Hyperparathyroidism and Associated Factors in Chronic Kidney Disease


  •   Shoukat Memon

  •   Ashar Alam

  •   Faiza Saeed

  •   Javeria Chughtai

  •   Salman Imtiaz

  •   Shahzad Ahmed

  •   Sobia Tariq


Background: The normal axis of calcium, phosphorus, vitamin D, and intact parathyroid hormone (iPTH) come under stress when chronic kidney disease (CKD) progresses beyond stage 3(GFR<30 ml/kg/1.732). This results in increased secretion of iPTH which is known as secondary hyperparathyroidism. This exacerbates further if simultaneous deficiency of nutritional vitamin D (Cholecalciferol) is also found. Secondary hyperparathyroidism results in vascular calcification and increases cardiac mortality. Early intervention in form of dietary modification (low phosphorus, low potassium), correcting vitamin D deficiency along with the addition of active vitamin D (calcitriol) would help in alleviating patients’ suffering and saving costs as well.

Material and method: This study was conducted from Jan 2017 to Jan 2018 at The Indus Hospital, Karachi with the age group ≥14 years of either gender who were suffering from chronic kidney disease (CKD). Patients on dialysis, chronic liver disease, and vitamin D supplementation were excluded. Their history, demographic, BMI, Calcium, Phosphorus, Alkaline Phosphatase, 25-Hyydorxyvitamin D, albumin, and intact parathyroid hormone (iPTH) were all noted.

Results: 265 patients were enrolled for final analysis in this data with a male to female ratio of 1:1.03 (146/121). Hyperparathyroidism (iPTH> 68 pg/ml) was seen in 190 (71.2%) patients. Mean values of all quantitative variables were not statistically significant when compared hyper parathyroid with normal parathyroid. Hyperparathyroidism was found significant in late CKD in comparison to early CKD (P-value <.001), While vitamin D deficiency was significantly associated with hyperparathyroidism in early CKD but not in late CKD.

Conclusion: Hyperparathyroidism is significantly present in CKD which is contributed by CKD progression and vitamin D deficiency.

Keywords: Chronic Kidney Disease, hyperparathyroidism, intact Parathyroid hormone, vitamin D


Jessani S, Bux R, Jafar TH. Prevalence, determinants, and management of chronic kidney disease in Karachi, Pakistan-a community based cross-sectional study. BMC Nephrology. 2014; 15(1): 1-9.

Brown EM, Pollak M, Seidman CE, Seidman JG, Chou YH, Riccardi D, et al. Calcium-ion-sensing cell-surface receptors. N Engl J Med. 1995; 333: 234–40

Portillo MR, Rodríguez-Ortiz ME. Secondary hyperparthyroidism: pathogenesis, diagnosis, preventive and therapeutic strategies. Reviews in Endocrine and Metabolic Disorders. 2017; 18(1): 79-95.

Rodríguez-Ortiz ME, Rodríguez M. Recent advances in understanding and managing secondary hyperparathyroidism in chronic kidney disease. F1000 Research. 2020; 9.

Kerby J, Rue L, Blair H, Hudson S, Sellers MT, Diethelm AG. Operative treatment of tertiary hyperparathyroidism: a single-center experience. Ann Surg. 1998; 227: 878.

Kilgo M, Pirsch J, Warner T, Starling JR. Tertiary hyperparathyroidism after renal transplantation: surgical strategy. Surgery. 1998; 124: 677.

Barreto FC, Barreto DV, Moyses RM, Neves KR, Canziani ME, Draibe SA, et al. K/DOQI-recommended intact PTH levels do not prevent low-turnover bone disease in hemodialysis patients. Kidney International. 2008; 73(6): 771-7.

KDIGO Clinical practice guidelines for diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Treatment of CKD–MBD targeted at lowering high serum phosphorus and maintaining serum calcium. Kidney International. 2009; 76(suppl 113): S50–S90.

Kalantar-Zadeh K, Kuwae N, Regidor DL, Kovesdy CP, Kilpatrick RD, Shinaberger CS, et al. Survival predictability of time-varying indicators of bone disease in maintenance hemodialysis patients. Kidney Int. 2006; 70(4): 771–80.

De Boer IH, Gorodetskaya I, Young B, Hsu CY, Chertow GM. The severity of secondary hyperparathyroidism in chronic renal insufficiency is GFR-dependent, race-dependent, and associated with cardiovascular disease. J Am Soc Nephrol. 2002; 13(11): 2762–9.

Block GA, Klassen PS, Lazarus JM, Ofsthun N, Lowrie EG, Chertow GM. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol. 2004; 15(8): 2208–18.

Ganesh SK, Stack AG, Levin NW, Hulbert-Shearon T, Port FK. Association of elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol. 2001; 12(10): 2131–8.

Jurkovitz CT, Qiu Y,Wang C, Gilbertson DT, Brown WW. The Kidney Early Evaluation Program (KEEP): program design and demographic characteristics of the population. Am J Kidney Dis. 2008; 51(suppl 2): S3–S12.

Yuen NK, Ananthakrishnan S, Campbell MJ. Hyperparathyroidism of renal disease. The Permanente Journal. 2016; 20(3).

Coen G, Ballanti P, Bonucci E, Calabria S, Costantini S, Ferrannini M, et al. Renal osteodystrophy in predialysis and hemodialysis patients: comparison of histologic patterns and diagnostic predictivity of intact PTH. Nephron. 2002; 91(1): 103-11.

Martin KJ, Gonzalez EA. Metabolic bone disease in chronic kidney disease. J Am Soc Nephrol. 2007; 18(3): 875–85.

Elias RM, Moysés RM. Elderly patients with chronic kidney disease have higher risk of hyperparathyroidism. International Urology and Nephrology. 2017; 49(10): 1815-21.

Zaheer S, de Boer I, Allison M, Brown JM, Psaty BM, Robinson-Cohen C, et al. Parathyroid Hormone and the Use of Diuretics and Calcium-Channel Blockers: The Multi-Ethnic Study of Atherosclerosis. Journal of Bone and Mineral Research. 2016; 31(6): 1137–1145.

Gimba ZM, Abene EE, Agbaji OO, Agaba EI. Secondary hyperparathyroidism among Nigerians with chronic kidney disease. African Health Sciences. 2018; 18(2): 446-57.

Andress DL, Coyne DW, Kalantar-Zadeh K, Molitch ME, Zangeneh F, Sprague SM. Management of secondary hyperparathyroidism in stages 3 and 4 chronic kidney disease. Endocrine Practice. 2008; 14(1): 18-27.

Saliba W, El-Haddad B. Secondary hyperparathyroidism: pathophysiology and treatment. J Am Board Fam Med. 2009; 22(5): 574-81.

Zisman AL, Hristova M, Ho LT, Sprague SM. Impact of ergocalciferol treatment of vitamin D deficiency on serum parathyroid hormone concentrations in chronic kidney disease. Am J Nephrol. 2007; 27(1): 36-43.

Tomasello S. Secondary hyperparathyroidism and chronic kidney disease. Diabetes Spectrum. 2008; 21(1): 19-25.

Moe SM, Chen NX. Mechanisms of vascular calcification in chronic kidney disease. Journal of the American Society of Nephrology. 2008; 19(2): 213-6.

Li Z, Wu J, Zhang X, Ou C, Zhong X, Chen Y, et al. CDC42 promotes vascular calcification in chronic kidney disease. The Journal of Pathology. 2019; 249(4): 461-71.

Kestenbaum B, Belozeroff V. Mineral metabolism disturbances in patients with chronic kidney disease. European Journal of Clinical Investigation. 2007; 37(8): 607-22.

Lishmanov A, Dorairajan S, Pak Y, Chaudhary K, Chockalingam A. Elevated serum parathyroid hormone is a cardiovascular risk factor in moderate chronic kidney disease. International Urology and Nephrology. 2012; 44(2): 541-7.


How to Cite
Memon, S., Alam, A., Saeed, F., Chughtai, J., Imtiaz, S., Ahmed, S., & Tariq, S. (2022). Hyperparathyroidism and Associated Factors in Chronic Kidney Disease. European Journal of Clinical Medicine, 3(2), 8–12. https://doi.org/10.24018/clinicmed.2022.3.2.173