Study of hyperparathyroidism among patients with chronic kidney disease at sohag university hospital

Document Type : Original Article


1 Lecturer of internal medicine, faculty of medicine, Sohag university, sohag, egypt

2 Department of Internal Medicine, Faculty of Medicine, Sohag University.

3 Department of Internal medicine, Faculty of Medicine, Sohag University.


Objectives:The aim of this study is to asses prevalence & clinical outcome of hyperparathyroidism among CKDpatients either on dialysis or not in Sohag University Hospital 1.To estimate serum intact parathormone(iPTH) and other biochemical parameters (calcium, inorganic phosphate, urea and creatinine)in CKDpatients2. To compare and find out correlation between serum intact parathormone and biochemicalparameters in the study group.
Patients &Methods: For the study of 5 stages of Chronic Kidney Disease(CKD) totally 100 patients in different stages inthe age group of 20-60 years were taken. Serum parathormone and other biochemical parameters were estimated using standard methods.Pelvi-abdominal ultrasonography,Plain x-ray,ECG & Echocardiography were also done.
Results:66 patients (66.00%) with PTH values above the normal range (hyperparathyroidism) (>72 pg/ml), with mean PTH = 481.92 ± 608.05,   and this is the prevalence rate of secondary hyperparathyroidism in the study population. The serum PTH levels were higher even in early stages of CKD and the higher values are directly related to the stage of CKD.  In the study, Serum phosphorus was found to be significantly positively correlated to PTH both in the total study population and in patients with hyperparathyroidism.The PTH was found to be significantly negatively correlated with serum total and ionized calcium of the patients, both in the total study population and in patients with hyperparathyroidism.Also the findings of this study as regard echocardiography in CKD patients;Left ventricular dysfunction was the commonest cardiovascular abnormality. LVH was the most common echocardiographic abnormality in CKD cases. Diastolic function was deranged in more number of patients as compared to systolic function in patients with CKD.
Conclusion: The estimation of serum PTH and other biochemical parameters can help to diagnose the secondary hyperparathyroidism in the early stage of CKD which inturn has advantage to manage the patients of CKD accordingly to prevent the future complications.

  1. Meguid El Nahas A, Bello AK. Chronic kidney disease: the global challenge. Lancet 2005; 365:331-40.
  2. Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization N Engl J Med 2004; 351:1296-305.
  3. Covic A, Kothawala P, Bernal M, Robbins S, Chalian A, Goldsmith D. Systematic review of the evidence underlying the association between mineral metabolism disturbances and risk of all-cause mortality, cardiovascular mortality and cardiovascular events in chronic kidney disease. Nephrol Dial Transplant 2009; 24:1506-23.
  4. Slatopolsky E, Delmez JA. Pathogenesis of secondary hyperparathyroidism. Am J    Kidney Dis 2009; 23:229-236
  5. Slatopolsky E, Finch J, Denda M, Ritter C, Zhong M, Dusso , MacDonald PN, Brown AJ: Phosphorus restriction prevents parathyroid gland growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest 2003; 97: 2534-2540.
  6. Drüeke TB. Cell Biology of Parathyroid Gland Hyperplasia in Chronic Renal Failure. AmSocNephrol 11:1141-1152, 2010.
  7. Brown EM: Gamba G, Ricardi D, et al. Cloning and characterization of an extracellular ca(2+)-sensing receptor from bovine parathyroid. Nature 1993; 366: 575-80.
  8. Bikle DD: Clinical counter point. Vitamin D: New actions, new analogs,new therapeutic potential. Endocr Rev13: 765-784, 2009.                                                                                                                                                                                                                                                                                                                                                 

9.Yalcindag C, Silver J, Naveh-Many T: Mechanism of increased parathyroid hormone mRNA in experimental uremia: Roles of protein RNA and RNA degradation. J Am Soc Nephrol10: 2562-2568, 1999. 

10.Slatopolsky E, Delmez JA. Pathogenesis of secondary hyperparathyroidism. Am J    Kidney Dis 2009; 23:229-236

11.Moe S, Drueke T, Cunningham J, et al. Definition, evaluation, and   Classification of renal osteodystrophy: a position statement from Kidney  Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006; 69:1945-53.

12.Schafer C, Heiss A, Schwarz A, et al. The serum protein alpha 2-   Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification. J Clin Invest 2003; 112:357-66.














13.Cannata-Andia JB, Rodriguez-Garcia M, Carrillo-Lopez N, Naves-Diaz M, Diaz-Lopez B. Vascular calcifications: pathogenesis, management, and impact on clinical outcomes. J Am SocNephrol 2006; 17:S267-73.

14.Massy ZA, Drueke TB. Vascular calcification. CurrOpinNephrolHypertens 2013; 22:405-12.

15.Shanahan CM, Cary NR, Metcalfe JC, Weissberg PL: High expression of genes for calcification-regulating proteins in human atherosclerotic plaques. J Clin Invest 2003; 93: 2393-2402.

16.Ian H, IninaGorodetskaya, Belinda Young, Chi-yuan, Glenn MC. The severity of secondary hyperpatathyeoidism in chronic renal insufficiency is GFR dependent, race dependent and associated with cardiovascular disease.