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Saudi Journal of Kidney Diseases and Transplantation
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RENAL DATA FROM THE ASIA - AFRICA Table of Contents   
Year : 2008  |  Volume : 19  |  Issue : 1  |  Page : 116-119
Evaluation of Secondary Hyperparathyroidism in Patients undergoing Hemodialysis


Department of Medicine, Division of Nephrology, Shahid Rahnemoon Hospital, Yazd Medical University, Iran

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   Abstract 

Renal osteodystrophy is a complication of chronic kidney disease (CKD) that present in low and high turnover patterns. This disorder has a key role in the disability of CKD patients in whom early diagnosis and treatment can result in better outcome. We studied hyperparathyroidism prevalence and its relationship with renal osteodystrophy in our advanced CKD population. We included 80 patients (of whom 44 (55%) were diabetic) during 6 months period. The patients answered a questionnaire about symptoms related to bone disease and blood levels of parathormone (PTH), calcium, phosphorus, and alkaline phosphatase were obtained, in addition to hand and skull radiographs in all the study patients. Prevalence of clinically evident hyperparathyroidism in our patients was 45%. Hyperparathyroidism had significant relationship with alkaline phosphatase and radiological findings, but did not have a significant relationship with dialysis duration, age, sex, familial history, diabetes mellitus, or hypertension. We conclude that secondary hyperparathyroidism is prevalent in our dialysis population and has high correlation with serum alkaline phosphatase levels and radiological changes.

Keywords: Osteodystrophy, Hyperparathyroidism, Chronic kidney disease

How to cite this article:
Rahimian M, Sami R, Behzad F. Evaluation of Secondary Hyperparathyroidism in Patients undergoing Hemodialysis. Saudi J Kidney Dis Transpl 2008;19:116-9

How to cite this URL:
Rahimian M, Sami R, Behzad F. Evaluation of Secondary Hyperparathyroidism in Patients undergoing Hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Sep 21];19:116-9. Available from: http://www.sjkdt.org/text.asp?2008/19/1/116/37450

   Introduction Top


Renal osteodystrophy is one of the metabolic disorders that occur in chronic kidney disease (CKD) patients. Patients with mild to moderate CKD rarely have clinical evident bone disease, however, recent studies have revealed that histological changes may deve­lop several years before presentation as clinically symptomatic disease. [1] Bone histo­pathological changes may include high or low turnover depending on over stimulated or over suppressed parathormone (PTH), respectively. Many CKD patients usually have a mixture of both patterns of the bone disease. [2]

In the 1980s, elevated PTH in CKD patients was introduced as the main the factor in osteodystrophy, [3] in addition to acidosis, calciteriol resistance and decreased synthesis of 1,25 dihydroxy Vitamin D 3 , and increased phosphorus blood levels. [4] New therapeutic methods were designed for prevention or controlling these causes.

Confirmation of diagnosis of renal osteo­dystrophy in CKD patients requires histo­logical, histomorphological and histodynamic studies. Although bone biopsy is the gold standard for the diagnosis of osteodystrophy, some clinical and biochemical markers such as the PTH level, phosphorus and calcium levels, and alkaline phosphatase (ALP) may be considered in lieu of bone biopsy.

The aim of our study is to evaluate the prevalence of hyperparathyroidism and its correlation with the other laboratory para­meters in our CKD patients undergoing hemodialysis.


   Methods and Patients Top


This cross-sectional study included 80 CKD patients who were undergoing chronic hemodialysis (HD). One of patients was died and 4 patients weren't agreeing to include the study. We included in the study the demographic data of the patients, HD duration, and HD frequency.

Blood samples for evaluation of PTH (immunoassay method) Calcium, phospho­rous, alkaline phosphatase (ALP) levels were obtained. Radiological studies of the hands and skull were evaluated by our radiologist for detection of osteodystrophy.


   Statistical Analysis Top


Data were analyzed with the aide of SPSS statistical software and appropriate statistical methods. P values < 0.05 were considered significant.


   Results Top


Of the study patients, 46 (57.5%) were males, and HD duration was 25 ± 20.4 months. The HD frequency was 2.6 ± 0.5 times per week. Forty four (55%) patients had diabetes mellitus as a cause of their CKD.

Elevated PTH levels were prevalent in 45% of our patients; 16 (36.4%) diabetic patients and 20 (55.6%) non-diabetics and 21 (45.7%) men were hyper parathyroid. [Table - 1] reveals the relationship between several parameters and the PTH. There were significant corre­lation only of the ALP levels and the radio­logical findings with the elevated PTH (p value < 0.05).


   Discussion Top


PTH and other bone markers of osteoclasts and osteoblasts have been studied; [5],[6],[7],[8] tartarat resistance acid phosphatase, c-terminal telo­peptide, collagen type I, and pyridinolin as bone reabsorption markers, in addition to alkaline phosphatase as marker osteoblasts' activity.

Correlation between PTH and ALP the levels to distinguish the patterns of renal osteodystrophy produced variable results. [9],[10],[11] Elevated PTH levels are prevalent in CKD patients. [12],[13] They were prevalent in our study patient. Moreover, there were signi­ficant correlations between ALP blood levels and the radiological findings with the ele­vated PTH. In similar study from England, the patients with elevated PTH blood levels and ALP had histological changes in their bones biopsy characteristic of high turn over pattern. [14] The radiological changes were also observed in an Italian study in patients with elevated levels of ALP and PTH. [15]

In our study, we did not observe a significant correlation between HD frequency, diabetes mellitus, age and gender of patients, bone pain, or muscle weakness with hyperpara­thyroidism.

PTH resistance, high levels of phosphorus, low levels calcium, and deficiency of 1, 25 dihydroxi vitamin D 3 can cause high levels of PTH in CKD patients. [16] Three to 5 times higher than normal level is a reliable marker for high turnover bone pattern. [2] PTH level higher than 450 pg/ml correlates with 100% sensitivity and 95.5% specificity for patients with high turnover bone disease, while levels from 450 - - 650 pg/ml in HD patients (espe­cially younger than 45 years old) correlated with 67.3%-87.1% positive predictive value. [17] However, several studies revealed variable results due to differences in the methodology of PTH measurements. [18],[19] Some of differences in PTH measurements maybe due to secretion of two hormones from para­thyroid gland; One of them stimulates bone turnover, while the other suppresses it. [20]

Finally, some dialysis related factors have been implicated in the pathology of bone and mineral disease in CKD patients. The type of dialyzer has a role in osteodystrophy; HD Patients dialyzed with cellulose membranes demonstrated more prevalence of hyperpara­thyroidism than those dialyzed with polyacrynitrile membranes. [21] In addition, low dia­lysate calcium level could decrease the pre­valence of bone metabolism and soft tissue calcifications. [22]

We conclude that secondary hyperparathyroidism is prevalent in our dialysis popu­lation and has high correlation with serum alkaline phosphatase levels and radiological changes

 
   References Top

1.Hamdy NA, Kanis JA, Beneton MN, et al. Effect of alfacalcidol on natural course of renal bone disease in mild to moderate renal failure. Br Med J 1995;310:358-63.  Back to cited text no. 1    
2.Coen G, Ballanti P, Bonucci E, et al. Bone markers in the diagnosis of low turnover osteodystrophy in haemodialysis patients. Nephrol Dial Transplant 1998;13:2294-­302.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Salusky IB, Coburn JW, Brill J, et al. Bone disease in pediatric patients undergoing dialysis with CAPD or CCPD. Kidney Int 1988;33:975-82.  Back to cited text no. 3  [PUBMED]  
4.Fukagawa M, Iwasaki Y. Molecular pathogenesis of secondary hyperpara­thyroidism in renal failure: Basic and clinical aspects. Nephrol Dial Transplant 1999;14:61-2.  Back to cited text no. 4    
5.Coen G, Mazzaferro S. Bone metabolism and its assessment in renal failure. Nephron 1994;67:383-401.  Back to cited text no. 5  [PUBMED]  
6.Gamero P, Delrnas PD. Assessment of the serum level of bone alkalin phosphatases with a new immunometric assay in patient with metabolic disease J Clin Endocrinol Metab 1993;77:1046-53.  Back to cited text no. 6    
7.Mazzaferro S, Pasquali M, Ballanti P, et al. Diagnostic value of serum peptides of collagen synthesis and degradation in dialysis renal osteodystrophy. Nephrol Dial Transplant 1995;10:52-8.  Back to cited text no. 7    
8.Urena P, Ferreira A, Kung VT, et al. Serum pyridinoline as a specific marker of collagen breakdown and bone metabolism in hemodialysis patients. J Bone Miner Res 1995;10:932-9.  Back to cited text no. 8    
9.Hruska K. New concepts in renal osteodystrophy. Nephrol Dial Transplant 1998;13:2755-60.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Gerakis A, Hutchison AJ, Apostolou T, Freemont AJ, Billis A. Biochemical markers for non-invasive diagnosis of hyper­parathyroid bone disease and adynamic bone in patients on haemodialysis. Nephrol Dial Transplant 1996;11:2430-8.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Kaida H, Ishibashi M, Nishida H, et al. Usefulness of whole PTH assay in patients with renal osteodystrophy-correlation with bone scintigraphy. Ann Nucl Med 2005; 19:179-84.  Back to cited text no. 11  [PUBMED]  
12.Gal-Moscovici A, Popovtzer MM. New worldwide trends in presentation of renal osteodystrophy and its relationship to parathyroid hormone levels. Clin Nephrol 2005;63:284-9.  Back to cited text no. 12  [PUBMED]  
13.Avbersek-Luznik I, Balon BP, Rus I, Marc J. Increased bone resorption in HD patients: Is it caused by elevated RANKL synthesis? Nephrol Dial Transplant 2005;20:566-70.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Hutchinson AJ. Correlation of bone histology with PTH and radiology in end stage renal disease. Kidney Int 1993:44:1071-7.  Back to cited text no. 14    
15.Rubin G, Anelli F. Renal osteodystrophy with hyperparathyroidism, the diagnostic value of intact PTH, ALP, osteocalcin. J Nucl Biol Med 1994;38:489-94.  Back to cited text no. 15    
16.Urena P, Kubrusly M, Mannstadt M, et al. The renal PTH/PTHrP receptor is down­regulated in rats with chronic renal failure. Kidney Int 1994;45:605-11.  Back to cited text no. 16    
17.Qi Q, Monier-Faugere MC, Geng Z, Malluche HH. Predictive value of serum parathyroid hormone levels for bone turnover in patients on chronic maintenance dialysis. Am J Kidney Dis 1995;26:622-31.  Back to cited text no. 17  [PUBMED]  
18.Reichel H, Esser A, Roth HJ, Schmidt-Gayk H. Influence of PTH assay methodology on differential diagnosis of renal bone disease. Nephrol Dial Transplant 2003;18: 759-68.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Koller H, Zitt E, Staudacher G, Neyer U, Mayer G, Rosenkranz AR. Variable para­thyroid hormone (1-84)/carboxylterminal PTH ratios detected by 4 novel parathyroid hormone assays. Clin Nephrol 2004;61: 337-43.  Back to cited text no. 19  [PUBMED]  
20.Cantor T, Sci B. The assay of the hypocalcemic PTH fragment inhibitor with PTH provides a more accurate assessment of renal osteodystrophy compared to the intact PTH assay. Nefrologia 2003;23:69-72.  Back to cited text no. 20  [PUBMED]  
21.Ferreira A, Ghazali A, Galvao J, et al. Effect of type of dialysis membrane on bone in hemodialysis patients. Nephrol Dial Transplant 2001;16:1230-8.  Back to cited text no. 21    
22.Fiedler R, Deuber HJ, Langer T, Osten B, Mohan S, Jehle PM. Effects of reduced dialysate calcium on calcium-phosphorus product and bone metabolism in hemodialysis patients. Nephron Clin Pract 2004;6:c1-2.  Back to cited text no. 22    

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Correspondence Address:
Mohammad Rahimian
Nephrology Ward, Yazd Medical University
Iran
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PMID: 18087140

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    Abstract
    Introduction
    Methods and Patients
    Statistical Analysis
    Results
    Discussion
    References
    Article Tables
 

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