Fibroblast growth factor 23 and lipid metabolism association in chronic kidney disease

  • M. I. Chaikovska HSME «I. Horbachevsky Ternopil State Medical University»
  • L. P. Martynyuk HSME «I. Horbachevsky Ternopil State Medical University»
Keywords: chronic kidney disease, mineral metabolism, fibroblast growth factor 23, lipid metabolism


Recent scientificstudies have demonstrated the effect of fibroblast growth factor 23 (FGF-23) on the volume and distribution of body fat. The aim of our study was to investigate of lipid metabolism in patients with chronic kidney disease (CKD) and its relationship with FGF-23.

Methods. We conducted a single-center, cohort retrospective study involved 106 patients with CKD 1-5 stages. Among the patients were 47 women (44%) and 59 men (56%) aged (49.6±13.9) years. All patients were determined the blood lipid spectrum: total cholesterol level (LDL), high density lipoproteins (HDL) and triglycerides (TG). The lipid profile was examined using a biochemical analyzer Cobas Integra 400 Plus. The C-terminal FGF-23 fragment was determined using a set of reagents for the enzyme immunoassay “Biomedica” (Astria). The glomerular filtration rate (GFR) was calculated using the CKD EPI formula (KDIGO 2012). All the statistical analyses were performed using Statistica 10.0.

Results. In patients with CKD, progressive decrease in the level of total cholesterol, LDL cholesterol, HDL cholesterol and the increase in TG concurrent with the fall in GFR was detected (p<0.001). The concentration of the C-terminal FGF-23 fragment progressively increased in parallel with the fall in GFR, reaching the highest values at CKD stage 5 (p<0.001). A significant relationship was found between FGF-23 and total cholesterol (r =-0.45, p<0.05), LDL (r=-0.29, p<0.05), HDL (r=-0.54, p<0.05), FGF-23 and TG (r=0.28, p<0.05).

Conclusions. CKD is characterized by a significant growth in TG levels, which increases with progression of renal dysfunction. The level of FGF-23 in CKD steadily increases in parallel with the decrease in GFR. The parameters of lipid metabolism, namely, total cholesterol, LDL, TG and HDL, have a reliable relationship with FGF-23 in CKD.


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Kottgen A, Russell SD, Loehr LR, Crainiceanu CM, Rosamond WD, Chang PP, et al. Reduced kidney function as a risk factor for incident heart failure: The atherosclerosis risk in communities (ARIC) study. J Am Soc Nephrol. 2007;18 (4):1307-15. doi: 10.1681/ASN.2006101159.

Dhingra R, Gaziano JM, Djoussé L. Chronic kid- ney disease and the risk of heart failure in men. Circ Heart Fail. 2011;4(2):138-44. doi: 10.1161/ CIRCHEARTFAILURE.109.899070.

Scialla JJ, Xie H, Rahman M,  Anderson  AH, Isakova T, Ojo A, et al. Fibroblast Growth Factor-23 and Cardiovascular Events in CKD.  J Am Soc Nephrol. 2014; 25(2):349-60. doi: 10.1681/ ASN.2013050465.

Okada S, Yoshida T, Hong Z, Ishii G, Hatano M, Kuro-o M, et al. Impairment of B lymphopoiesis in precocious aging (klotho) mice. Int Immunol. 2000;12(6):861-71. doi: 10.1093/intimm/12.6.861.

Streicher C, Zeitz U, Andrukhova O, Rupprecht A, Pohl E, Larsson TE, et al. Long-term Fgf23 de- ficiency does not influence aging, glucose ho- meostasis, or fat metabolism in mice with a non- functioning vitamin D receptor. Endocrinology. 2012;153(4):1795-805.  doi:  10.1210/en.2011-1878.

Mirza MA, Alsio J, Hammarstedt A, Erben RG, Micha elsson K, Tivesten A, et al. Circulating fi- broblast growth Factor-23 is associated with fat mass and dyslipidemia in two independent co- horts of elderly individuals. Arterioscler Thromb Vasc Biol. 2011;31(1):219-27. doi: 10.1161/ ATVBAHA.110.214619.

Gutierrez OM, Wolf M, Taylor EN. Fibroblast growth factor 23, cardiovascular disease risk fac- tors, and phosphorus intake in the health profes- sionals followup study. Clin J Am Soc Nephrol. 2011;6(12):2871-8.  doi:  10.2215/CJN.02740311.

Ali FN, Falkner B, Gidding SS, Price HE, Keith SW, Langman CB. Fibroblast growth factor-23 in obese, normotensive adolescents is associated with adverse cardiac structure. J Pediatr. 2014;165(4): 738-43. doi:  10.1016/j.jpeds.2014.06.027.

Grethen E, Hill KM, Jones R, Cacucci BM, Gupta CE, Acton A, et al. Serum leptin, parathyroid hormone, 1,25-dihydroxyvitamin D, fibroblast growth fac- tor 23, bone alkaline phosphatase, and sclerostin relationships in obesity. J Clin Endocrinol Metab. 2012;97(5):1655-62.  doi:  10.1210/jc.2011-2280.

Abbas  MA.  Physiological  functions  of  vitamin D   in  adipose  tissue.  J  Steroid  Biochem  Mol Biol. 2017;165(Pt B):369-381. doi: 10.1016/j.js- bmb.2016.08.004.

Tsuji K, Maeda T, Kawane T, Matsunuma A, Horiuchi N. Leptin stimulates fibroblast growth factor 23 expression in bone and suppresses re- nal 1alpha,25-dihydroxyvitamin D3 synthesis in leptin-deficient mice. J Bone Miner Res. 2010; 25(8):1711-23. doi: 10.1002/jbmr.65.

Rutkowski JM, Pastor J, Sun K, Park SK, Bobulescu IA, Chen CT, et al. Adiponectin alters renal cal- cium and phosphate excretion through regulation of klotho expression. Kidney Int. 2017 Feb; 91(2): 324-337. doi: 10.1016/j.kint.2016.09.016.

Saini RK, Kaneko I, Jurutka PW, Forster R, Hsieh A, Hsieh JC, et al. 1, 25-dihydroxyvitamin D(3) regu- lation of fibroblast growth factor-23 expression in bone cells: evidence for primary and secondary mechanisms modulated by leptin and interleukin-6. Calcif Tissue Int. 2013; 92(4):339-53. doi: 10.1007/ s00223-012-9683-5.

Wagner CA, Imenez Silva PH, Rubio-Aliaga I. And the fat lady sings about phosphate and calcium. Kidney Int. 2017;91(2):270-2. doi: 10.1016/j. kint.2016.11.009.

Krane V, Wanner C. The metabolic burden of dia- betes and dyslipidaemia in chronic kidney disease. Nephrol Dial Transplant. 2002;17[Suppl 11]:23-7. doi: 10.1093/ndt/17.suppl_11.23.

Ritz E, Wanner C. Lipid Abnormalities and Cardiovascular Risk in Renal Disease. J Am Soc Nephrol. 2008;19(6):1065-70. doi: 10.1681/ ASN.2007101128.

Vaziri ND. Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences. Am J Physiol Renal Physiol. 2006;290(2):F262-72. doi:10.1152/ajprenal.00099.2005.

Lowrie EG, Lew NL. Death risk in hemodialysis patients: the predictive value of commonly mea- sured variables and an evaluation of death rate differences between facilities. Am J Kidney Dis. 1990;15(5):458-82.

Park J, Ahmadi SF,  Streja  E,  Molnar  MZ, Flegal  KM,  Gillen  D,  et  al.   Obesity   para- dox in endstage kidney disease patients. Prog Cardiovasc Dis. 2014;56(4):415-25. doi: 10.1016/j. pcad.2013.10.005.

Nishizawa Y, Shoji T, Kakiya R, Tsujimoto Y, Tabata T, Ishimura E, et al. Non-high-density lipo- protein cholesterol (non-HDL-C) as a predictor of cardiovascular mortality in patients with endstage renal disease. Kidney Int Suppl. 2003;(84):S117- 20.  doi:  10.1046/j.1523-1755.63.s84.30.x

Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, et al. FGF23 induces left ventricular hy- pertrophy. J Clin Invest. 2011;121(11):4393-408. doi: 10.1172/JCI46122.

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How to Cite
Chaikovska, M. I., & Martynyuk, L. P. (2018). Fibroblast growth factor 23 and lipid metabolism association in chronic kidney disease. Ukrainian Journal of Nephrology and Dialysis, (2(58), 34-40.