequently exhibit elevated urinary calcium excretion, contributing to kidney stone formation and osteoporosis. The underlying mechanism of hypercalciuria in β-thalassemia remains elusive, with FGF23 playing a potential role. FGF23, a bone-derived hormone, primarily acts on the kidneys by inhibiting phosphate reabsorption in the proximal tubules while enhancing calcium uptake in the distal tubules. Few studies have evaluated FGF23 levels in β-thalassemic patients as compared to the general population with contradictory results.

Objective: This study aims to investigate FGF23 levels in patients with TDT and hypercalciuria vs those without.

Methods: Our study included 126 patients referring to the Regional HUB Centre for Thalassaemia and Haemoglobinopathies in Ferrara in 2023. The parameters we assessed are shown in the Table. Hypercalciuria was defined as a 24-hour urinary calcium level ≥4 mg/kg/day. The intact FGF23 polypeptide was quantified using the chemiluminescence immunoassay "LIAISON® FGF 23 test".

Results:


	Normocalciuric	Hypercalciuric
N=126	39 (31%)	87 (69%)
Sex (F/M)	27/12	44/43
	Median [IQR]	Median [IQR]
Age (years)	51 [45; 56]	49 [44; 53]
BMI (kg/m²) *	23.8 [21.4; 26.7]	21.9 [20.2; 24.8]
FGF23 (pg/ml) **	42.6 [30.1; 58.7]	32.5 [23.8; 42.7]
Urinay creatinine (g/day) *	0.9 [0.8; 1.1]	1.1 [0.8; 1.4]
Urinary phosphate (g/day) ***	0.55 [0.3; 0.7]	0.8 [0.6; 1]
Urinary proteins (mg/day)	131 [101; 207]	176 [114; 242]
Calcium (mg/dl)	9.3 [9; 9.7]	9.5 [9.3; 9.8]
Phosphate (mg/dl)	3.6 [3.2; 3.9]	3.5 [3.3; 3.9]
Vitamin D (ng/ml) *	34.9 [27.2; 37.5]	28.8 [19.4; 34.6]
PTH (pg/ml)	28 [21.5; 41.5]	25 [19; 33.8]
Magnesium (mg/dl)	2.2 [2; 2.4]	2.1 [2; 2.3]
Ferritin (ng/ml)	548 [334; 889]	447 [298; 676]
ron (ug/dl)	223.5 [195.8; 272.3]	241 [215.5; 270]
eGFR (ml/min)	91.6 [75; 109]	90.8 [77.1; 116.7]
Creatinine (mg/dl)	0.74 [0.59; 0.89]	0.73 [0.61; 0.9]
Mann-Whitney test was applied. P<0.05; P<0.01; P<0.001**

Conclusions: Hypercalciuric patients exhibited lower FGF23 levels combined with higher urinary creatinine and phosphate levels as compared to normocalciuric patients. This smggests a potential role of FGF23 in the development of hypercalciuria, but additional mechanisms (i.e., renal impairment due to iron overload or chelation therapy) may contribute to the increased phosphate and calcium renal losses in these patients. Further studies are warranted to better explore this issue.