A Biochemical Study of Fibroblast Growth Factor -23 and Phosphorus Metabolism in Adult Patients with Obstructive Renal Failure in Babylon-Iraq

Document Type : Original Article


1 Department of chemistry and Biochemistry, Faculty of Medicine, Babylon University, Babel, Iraq

2 Assistant Professor, College of Medicine, Department of Chemistry and Biochemistry, Faculty of Medicine – University of Babylon/ Babel, Iraq

3 Professor of Urology at the Faculty of Medicine - University of Babylon/ Babel, Iraq


Complete or partial obstruction to the urine's flow can cause gradual and cumulative kidney damage, and this is what is known as obstructive uropathy (OU). The obstruction could be caused by a problem with one or both ureters, and it could occur close to or far from the bladder neck (such as in the urethra). Multiple research have sought to understand the origins and implications of obstructive uropathy, which is a primary cause of renal failure. Fibroblast growth factor23 (FGF23) Osteocytes and osteoblasts create this phosphaturic hormone, which binds to FGF receptors via the transmembrane protein Klotho. Specifically, FGF23 inhibits sodium/phosphate cotransporters NaPi2a and NaPi2c, which in turn inhibits renal phosphate reabsorption, by targeting the renal proximal tubule and decreasing calcitriol synthesis. FGF23 also inhibits the synthesis and secretion of parathyroid hormones by the parathyroid glands. Calcitriol, phosphate, and parathyroid hormone are all involved in the control of FGF23 at the cellular and molecular levels. More FGF23 is found in rare hereditary and acquired illnesses, but chronic kidney disease is also linked to an increase in FGF23 as a reaction to Hyperphosphatemia. However, Increased levels of FGF23 have been associated to deterioration of chronic kidney disease. Whether FGF23 is linked to renal impairment and an increased risk of death .The study's objective was to take measurements of serum level of Fibroblast growth factor- 23 (FGF-23) and phosphorus in people suffering from obstructive renal failure and healthy control subject and to assess the relation of each of them. The study involved collecting blood samples from 100 volunteers, 50 healthy subjects (38 men and 12 women), (34 men and 16 women) suffering from obstructive renal failure.age was (15 –65) years BMI with (18.5-24.9) Kg m-2. Patients were subjected to Kidney Surgery Department at Hillah Hospital from The period from1st of December, 2020 to 1 of June, 2021. The findings revealed statistically significant variations (P<0.0001) in the serum FGF23 level between obstructive renal failure group (501.3±230.89 Pg ml-1) compared with control group (119.63±29.8 Pg ml-1). P = <0.001 for Phosphorus obstructive renal failure group (2.01±0.76 mmol L-1) compared with control group (0.68±0.39 mmol L-1).The results of levels of Hemoglobin& GFR in the of people with obstructive renal disease were significantly lower than healthy people and significantly, as the value of P <0.05. The level of occurrence of The Fibroblast growth factore23 & phosphors is higher in patient with obstructive renal failure than those healthy control, The FGF23 could be served as a diagnostic marker in obstructive renal failure patients to predict the possibility to develop chronic kidney disease, The occurrence of obstructive renal disease at a large rate in old age and in men more than women.


  1. Undre S., Marks S.D., 2016. Obstructive Uropathy Pediatric Kidney Disease. pp. 1121-1133: Springer.
  2. Cheungpasitporn W., Rossetti S., Friend K., Erickson S.B., Lieske J.C., 2016. Treatment effect, adherence, and safety of high fluid intake for the prevention of incident and recurrent kidney stones: a systematic review and meta-analysis. Journal of Nephrology. 29(2), 211-219.
  3. Stevens S., 2018. Obstructive Kidney Disease. Nurs Clin North Am. 53(4), 569-578.
  4. Dousdampanis P., Trigka K., Stefanidis I., 2020. "Obstructive Nephropathy.pp. 502-511.
  5. Klahr S., 2000. The geriatric patient with obstructive uropathy. Nephrology and Geriatrics Integrated. 167-177.
  6. Wolf M., 2012. Update on fibroblast growth factor 23 in chronic kidney disease. Kidney International. 82(7), 737-747.
  7. Bär L., Stournaras C., Lang F., Föller M., 2019. Regulation of fibroblast growth factor 23 (FGF 23) in health and disease. FEBS letters. 593(15), 1879-1900.
  8. Murali S.K., Roschger P., Zeitz U., Klaushofer K., Andrukhova O., Erben R.G., 2016. FGF23 regulates bone mineralization in a 1, 25 (OH) 2D3 and klotho‐independent manner. Journal of Bone and Mineral Research. 31(1), 129-142.
  9. Leifheit-Nestler M., Haffner D., 2018. Paracrine effects of FGF23 on the heart. Frontiers in Endocrinology. 9, 278.
  10. Scialla J.J., Xie H., Rahman M., Anderson A.H., Isakova T., Ojo A., Zhang X., Nessel L., Hamano T., Grunwald J.E., 2014. Fibroblast growth factor-23 and cardiovascular events in CKD. Journal of the American Society of Nephrology. 25(2), 349-360.
  11. Neyra J.A., Hu M.C., Moe O.W., 2020. Fibroblast Growth Factor 23 and αKlotho in Acute Kidney Injury: Current Status in Diagnostic and Therapeutic Applications. Nephron. 144(12), 665-672.
  12. Christov M., Neyra J.A., Gupta S., Leaf D.E., 2019, January. Fibroblast growth factor 23 and klotho in AKI. In Seminars in Nephrology.  39(1), 57-75). WB Saunders.
  13. Leaf D.E., Wolf M., Waikar S.S., Chase H., Christov M., Cremers S., Stern L., 2012. FGF-23 levels in patients with AKI and risk of adverse outcomes. Clinical Journal of the American Society of Nephrology. 7(8), 1217-1223.
  14. Muñoz‐Castañeda J.R., Herencia C., Pendón‐Ruiz de Mier M.V., Rodriguez‐Ortiz M.E., Diaz‐Tocados J.M., Vergara N., Martínez‐Moreno J.M., Salmerón M.D., Richards W.G., Felsenfeld A., 2017. Differential regulation of renal Klotho and FGFR1 in normal and uremic rats. The FASEB Journal. 31(9), 3858-3867.
  15. Rodríguez-Ortiz M.E., Díaz-Tocados J.M., Muñoz-Castañeda J.R., Herencia C., Pineda C., Martínez-Moreno J.M., Montes de Oca A., López-Baltanás R., Alcalá-Díaz J., Ortiz A., 2020. Inflammation both increases and causes resistance to FGF23 in normal and uremic rats. Clinical Science. 134(1), 15-32.
  16. Rodríguez M., 2020. FGF23: Is It Another Biomarker for Phosphate–Calcium Metabolism? Advances in Therapy. 37(2), 73-79.
  17. Andrukhova O., Zeitz U., Goetz R., Mohammadi M., Lanske B., Erben R.G., 2012. FGF23 acts directly on renal proximal tubules to induce phosphaturia through activation of the ERK1/2–SGK1 signaling pathway. Bone. 51(3), 621-628.
  18. Andrukhova O., Smorodchenko A., Egerbacher M., Streicher C., Zeitz U., Goetz R., Shalhoub V., Mohammadi M., Pohl E.E., Lanske B., 2014. FGF 23 promotes renal calcium reabsorption through the TRPV 5 channel. The EMBO Journal. 33(3), 229-246.
  19. Mace M.L., Gravesen E., Nordholm A., Olgaard K., Lewin E., 2018. Fibroblast growth factor (FGF) 23 regulates the plasma levels of parathyroid hormone in vivo through the FGF receptor in normocalcemia, but not in hypocalcemia. Calcified tissue International. 102(1), 85-92.
  20. Micarelli D., Cristi E., Taddei A.R., Della Rovere F.R., Mercanti C., Feriozzi S., 2020. A case of acute renal failure with multiple origins of the renal injury. CEN Case Reports. 9(4), 437-441.
  21. Agoro R., Montagna A., Goetz R., Aligbe O., Singh G., Coe L.M., Mohammadi M., Rivella S., Sitara D., 2018. Inhibition of fibroblast growth factor 23 (FGF23) signaling rescues renal anemia. The FASEB Journal. 32(7), 3752-3764.
  22. Tolani M.A., Ahmed M., Nasir O., Sudi A., 2020. Obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction: analysis of burden and associations in a university teaching hospital in Nigeria. Journal of Medicine in the Tropics. 22(2), 127.
  23. Rygasiewicz K., Hryszko T., Siemiatkowski A., Brzosko S., Rydzewska-Rosolowska A., Naumnik B., 2018. C-terminal and intact FGF23 in critical illness and their associations with acute kidney injury and in-hospital mortality. Cytokine. 103, 15-19.