Biological Trace Element Research

, Volume 137, Issue 3, pp 335–339

Diminished Selenium Levels in Hemodialysis and Continuous Ambulatory Peritoneal Dialysis Patients


  • Maryam Pakfetrat
    • Shiraz Nephro-Urology Research CenterShiraz University of Medical Sciences
    • Shiraz Nephro-Urology Research CenterShiraz University of Medical Sciences
  • Mahshid Hasheminasab
    • Shiraz Nephro-Urology Research CenterShiraz University of Medical Sciences

DOI: 10.1007/s12011-009-8588-2

Cite this article as:
Pakfetrat, M., Malekmakan, L. & Hasheminasab, M. Biol Trace Elem Res (2010) 137: 335. doi:10.1007/s12011-009-8588-2


In this cross-sectional study, selenium (Se) levels in the sera of 35 hemodialysis (HD) patients and 34 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) for more than 3 months were compared with the serum Se levels of 34 healthy volunteers. The observed Se levels of 100.8 ± 51.9 µg/L in the sera of the HD patients and of 65.5 ± 32.1 µg/L in the sera of the CAPD patients were significantly lower than the 134.9 ± 81.2 µg/L of the controls, with p = 0.002 and 0.02, respectively. Furthermore, the Se levels were significantly higher in the HD rather than the CAPD patients (p = 0.01). In the spent dialysate effluent fluid of 32 of the CAPD patients Se was undetectable, in the remaining two CAPD patients the Se levels were 1.9 and 4.6μg/l, respectively. The low Se levels of HD and CAPD patients as compared to healthy persons are attributed to diminished Se retention due to chronic oxidative stress.


HemodialysisPeritoneal dialysisSelenium


Dialysis patients are subject to chronic oxidative stress that can trigger defense mechanisms for protection against oxidative damage [1]. The seleno-enzyme GSH-Px plays a significant role in protecting cell membranes from oxidative damage [2, 3]. The relationship between antioxidant competence and the severity of renal failure might be one of the reasons of various pathologies which are associated with the end stage renal disease (ESRD) such as shortening of red blood cell life span, platelet dysfunction, accelerated aging, and cardiovascular diseases [4].

In patients with ESRD serum, Se is generally found to be lower than in normal healthy subjects for as yet unexplained reasons [2, 3]. The aim of the present study was to determine the serum Se of hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) patients and to compare it with that of healthy controls since it is possible that HD and CAPD patients due to their special diets receive Se mainly in inorganic form such as sodium selenite rather than as L (+) selenomethionine, the chief organic nutritional form of Se normally present in food [5, 6]. This could explain the observed differences between patients and controls since selenomethionine will raise serum Se levels more than inorganic Se as it may replace methionine in the plasma proteins.

Materials and Methods


This is a cross-sectional study based on data collected from HD and CAPD patients treated at the Shiraz University of Medical Sciences in Iran. In this research about 67 cases were selected randomly (between 18 and 75 years old); 35 HD and 34 CAPD patients who were under HD or CAPD for more than 3 months were selected. This study is in conformity with the Declaration of Helsinki and was approved by the local Ethics Committee. All patients filled the written consent form. The liver disease, neoplasia, diarrhea, or parathyroidectomy, previous kidney transplant, and current or recent intake of drugs which affected on Se or Se supplement were excluded. Meanwhile, 34 healthy volunteers' subjects from health care workers with no medical problems were selected for control group randomly. The controlled patients were all generally healthy according to the medical history and examinations: baseline tests for blood urea nitrogen (BUN), creatinine (Cr), glucose, AST, ALT, and ALP were all in normal range.

Study Protocol

HD is generally performed three times per week over a period of 4 h with using Fresenius 4008B machines and a low flux synthetic, polysulfone membrane. In all patients, bicarbonate-based dialysate fluid was used. It contains sodium (Na) 136 meq/l, potassium (K) 2 meq/l, Mg 0.5 mmol/l, and calcium (Ca) 1.25 mmol/l. It must be mentioned that those settings were the same for all patients during the HD session. Blood and dialysate flow rates were 300–350 and 500 ml/min, respectively. Blood samples of patients were collected from the arterial line immediately before a mid week single dialysis session before heparin administration in a fasting state, which were centrifuged and frozen at −70°C before the measurements.

Serum levels of BUN, Cr, Se, zinc (Ze), triglyceride (TG), cholesterol, LDL, HDL, albumin (Alb), hemoglobulin (Hb), serum iron, frettin, Na, K, and uric acid were measured. Also Aliquots of 10 cc from pre and post HD fluid were collected and frozen at −70° to measure Se level.

In CAPD patients, depending on the desired volume of fluid removal, an isotonic (i.e., containing D 1.5%) dialysate fluid or higher concentrations of D (2.5% or 4.5%) were used (Dianeal PD-2, Baxter Health Care, Singapore). The usual volume of dialysate fluid was 2 L for each exchange. This rate was variable from three to four exchanges per day. The aim was to achieve a negative fluid balance of 1 to 2 L per day. On usual monthly clinical visit venous blood sample was drawn after an overnight fast which were centrifuged and frozen at −70°C before the measurements. Dialysate effluents which had been removed by the first exchange in the morning, were investigated .Aliquots of 10 cc were collected from the effluent. The specimens were refrigerated for evaluating Se.

The Se determinations were performed using a graphite furnace atomizer (GFA-4B). Ze was measured by the manual extraction (CTA 2000, England). BUN, sCr, sCa, and P were performed by using a profile analyzer (Prestige 24I, Tokio, Nippon). TG and cholesterol were measured by the enzymatic method (End point). Alb was measured by using BCG method (Brown Crezo Green). Hb was measured by using the cell counter, serum Na and K were measured by using flame photometer (Fater electronic, Tehran, Iran). All measurements were performed at the GHRC laboratory of Shiraz Medical University.

Statistical Analysis

Data were analyzed by Statistical Package for the Social Sciences software version 15.0 (SPSS Inc., Chicago, IL, USA). Comparison of the quantities data was made using the Student’s t test, and analysis of variance (ANOVA; Mann–Whitney and Kruskal–Wallis tests as nonparametric test). Correlation between quantitative data was determined by Pearson’s correlation coefficient (Spearman's rho as nonparametric correlation coefficient). Also Chi-square test was performed for comparison of the qualitative data. A p value of <0.05 was considered as a significant factor.


Sixty-seven dialysis patients (35 HD and 34 CAPD patients), and 34 healthy persons with the average age 49.9 ± 15 years participated in this study.

There was no significant difference in demographic data between these three groups. There was a significant difference between Se for the three groups (ANOVA test, p = 0.006) according to LSD, there was a significance difference between control and CAPD groups (134.9 ± 81.2 µg/l, 65.5 ± 32.1 µg/l, p = 0.002) as well as control and HD groups (134.9 ± 81.2 µg/l, 100.8 ± 51.8 µg/l, p = 0.02). The rate of Se level was significantly higher in HD group in comparison with CAPD patients (p = 0.01). Values of biochemical data which have been compared between the CAPD and HD patients are shown in Table 1.
Table 1

Laboratory Findings are Compared Among All Cases and Two Studied Groups


Total (n = 101)

PD group (n = 34)

HD group (n = 35)


p value

Age (years)

49.9 ± 15.9

51.5 ± 15.0

55.6 ± 13.9

Student’s t


Sex/male (n, %)

54 (53.5%)

14 (43.8%)

23 (65.7%)



Selenium (µg/l)

85.8 ± 51.3

69.5 ± 46.1

100.8 ± 51.8

Student’s t


Hemoglobulin (g/dl)

10.7 ± 1.9

11.1 ± 1.8

10.4 ± 2.0



Triglyceride (mg/dl)

159.9 ± 96.5

205.2 ± 107

120.8 ± 66.3



Cholesterol (mg/dl)

177.5 ± 53.1

206.5 ± 55.6

159.5 ± 34.7

Student’s t


LDL (mg/dl)

109.0 ± 39.8

120.6 ± 44.3

93.5 ± 27.2

Student’s t


HDL (mg/dl)

37.5 ± 13.1

42.0 ± 13.3

30.9 ± 9.8

Student’s t


Total protein (mg/dl)

6.95 ± 0.8

6.94 ± 0.80

7.0 ± 1.2

Student’s t


Albumin (mg/dl)

4.0 ± 0.6

3.9 ± 0.6

4.1 ± 0.5

Student’s t


BUN (mg/dl)

52.9 ± 17.1

45.3 ± 14.7

60.6 ± 16.1

Student’s t


Creatinine (mg/dl)

7.9 ± 3.1

7.2 ± 3.5

8.5 ± 2.6

Student’s t


Sodium (meq/dl)

140.6 ± 4.6

139.3 ± 3.5

141.7 ± 5.2

Student’s t


Potasium (meq/dl)

5.0 ± 0.9

4.4 ± 0.7

5.5 ± 0.9

Student’s t


Zinc (µg/dl)

77.5 ± 34.8

75.2 ± 21.9

79.7 ± 44.0



Calcium (mg/dl)

8.8 ± 0.8

8.8 ± 0.9

8.8 ± 0.8

Student’s t


Phosphorus (mg/dl)

5.3 ± 1.6

4.8 ± 1.1

5.7 ± 1.9

Student’s t


PD peritoneal dialysis, HD hemodialysis, n Number, ± mean ± standard deviation, NS not significant, LDL low-density lipoprotein, HDL high-density lipoprotein

aNone normal distribution (after Kolmogorov–Smirnov test)

Only 35.3% of control group had Se in normal range (35.3% of PD group and 34.3% of HD). Se concentration in spent dialysate effluent in HD patients (780.2 ± 103.4 µg/l) was significantly higher than dialysate influent (532.5 ± 92.7 µg/l; p = 0.004). The range of Se levels in the spent dialysate effluent fluid in CAPD patients was undetectable (range 0 µg/l in 33 patients, 1.9 and 4.6 µg/l in two others).


The present study indicated that serum level of Se was significantly lower in HD and peritoneal dialysis patients in comparison with healthy subjects; meanwhile, CAPD patients were more at risk of Se deficiency than HD patients. Although normal Se concentrations have been reported in the advanced stage of CRF [7], lower values have been noted frequently [810].

Se deficiency may contribute to cardiovascular disease, anemia [11], and immune dysfunction, all of them are common in patients with renal failure [12]. The reason for Se depletion in ESRD patients is not clear and several of the following factors should be taken into account to explain this phenomenon: decreased dietary intake combined with protein restrictions, impaired gastrointestinal absorption of Se compounds and HD treatment [4, 13]. Our study indicated that a significant loss of Se occurred through HD membrane. It was in agreement with the study of Bogye et al. that indicated selenium is lost through the pores of polysulfone membranes during HD which is associated with their protein permeability [13].

Another important aspect of Se metabolism in ESRD patients is likely derangement of the plasma Se carrier environment. Se in human plasma is incorporated specifically (as selenocysteine) in selenoprotein P and GSH-Px and nonspecifically (as selenide or selenomethionine) in the Alb fraction [14, 15]. The fraction of Se bound to these proteins varies with a dietary intake and health status .Particularly, acute-phase response, as documented by elevated plasma C-reactive protein levels, causes plasma Se to decrease and selenoproteins redistribution [16, 17].

With regard to the previous studies, this study also indicated that Se deficiency [18, 19] is more prevalent in CAPD in comparison with HD patients. It may occur as a result of differences in serum volume or nutritional factors. Otherwise urinary loss of Se [20] may be more prevalent in CAPD than HD patients because of higher residual renal function in CAPD patients. Theoretically, peritoneal dialysis might lead to a greater depletion of elements than HD because most elements are protein bound and peritoneal protein loss may occur significantly, where the loss is in the form of amino acids and not intact proteins. But in our study, Se loss in CAPD patients was undetectable in spent peritoneal fluid. This result is in conformity with previous study which has been performed by Apostolidis [19] and Sriram et al. [21]. Although in the present study, loss of selenium from HD membrane is significantly more in comparison with peritoneal membrane, the mechanism(s) of occurring Se depletion in CAPD is being studied now.


This study was funded by The Shiraz Nephro-Urology Research Center of Shiraz University of Medical.

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© Springer Science+Business Media, LLC 2009