Fibroblast growth Factor-23 in pre-dialysis chronic kidney disease patients and its correlation with carotid artery calcification

Tarun Kumar; Smita Mohanty; Anita Rani; Amita Malik; Rajesh Kumar; Gaurav Bhashker

doi:10.4103/ijn.IJN_506_20

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ORIGINAL ARTICLE

Year : 2022 | Volume : 32 | Issue : 6 | Page : 560-566

Fibroblast growth Factor-23 in pre-dialysis chronic kidney disease patients and its correlation with carotid artery calcification

Tarun Kumar¹, Smita Mohanty², Anita Rani³, Amita Malik⁴, Rajesh Kumar¹, Gaurav Bhashker¹
¹ Department of Nephrology, V.M.M.C. and Safdarjung Hospital, New Delhi, India
² Department of Medicine, V.M.M.C. and Safdarjung Hospital, New Delhi, India
³ Department of Biochemistry, V.M.M.C. and Safdarjung Hospital, New Delhi, India
⁴ Department of Radiodiagnosis, V.M.M.C. and Safdarjung Hospital, New Delhi, India

Correspondence Address:
Rajesh Kumar
Associate Professor, Department of Nephrology, V.M.M.C. and Safdarjung Hospital, New Delhi
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/ijn.IJN_506_20

Introduction: Fibroblast growth factor 23 (FGF-23) is a phosphate metabolism regulator in patients with chronic kidney disease (CKD). The present study is aimed to examine the FGF-23 level in pre-dialysis patients with CKD and its correlation with carotid artery calcification (CAAC). Methods: This cross-sectional study included patients with CKD and controls. The patients were compared with controls having similar distribution of age and sex to determine serum FGF-23 level in Indian healthy adult population. Detailed medical history, physical examination, and investigations were done for each patient. Atherosclerotic risk factors, cardiovascular comorbidities, and drug history were recorded. Carotid calcification was observed using carotid ultrasound. Results: In total, 62 patients with a mean age of 50.0 years were enrolled. Majority of the patients had hypertension (66.1%), followed by diabetes (27.4%) and dyslipidemia (3.2%). Mean serum corrected calcium levels were significantly higher in patients with CAAC compared to the patients without CAAC (9.21 ± 1.34 vs. 8.53 ± 0.93 mg/dL; P = 0.014). The FGF-23 levels were significantly higher in patients with CAAC compared to those without CAAC (396.0 vs. 254.0 pg/mL; P = 0.008). CAAC was found to be present in both early and late stages of CKD. Multivariate analysis showed that log FGF-23 and serum corrected calcium remained as independent determinants of CAAC. The prevalence of CAAC increased with the ascending quartiles of FGF23. Conclusion: In conclusion, FGF-23 was found to be independently associated with CAAC in CKD.

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