Document Type : Research Paper


1 Department of Pharmaceutical Chemistry, College of Pharmacy, University of Ninevah, Mosul, Iraq

2 Department of Laboratory, Al-Hadbaa Blood and Bone Marrow Transplantation Hospital, Mosul, Iraq


Background: As a key regulator of bone metabolism, parathyroid hormone (PTH) also modulates the homeostatic response to changes in plasma calcium concentrations. PTH values are often used in patients with “chronic kidney disease (CKD)” as a surrogate for assessing bone and mineral disease associated with CKD. Objectives: The present study sought to evaluate the PTH level alongside measured serum electrolytes and renal function in CKD patients. Method: This study was based on a cross-sectional comparative study which considered the sample size of 120 individuals who were divided into two groups, the control group (n=30) which had apparently healthy individuals, and the second group which consisted of (n=90) patients diagnosed with CKD, and associated medical conditions including hypertension and diabetes. Parathyroid hormone, calcium, phosphate, fasting blood sugar, creatinine, blood urea, serum sodium were measured. Results: The results summarize that the levels of PTH, FBS, phosphate, urea, and creatinine were significantly increased in the patients with CKD as compared to the healthy individuals. However, no marked differences were found in the values of Na, K, and Ca. Conclusion: PTH should be considered as a marker for CKD and outlined in the investigation and follow-up of the prognosis of these patients.


Main Subjects

  1. Sah DK, Haque SS, Shah S, Yadav SS. Role of Calcium, Phosphorus and Intact Parathyroid Hormone in Different Stages of Chronic Kidney Disease. J Clin Exp Nephrol, 2023; 8 (2): 185.
  2. Singh S, Bhatta S. Biochemical and hematological parameters in chronic kidney disease. Journal of Manmohan Memorial Institute of Health Sciences. 2018;4(1):4-11.
  3. Treacy O, Brown NN, Dimeski G. Biochemical evaluation of kidney disease. Translational andrology and urology. 2019;8(Suppl 2):S214.
  4. Valente-Da-Silva HG, Maya MC, Moreira AS. Parathyroidectomy in chronic kidney disease: effects on weight gain and on quality of life improvement. Revista do Colégio Brasileiro de Cirurgiões. 2017;44:263-9.
  5. González-Casaus ML, González-Parra E, Sánchez-González C, Albalate M, de La Piedra-Gordo C, Fernández E, Torregrosa V, et al. A lower proportion of circulating active parathyroid hormone in peritoneal dialysis does not allow the pth inter-method adjustment proposed for haemodialysis. Nefrología. 2014;34(3):330-40.
  6. Hsiao PJ, Liao CY, Kao YH, Chan JS, Lin YF, Chuu CP, et al. Comparison of fractional excretion of electrolytes in patients at different stages of chronic kidney disease: A cross-sectional study. Medicine. 2020;99(2).
  7. Vhora RS, Munde A, Bale C, Kakrani AL. Correlation of serum parathyroid hormone with mineral bone disease in chronic kidney disease patients. Medical Journal of Dr. DY Patil University. 2015;8(6):708-12.
  8. Cozzolino M, Ketteler M. Evaluating extended-release calcifediol as a treatment option for chronic kidney disease-mineral and bone disorder (CKD-MBD). Expert Opinion on Pharmacotherapy. 2019;20(17):2081-93.
  9. D'Arrigo G, Mallamaci F, Pizzini P, Versace MC, Tripepi GL, Zoccali C, et al. MO499 CKD-MBD biomarkers and CKD progression: an analysis by joint models. Nephrology Dialysis Transplantation. 2021;36(Supplement_1):gfab087-0019.
  10. Block GA, Kilpatrick RD, Lowe KA, Wang W, Danese MD. CKD–mineral and bone disorder and risk of death and cardiovascular hospitalization in patients on hemodialysis. Clinical journal of the American Society of Nephrology: CJASN. 2013;8(12):2132.
  11. Wesseling-Perry K, Harkins GC, Wang HJ, Elashoff R, Gales B, Horwitz MJ, et al. The calcemic response to continuous parathyroid hormone (PTH)(1-34) infusion in end-stage kidney disease varies according to bone turnover: a potential role for PTH (7-84). The Journal of Clinical Endocrinology & Metabolism. 2010;95(6):2772-80.
  12. Tejwani V, Qian Q. Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease. 2013;5(6):1913-36.
  13. Svajger BA, Pruss CM, Laverty KJ, Zelt JG, Jones G, Kaufmann M, et al. PTH suppression by calcitriol does not predict off‐target actions in experimental CKD. Pharmacology Research & Perspectives. 2020;8(3):e00605.
  14. Liamis G, Liberopoulos E, Barkas F, Elisaf M. Diabetes mellitus and electrolyte disorders. World Journal of Clinical Cases: WJCC. 2014;2(10):488.
  15. Chen NX, Srinivasan S, O'Neill K, Nickolas TL, Wallace JM, Allen MR, et al. Effect of advanced glycation end‐products (AGE) lowering drug ALT‐711 on biochemical, vascular, and bone parameters in a rat model of CKD‐ Journal of Bone and Mineral Research. 2020;35(3):608-17.
  16. Goodman WG, Goldin J, Kuizon BD, Yoon C, Gales B, Sider D, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. New England Journal of Medicine. 2000;342(20):1478-83.
  17. Wang P, Zhou P, Chen W, Peng DA. Combined effects of hyperphosphatemia and hyperglycemia on the calcification of cultured human aortic smooth muscle cells. Experimental and Therapeutic Medicine. 2019;17(1):863-8.
  18. Tran L, Batech M, Rhee CM, Streja E, Kalantar-Zadeh K, Jacobsen SJ, et al. Serum phosphorus and association with anemia among a large diverse population with and without chronic kidney disease. Nephrology Dialysis Transplantation. 2016;31(4):636-45.
  19. Wang P, Zhou P, Chen W, Peng DA. Combined effects of hyperphosphatemia and hyperglycemia on the calcification of cultured human aortic smooth muscle cells. Experimental and Therapeutic Medicine. 2019;17(1):863-8.