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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2010  |  Volume : 21  |  Issue : 4  |  Page : 707-711
Relation of serum albumin and C-reactive protein to hypotensive episodes during hemodialysis sessions

1 Department of Internal Medicine, Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
2 Interventional Electrophysiology, Fars Heart Foundation, Shiraz, Iran
3 Department of Biostatistics, Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
4 Kousar Hospital, Shiraz, Iran

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Date of Web Publication26-Jun-2010


To evaluate the effect of albumin serum levels and C-reactive protein (CRP) on the course of dialysis induced hypotension (DIH) in chronic hemodialysis (HD) patients, we studied 58 chronic hemodialysis patients in our center during 2007. We investigated the correlation bet­ween serum albumin, highly sensitive CRP (hs-CRP) and DIH. The mean of the serum albumin levels was 4.2 ± 0.5 g/dL, and 32.8% of the patients revealed hypoalbuminemia. Occurrence of DIH among HD patients was 27.6%. The mean of serum albumin levels in the DIH group was significantly lower compared with the normotensive group (3.9 ± 0.4 vs 4.3 ± 0.5g/dL, respec­tively, P= 0.008). The mean of the hs-CRP levels was significantly higher in the DIH group compared with the normotensive group (12.9 ± 12 vs. 7.2 ± 5.2 mg/dL, respectively, P= 0.01). We conclude that high level of CRP and hypoalbuminemia may be predictors of DIH.

How to cite this article:
Pakfetrat M, Roozbeh J, Malekmakan L, Zare N, Nasab MH, Nikoo MH. Relation of serum albumin and C-reactive protein to hypotensive episodes during hemodialysis sessions. Saudi J Kidney Dis Transpl 2010;21:707-11

How to cite this URL:
Pakfetrat M, Roozbeh J, Malekmakan L, Zare N, Nasab MH, Nikoo MH. Relation of serum albumin and C-reactive protein to hypotensive episodes during hemodialysis sessions. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2019 Dec 7];21:707-11. Available from: http://www.sjkdt.org/text.asp?2010/21/4/707/64654

   Introduction Top

Dialysis-induced hypotension (DIH) observed in 20-33% of hemodialysis (HD) patients, and the pathogenesis is multifactor. [1],[2] Hypoalbumi­nemia is a strong predictor of mortality and morbidity among HD patients, [3],[4],[5] and is asso­ciated with increased risk of infection in dia­lysis patients. [6] Hypoalbuminemia is a major risk factor of hypotension during HD, [7] and can result from protein malnutrition, increased dia­lysate protein loss, systemic illness, and infla­mmatory disorders. [8],[9],[10]

In addition, immune activation working through IL-6, CRP and other cytokines play a role in pathogenesis of DIH in some patients. [11]

In the present study, we evaluated serum Alb and CRP in HD patients and their correlation with DIH.

   Patients and Methods Top

This is a cross sectional study based on data collected from HD patients treated at the Sahraee HD Center of Shiraz, Iran during 2007. We recruited 58 chronic HD patients without a history of endocrine tumors, diabetes mellitus, liver failure, heart failure, or unstable coronary artery disease. Patients with hemoglobin less than 9 mg/dL were excluded. The age of the patients ranged from over 18 to less than 75 years of age.

All the patients were dialyzed for at least three months before entering the study. They were dialyzed three times a week for 4 h each time on Fresenius 4008B machines and low flux synthetic polysulfone membrane dialy­zers. Dialysate temperature, sodium and cal­cium concentration were also kept constant. In all patients, we used bicarbonate-based dialy­sate fluid that contained sodium 136 mmol/L, potassium 2 mmol/L, magnesium 1 mmol/L, and calcium 1.25 mmol/L, and those settings were the same for all the patients during the HD session. Blood and dialysate flow rates were 300-350 and 500 mL/min, respectively. The ultrafiltration rate was fixed over the course of a dialysis session with meticulous adjust­ment of dry weight. The administration of any drugs that could influence blood pressure (BP) was stric-tly avoided during dialysis.

Blood samples from HD patients in a fasting state were collected from the arterial line im­mediately before the mid week dialysis session before heparin administration, and they were centrifuged and frozen at -70΀ C before the measurements. Biochemical determinations in­cluded levels of: serum albumin (Alb), lipid profile, blood urea nitrogen (BUN), serum creatinine (cr), magnesium (Mg), calcium (Ca), phosphorus (P), sodium (Na), potassium (K) and highly sensitive C-reactive protein (hs­CRP). All measurements were performed at the gastrohepatology research center labora­tory of Shiraz Medical University. Serum Alb levels were measured using a bromocresol pur­ple dye-binding method. The levels of hs-CRP were assayed with the Nephelometric method; normal range of hs-CRP was defined ≤ 3.3 mg/dL.

Blood pressure (BP) was measured with an automatic sphygmomanometer every 30 mi­nutes. Electrocardiogram was performed be­fore and after dialysis sessions. According to national kidney foundation guideline (NFK­DOQI guideline), DIH was defined as a dec­rease of systolic BP of more than 20 mmHg of the basal value associated with signs and symp­toms (dizziness, nausea, sweating, and pallor). DIH episodes were treated conventionally by decreasing the ultrafiltration volume or admi­nistering hypertonic salt solution.

Hypoalbuminemia was defined as Alb < 4 g/dL (NFK-DOQI guideline).

This study complies with the Declaration of Helsinki and was approved by the local Ethics Committee. All patients signed written informed consents.

   Statistical Analysis Top

Data were analyzed by SPSS, V15. Quantita­tive data are presented using the mean and standard deviation. Comparison of quantitative data was made using the Mann-Whitney test as nonparametric test. Qualitative data were ana­lyzed by the Chi-Square test. The correlation was determined by the Pearson's correlation coefficient. A P value of less than 0.05 was considered significant.

   Results Top

The average age of the study patients was 51.1 ± 17.5 years, and 62.1% (36/58) of them were male. The causes of ESRD included dia­betes mellitus (n=17), nephrosclerosis (n=18), glomerulonephritis (n=6), renal stone (n=5), polycystic kidney disease (n=2), and unknown causes (n=10).

The mean of the patients KT/V was 1.2 ± 0.5. The mean of the serum Alb levels in the study patients was 4.2 ± 0.5g/dL and 32.8% (19/58) of patients revealed hypoalbuminemia. DIH among our patients was 27.6% (16/58). Patients were divided in to two subgroups: with DIH and without DIH (non-DIH) group. [Table 1] shows the blood chemistry value between the DIH and the non-DIH patients. Electro-cardiogram did not show any significant changes after HD sessions in any patients in either subgroup.

The mean of serum Alb levels in the DIH group was significantly lower compared with the non-DIH group group (3.9 ± 0.4 vs 4.3 ± 0.5g/dL, P= 0.008). DIH occurred in 52.6% of patients with hypoalbuminemia compare to 15.4% of patients with normal serum Alb (P= 0.005). The mean of the hs-CRP levels was signifi­cantly higher in the DIH group compared with the non-DIH group (12.9 ± 12 vs. 7.2 ± 5.2 mg/dL, P= 0.01). However, there was no sig­nificant difference in the other biochemical markers including BUN, serum Cr, Ca, P, and lipid profile between the DIH and the non-DIH groups. There was a negative correlation bet­ween the serum alb and hs-CRP levels, but this correlation was not significant (r=-0.13, P= 0.33).

   Discussion Top

In this study, we investigated some bioche­mical markers of patients during HD and its relation to DIH. Serum alb level in patients with DIH was significantly lower compared with patients without DIH. In addition, high serum level of hs-CRP was a significant risk factor for developing DIH.

Some features of DIH are directly related to the dialysis procedure itself such as ultrafiltra­tion rate, meal during dialysis, increased tem­perature, and acetate dialysate. [12],[13] Several pa­tient characteristics increase the risk of DIH, such as older age, diabetes, left ventricular hy­pertrophy, coronary artery disease, autonomic neuropathy, excessive intradialytic weight gain and low ejection fraction. [14],[15],[16],[17]

In some but not all studies, a positive asso­ciation between serum Alb concentration and BP was found as a prime risk factor for stroke and coronary heart disease. [18] Whitfield et al, demonstrated a strong correlation between BP and plasma Alb. [19] Hostmark et al, showed that systolic BP and diastolic BP increased with increasing serum Alb concentration up to the physiological range. [20]

A rise in serum Alb of 1 gr/dL was associated with a 1.8 mmHg and 0.9 mmHg increase in SBP and DBP, respectively. This phenomenon may be related to experimental studies linking tryptophan, the only amino acid to bind non­covalently to serum Alb, to a BP lowering ef­fect mediated by promotion of 5-hydroxy-tryp­tamine synthase in the brain. [18] Some authors have suggested that the observed effect of se­rum Alb on BP might be actually due to serum Ca. [18] However, another study found no asso­ciation between ionized Ca and BP. [21] Futher­more, associations of serum Alb concentra­tions and BP could result from increased hy­drostatic pressure producing hemoconcentra­tion. [22] Nakamato et al compared background characteristics of hypotensive patients during HD and showed that serum Alb in the DIH group was significantly lower compared with the normotensive group; our results were com­parable to those found by Nakamato. [7] However, some studies failed to demonstrate an asso­ciation between Alb and BP. [23],[24]

In our study, about 50% of our patients showed a high hs-CRP level. Incidence of DIH was significantly higher in patients with high level of hs-CRP compared with normal hs-CRP pa­tients (41.4% vs 13.8%, P= 0.038). Tometa et al examined the relationship between HD­induced immune activation and DIH, using the acute phase reactant, serum CRP as a surrogate for immunogenic activation. The maximum per­cent change in the mean arterial pressure was found to correlate significantly with CRP (r= 0.67, P< 0.05) in nine consecutive patients with a history of symptomatic DIH. Immune activation mediated by interleukine-6, CRP and other cytokines plays a role in pathogenesis of DIH in some patients. [11]

An elevated CRP has been reported to negate the relationship with serum Alb. [25] In our study, the incidence of hypoalbuminemia in the pa­tients with high hs-CRP level was higher com­pared with patients with normal hs-CRP, but the correlation was not significant. However, some studies suggest that serum Alb is inde­pendently affected by both inflammation and nutritional intake. [26]

Our study has some limitation. Assessment of DIH and measurement of serum Alb was done in only single session of HD.

We conclude that low serum Alb levels and high level of hs-CRP may predict an increased risk of DIH in HD patients.

   References Top

1.Kaczmarczyk I, Krasniak A, Drozdz M, et al. The influence of sodium profiling on blood volume and intradialytic hypotension in pa­tients on maintenance hemodialysis. Przegl Lek 2007;64(7-8):476-80.  Back to cited text no. 1      
2.Duman D, Demirtunc R, Erdogan B, Sahin GM, Karadag B. Dialysis-induced hypotension is associated with impaired aortic elasticity in patients undergoing chronic hemodialysis. Blood Press Monit 2008;13(2):73-8.  Back to cited text no. 2      
3.Iseki K, Kawazoe N, Fukiyama K. Serum albumin is a strong predictor of death in chro­nic dialysis patient. Kidney Int 1993;44(1): 115-9.  Back to cited text no. 3      
4.Leon JB, Albert JM, Gilchrist G, et al. Im­proving albumin levels among hemodialysis patients: a community-based randomized con­trolled trial. Am J Kidney Dis 2006;48(1):28-­36.  Back to cited text no. 4      
5.Hossli SM. Clinical management of intra­dialytic hypotension; survey results. Nephrol Nurs J 2005;32(3):287-91.  Back to cited text no. 5      
6.Adeniyi OA, Tzamaloukas AH. Relation bet­ween access-related infection and pre-infection serum albumin concentration in patients on chronic hemodialysis. Hemodial Int 2003;7(4): 304-10.  Back to cited text no. 6      
7.Nakamoto H, Honda N, Mimura T, Suzuki H. Hypoalbuminemia is an important risk factor of hypotension during hemodialysis. Hemodial Int 2006;10:10-5.  Back to cited text no. 7      
8.Kalantar-Zadeh K, Ikizler TA, Block G, Avram MM, Kopple JD. Malnutrition-inflammation complex syndrome in dialysis patients: causes and consequences. Am J Kidney Dis 2003;42: 864-81.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]  
9.Cheng CH, Chen MY, Lee YJ, et al. Assess­ment of nutritional status in continuous ambu­latory peritoneal dialysis patients: a com­parison of bioelectric impedance and conven­tional methods. Zhong-hua Yi Xue Za Zhi (Taipei) 2000;63(10):758-64  Back to cited text no. 9      
10.Acchiardo SR, Moore LW, Latour PA. Malnu­trition as the main factor in morbidity and mortality of hemodialysis patients. Kidney Int 1983;24:99-203.  Back to cited text no. 10      
11.Tomita M, Malhotra D, Dheenan S, Shapiro JI, Henrich WL, Santoro TJ. A potential role for immune activation in hemodialysis hypoten­sion. Ren Fail 2001;23(5):637-49.  Back to cited text no. 11      
12.Tisler A, Akocsi K, Borhas B, et al. The effect of frequent or occasional dialysis-associated hypotension on survival of patients on mainte­nance of hemodialysis. Nephrol Dial Transplant 2003;18:2601-5.  Back to cited text no. 12      
13.Thaha M, Yogiantoro M, soewanto. Corre­lation between intradialytic hypotension in patients undergoing routine hemodialysis and use of acetate compared in bicarbonate dialy­sate. Acta Med Indones 2005;37(3):145-8.  Back to cited text no. 13      
14.Daugirdas JT. Pathophysiology of dialysis hypotension: an update. Am J Kidney Dis 2001;38:11-7.  Back to cited text no. 14      
15.Passauer J, Bussemarker E, Gross P. Dialysis hypotension; Do we see the end of tunnel? Nephrol Dial Transplant 1998;13:3024-9.  Back to cited text no. 15      
16.Takeda A, Toda T, Fujii T, Sasaki S, Matsui N. Can predialysis hypertension prevent intra­dialytic hypotension in hemodialysis patients? Nephron Clin Pract 2006;103(4):137-43.  Back to cited text no. 16      
17.Schreiber MJ. Clinical dilemmas in dialysis: managing the hypotensive patients setting the stage. Am J kidney Dis 2007;38:1-10.  Back to cited text no. 17      
18.Hu H, Sparrow D, Weiss S. Association of serum albumin with blood pressure in the normative aging study. Am J Epidemiol 1992; 136(12):1465-73  Back to cited text no. 18      
19.Whitfield JB, Martin NG. Blood pressure and chemistry, some correlations and apparent cor­relations. Ann Clin Biochen 1984;21(4):257-­60.  Back to cited text no. 19      
20.Hostmark AT, Tomten SE, Berg JE. Serum albumin and blood pressure: a population- based, cross-sectional study. J Hypertens 2005;23(4):725-30.  Back to cited text no. 20      
21.Vargas CM, Obisesan TH, Cillum RF. Asso­ciation of serum albumin concentration, serum ionized calcium concentration, and blood pre­ssure in the third national health and nutrition examination survey .J clin Epidemiol 1998;51 (9):739-46  Back to cited text no. 21      
22.Tibblin G, Bergentz SE, Bjure J, Wilhelmsen L. Hematocrit, plasma protein plasma volume, and viscosity in early hypertensive disease. Am Heat J 1966;72:165-76.  Back to cited text no. 22      
23.Bulpitt CJ, Hodes C, Everitt MG. The rela­tionship between blood pressure and bioche­mical risk factors in a general population. Br J Prev Soc Med 1976;30:158-62.  Back to cited text no. 23  [PUBMED]  [FULLTEXT]  
24.Walker AR, Walker BF, Manetsi B, Molefe O, Walker AJ. Serum Albumin level in elderly rural Africans. Int J Vit Nutr Res 1991;61:339­45.  Back to cited text no. 24      
25.Coutinho HM, Leenstra T, Acosta LP, et al. Pro-inflammatory cytokines and C-reactive protein are associated with undernutrition in the context of Schistosoma japonicum infec­tion. Am J Trop Med Hyg 2006;75(4):720-6.  Back to cited text no. 25      
26.Kaysen GA, Stevenson FT, Depner TA. Determinants of albumin concentration in hemodialysis patients. Am J Kidney Dis 1997; 29:658-68.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]  

Correspondence Address:
Leila Malekmakan
Nephro-Urology Research Center, Shiraz University of Medical Sciences, P.O. Box 71348-14336, Shiraz
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