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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 4  |  Page : 573-576
Risk factors of post renal transplant hyperparathyroidism

1 Renal Transplant Unit, St. George's Healthcare NHS Trust, London , United Kingdom; NemazeeHospital Organ Transplantation Unit, Shiraz University of Medical Sciences, Shiraz , Iran
2 NemazeeHospital Organ Transplantation Unit, Shiraz University of Medical Sciences, Shiraz, Iran

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Date of Web Publication8-Jul-2009


It is well recognized that patients with end stage renal diseases (ESRD) have hyper­plastic parathyroid glands. In most patients, a decrease in parathyroid hormone (PTH) occurs by about 1 year after renal transplantation. However, some renal transplant recipients continue to have elevated level of PTH. We prospectively evaluated 121 patients undergoing renal transplantation between August 2000 and 2002. The duration of dialysis, calcium (Ca), phosphorus (P), albumin, creatinine and iPTH levels were recorded prior to transplantation and three months and one year after transplantation. These 121 patients were on dialysis for an average period of 17.4 months prior to transplantation. An increase in the serum Ca and a decrease in serum P and iPTH level was seen in the patients after transplantation (P< 0.001). Hyperparathyroidism was in 12 (9.9%) and 7 (5.7%) patients three months and one year after transplantation respectively. Elderly patients and patients with longer duration on dialysis had an increased risk of developing post transplant hyperpara­thyroidism and hypercalcemia in the first year post transplant (P< 0.05). In conclusion age and duration on dialysis before transplantation seems to be important risk factors for post transplant hyperparathyroidism.

Keywords: Hypercalcemia, Hyperparathyroidism, Risk factor, Transplantation

How to cite this article:
Jahromi AH, Roozbeh J, Raiss-Jalali GA, Dabaghmanesh A, Jalaeian H, Bahador A, Nikeghbalian S, Salehipour M, Salahi H, Malek-Hosseini A. Risk factors of post renal transplant hyperparathyroidism. Saudi J Kidney Dis Transpl 2009;20:573-6

How to cite this URL:
Jahromi AH, Roozbeh J, Raiss-Jalali GA, Dabaghmanesh A, Jalaeian H, Bahador A, Nikeghbalian S, Salehipour M, Salahi H, Malek-Hosseini A. Risk factors of post renal transplant hyperparathyroidism. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Jan 23];20:573-6. Available from: https://www.sjkdt.org/text.asp?2009/20/4/573/53244

   Introduction Top

It is well recognized that patients with end stage renal diseases (ESRD) have altered bone mineral metabolism and hyperplastic parathy­roid glands. In most patients subsequent to res­toration of renal function and normalization of calcium, phosphorus, and calcitriol a decrease in serum parathyroid hormone (PTH) occurs by about 1 year after successful renal transplan­tation. [1] ,[2] However, some renal transplant reci­pients with even good renal function even by one year may continue to have elevated level of PTH and persistent hypercalcemia. [3] ,[4]

In some studies, incomplete resolution of hyper­parathyroidism is reported in more than 50% of patients despite excellent allograft function. [5] This may be due to incomplete normalization of renal function and/or to an incomplete resolu­tion of the pre-transplant parathyroid hyperpla­sia. [2] Although some improvement has occurred, risk factors for this morbidity remain poorly understood. [6]

The aim of the present study was to examine the parathyroid status of renal transplant patients immunosuppressed with cyclosporine and with a functioning graft (Creatinine < 2 mg/dL) and analyze the factors responsible for the persis­tence of hyperparathyroidism.

   Materials and Methods Top

In a prospective study, 121 patients with ESRD who consequently underwent renal transplan­tation in our center between August 2000 and August 2002 were studied. Inclusion criteria consisted of: (i) age at the time of transplant > 18 years; (ii) cyclosporine (CsA) based immu­nosuppression; (iii) good and stable graft func­tion ascertained by Creatinine (Cr) < 2 mg/dL in the first year post transplantation; (iv) Com­plete record of the patient with follow up.

The duration of dialysis prior to transplan­tation and past medical history of the patients were recorded. Results of total serum calcium (Ca) corrected for albumin, phosphorus (P), al­bumin and Cr were recorded before and, three months and one year after transplantation.

For the purpose of this study, hypercalcemia was defined as serum Ca > 10.8 mg/dL, high iPTH as iPTH > 60 pg/mL, hypophosphatemia as serum P < 2.3 mg/dL and graft dysfunction as serum Cr > 2 mg/dL. None of the patients received calcium, phosphorus, vitamin D supple­ments, estrogen and anti-epileptics after trans­plantation or had undergone parathyroidectomy.

The immunosuppression protocol consisted of Cyclosporine (CsA), Imuran, Cellcept, and Pre­dnisolone in all of the patients.

Results were analyzed using SPSS-11 software for Windows® (Chicago, IL) and for statistical interpretation student's t-test, chi-square test and independent t-test were used when indicated. In this study, p-value < 0.05 is considered statis­tically significant. Results are expressed as mean ± Standard Deviation (SD).

   Results Top

Total 121 patients (male = 84, female= 37) with mean age of 35.5 ± 12.5 were included in the study. Duration of dialysis prior to transplanta­tion was 17.4 ± 6 months. Serum calcium, phos­phorus and iPTH level changed significantly after transplantation.

A significant increase in the serum Ca (from 6.76 ± 0.67 to 9.7 ± 1.36 mg/dL) and a decrease in serum phosphorus (from 9.29 ± 1.87 to 2.76 ± 0.82 mg/dL) and iPTH levels (from 153.21 ± 131 to 43.24 ± 37.23 pg/mL) was seen in the first three months after transplantation (P< 0.001).

Three months post transplantation, 100 (82.6%) patients had normal calcium levels and 21 (17.4%) were hypercalcemic, with mean age of 34.3 ± 11.5 and 40.61 ± 14.14 years, respec­tively (P< 0.05). All normocalcemic participants had normal iPTH values; however, 12 hyper­calcemic subjects (9.9%) demonstrated elevated iPTH (> 60 pg/mL) and other 9 (7.4%) hyper­calcemic patients had iPTH < 60 pg/mL. None had suppressed iPTH values (< 5 pg/mL).

Furthermore, mean calcium level in patients with iPTH < 60 pg/mL was considerably lower than those with iPTH > 60 pg/mL (9.4 ± 1.07 vs 12.81 ± 0.75 mg/dL; P< 0.001). However, mean phosphorus levels were not statistically diffe­rent (2.68 ± 0.9 vs 2.77 ± 0.82 mg/dL; P> 0.05).

Hypercalcemia was seen in 21 (17.4 %) and 7 (5.7%) patients three months and one year after transplantation respectively. Hyperparathyroidism was documented in 12 (9.9%) and 7 (5.7%) pa­tients three months and one year after trans­plantation.

Patients with longer duration of dialysis prior to transplantation had an increased risk of deve­loping post transplant hyperparathyroidism and hypercalcemia in the first year post transplant. In hypercalcemic patients compared to normo­calcemic subjects, mean duration of dialysis prior to transplantation was 31 ± 26.43 vs 14.58 ± 8.54 months, P= 0.01; in patients with hyper­parathyroidism compared to the patients with iPTH < 60 pg/mL it was 58 ± 18.68 vs 14.26 ± 8.34 months, P< 0.001.

Elderly patients had an increased risk of deve­loping post transplant hyperparathyroidism in the first year post transplant, P< 0.05. Mean age of subjects with iPTH < 60 pg/mL was signi­ficantly lower than those with iPTH > 60 pg/mL. (38.7 ± 12 vs 50.5 ± 7 years; P< 0.05). The maximum level of calcium in our patients was 11.7 mg/dL and none of the patients developed indications for parathyroidectomy.

   Discussion Top

Successful kidney transplantation normalizes the endocrine and metabolic imbalances res­ponsible for secondary hyperparathyroidism in the first few months. [1] ,[4] In this study, post trans­plant calcium, phosphorus, creatinine, and iPTH levels considerably normalized in majority of the patients.

Nevertheless, the early favorable events are not always followed by the normalization of PTH secretion. 9.9% and 5.7 % of our patients had elevated PTH levels at three months and one year post transplantation. Several studies have reported elevated PTH levels up to 50% of pa­tients one year after transplantation in the pre­sence of good renal function. [3] ,[5]

Similarly post transplant hypercalcemia varies widely from 8.5% to 65 % [7] ,[8] necessitating para­thyroidectomy in 1.6-17% of cases usually after the first year following renal transplantation. [5] In general, the indications for parathyroidectomy include the persistence of an elevated iPTH level (> 150 pg/mL) accompanied by hypercal­cemia (> 11.5 mg/dL), with or without associa­ted complications (eg, renal function impair­ment, nephrolithiasis, pancreatitis, pathologic fractures); calciphylaxis or severe vascular cal­cifications; or gland larger than 1 cm on ultra­sound or monoisobutilisonitrile (MIBI) scan. [5] ,[9]

The maximum post-op Ca level in our patients was 11.7 mg/dL and none developed indica­tions for parathyroidectomy possibly due to proper pretransplant management of hyperpa­rathyroidism, having younger group of patients in comparison to some other studies.

Age, duration of dialysis prior to transplan­tation, parathyroid gland size, and development of nodular and/or monoclonal hyperplasia of parathyroid glands are the main factors respon­sible for persistent hyperparathyroidism. [6] ,[10] ,[11]

Patients in our study with longer duration of dialysis and elderly had more chance of per­sistent hyperparathyroidism. Other factors cau­sing persistent parathyroid hyperplasia include, suboptimal graft function and some immuno­suppressive drugs are thought to contribute to persistent hyperparathyroidism. [2] ,[12] In the present study, however, none of these contributing fac­tors (suboptimal graft function, immunosup­pressive medication) were associated with per­sistent hyperparathyroidism.

Although the improvement of parathyroid func­tion occurring between three and six months after transplantation has been attributed to a re­duced parathyroid functional mass, [1] the process of involution may take many years. [5] The long lifespan of parathyroid cells (approximately 20 yr) with a cell renewal rate of approximately 5% per year [13] contributes to the very slow invo­lution of the gland after renal transplantation.

In conclusion, spontaneous resolution of se­condary hyperparathyroidism occurred in the majority of our post transplant patients. Age and duration of pretransplant dialysis was found to be a risk factor for post transplant hypercal­cemia and hyperparathyroidism. Early trans­plantation strategy along with proper attention to the levels of calcium, phosphate and PTH may prevent persistent hyperparathyroidism post transplantation.

   Acknowledgment Top

The authors would like to thank Ms. Samira Mazloom for her kind support in editing this article.

   References Top

1.Bonarek H, Merville P, Bonarek M, et al. Reduced parathyroid functional mass after successful kidney transplantation. Kidney Int 1999;56:642-9.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Torres A, Rodrigues AP, Concepcion MT, et al. Parathyroid function in long-term renal trans­plant patients: Importance of pre transplant PTH concentrations. Nephrol Dial Transplant 1998; 13( Suppl 3):94-7.  Back to cited text no. 2    
3.Reinhardt W, Bartelworth H, Jockenhovel F, et al. Sequential changes of biochemical bone parameters after kidney transplantation. Nephrol Dial Transplant 1998;13:436-42.  Back to cited text no. 3    
4.Messa P, Sindici C, Cannella G, et al. Persistent secondary hyperparathyroidism after renal trans­plantation. Kidney Int 1998;54:1704-13.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Torres A, Lorenzo V, Salido E. Calcium meta­bolism and skeletal problems after transplan­tation. J Am Soc Nephrol 2002;.13:551-8.  Back to cited text no. 5    
6.Evenepoel P, Claes K, Kuypers D, Maes B, Bammens B, Vanrenterghem Y. Natural history of parathyroid function and calcium metabolism after kidney transplantation: a single centre study. Nephrol Dial Transplant 2004;19:1281-7.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Apaydin S, Sariyar M, Erek E, et al. Hyper­calcemia and hyperparathyroidism after renal transplantation. Nephron 1999;81:364-5.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Lewin E. Involution of the parathyroid glands after renal transplantation. Curr Opin Nephrol Hypertens 2003;12:363-71.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Schomig M, Ritz E. Management of disturbed calcium metabolism in uremic patients. 2. Indi­cations for parathyroidectomy, Nephrol Dial Transplant 2000;15(suppl 5):25.  Back to cited text no. 9    
10.Koch Nogueira PC, David L, Cochat P. Evolu­tion of secondary hyperparathyroidism after renal transplantation. Pediatr Nephrol 2000;14: 42-6.  Back to cited text no. 10    
11.Spasovski GB, Bervoets AR, Behets GJ, et al. Spectrum of renal bone disease in end stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003;18:1159-66.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Dumoulin G, Hory B, Nguyen NU, et al. No trend toward a spontaneous improvement of hyperparathyroidism and high bone turnover in normocalcemic long-term renal transplant recipients. Am J Kidney Dis 1997;29:746-53.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Parfitt AM. The hyperparathyroidism of chronic renal failure: a disorder of growth. Kidney Int 1997;52:3-9.  Back to cited text no. 13  [PUBMED]  

Correspondence Address:
Alireza Hamidian Jahromi
General Surgery Department, Cheltenham General Hospital, Sandford road, Cheltenham , GL53 7AN UK

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PMID: 19587496

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