Association between extracellular water, left ventricular mass and hypertension in haemodialysis patients

Riccardo Maria Fagugli1, Paolo Pasini2, Giuseppe Quintaliani1, Franca Pasticci1, Giovanni Ciao1, Beatrice Cicconi1, Daniela Ricciardi1, Paola Vittoria Santirosi1, Emanuela Buoncristiani1, Francesca Timio1, Fabrizio Valente1 and Umberto Buoncristiani1

1Department of Nephrology-Dialysis and 2Department of Cardiology, Silvestrini Hospital, Perugia, Italy

Correspondence and offprint requests to: Riccardo Maria Fagugli, MD, S. C. Nefrologia e Dialisi, Ospedale Silvestrini, Azienda Ospedaliera di Perugia, S. Andrea delle Fratte, 06100 Perugia, Italy. Email: rmfag{at}tin.it



   Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Background. Hypertension and left ventricular hypertrophy (LVH) are present in the majority of patients undergoing haemodialysis (HD). These two pathologies persist after dialysis onset, and pharmacological therapy is often required for adequate control of blood pressure (BP). Although fluid overload is a determinant of hypertension, clinical assessment of this parameter remains difficult and unsatisfactory. Bioimpedance analysis (BIA) spectroscopy and the relative determination of extracellular water (ECW%) may provide a simple and inexpensive tool for investigating fluid overload. We studied 110 patients on thrice-weekly HD to determine whether ECW body content correlates with hypertension and LVH in this patient population.

Methods. Hypertension was determined according to the WHO criteria (office BP >= 140/90 and/or the use of antihypertensive therapy). Twenty-four hour BP monitoring and echocardiography were performed on midweek inter-HD days. Blood chemistries, dialysis dose (spKt/V) and bioimpedance were analysed on midweek HD days.

Results. Hypertension was present in 74.5% of patients. There were no differences for age, spKt/V, haemoglobin, serum creatinine and residual renal function between normotensive and hypertensive patients. Twenty-four hour systolic BP (SBP), 24 h diastolic BP and 24 h pulse pressure were higher in hypertensive patients, in spite of antihypertensive therapy. LVH was present in 61.8% of patients. BIA revealed that ECW% was increased in LVH+ patients (LVH+ = 47.5 ± 7.9%, LVH– = 42.4 ± 6.2%, P = 0.01) and in hypertensive patients compared with normotensives (46.5 ± 7.7% vs 43 ± 7.2%, P = 0.02). Dry body weights and inter-HD body weight increases did not differ between hypertensive and normotensive patients nor between patients with or without LVH. ECW was correlated with SBP (r = 0.35, P < 0.01) and with left ventricular mass index (LVMig/sqm) (r = 0.49, P < 0.001). A stepwise multiple linear regression model revealed that LVMig/sqm was significantly correlated with ECW%, SBP and male gender (r = 0.65, P < 0.001).

Conclusions. LVH and hypertension are present in a majority of HD patients and they are closely correlated with one another. We found associations between fluid load, measured by BIA and expressed as ECW, and BP and LVM.

Keywords: extracellular water; haemodialysis; hypertension; left ventricular hypertrophy



   Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
According to the United States Renal Data System (http://www.usrds.org/2001pdf/h.pdf) and the Italian Hemodialysis Register (http://www.sin-ridt.org/), cardiovascular diseases are the most important cause of mortality in haemodialysis (HD) patients. Left ventricular hypertrophy (LVH) is present in a majority of HD patients and is accompanied in the long term by cardiac myocyte apoptosis, fibrosis, capillary rarefaction and, consequently, ischaemic heart disease [1]. LVH is correlated with patient survival, and its regression is associated with an improved cardiac outcome [2]. Hypertension and LVH are strongly correlated, and their pathogenesis is linked to a number of causes, including fluid and salt overload, hyperkinetic flow secondary to anaemia or arteriovenous fistula, hyperparathyroidism, accelerated atherosclerosis due to advanced glycation end-products accumulation, oxidative stress and hyper-homocysteinaemia [3]. Although fluid overload is likely to play a role in hypertension and LVH, this possibility has not been tested using diagnosis and clinical follow-up [4]. Bioimpedance analysis (BIA), a method of body water composition analysis, has provided a simple and inexpensive means to assess various parameters in HD patients [5,6]. The aim of our study was to investigate associations between derived parameters of fluid load measured by BIA, such as extracellular water (ECW), and blood pressure (BP) and left ventricular mass index (LVMi) in HD patients.



   Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
We performed a cross-sectional study on a population of 120 HD patients (73 male and 47 female, age 57 ± 17.1 years) treated thrice-weekly for a total of 12 h. The patients had been on HD (HD age) for 34 ± 45.2 months. They were treated at the Department of Nephrology-Dialysis at the Regional Hospital of Perugia. Inclusion criteria were age >15 and <75 years, stable clinical and biochemical conditions for at least the previous 3 months and a spKt/V of >1.2. Ultrafiltration was under strict control, and ideal dry body weight (dBw) presumably achieved when intolerance became evident through muscle cramps or hypotensive episodes. Exclusion criteria were limb amputation, severe malnutrition [a narrow phase angle (PA) of <3° during BIA, a decrease of dBw of >=10% over the previous 3 months, a body mass index of <=18, a serum albumin level of <=3.2 g/dl and a serum cholesterol level of <=150 mg/dl] and other malignancies. All patients provided informed consent for participation in the study.

Hypertension was determined according to the WHO criteria (office BP>=140/90 and/or the use of antihypertensive therapy). Blood chemistries were determined at the beginning of midweek HD sessions. On the same day, body composition was studied by BIA at 20 min after the end of dialysis. On the following midweek inter-HD day, 24 h ambulatory BP monitoring and echocardiography were performed. These examinations were performed using the following methods.

Blood chemistries
Haemoglobin, uric acid, serum urea and serum creatinine were determined using standard procedures.

Office pre-HD blood pressure (OBP)
During the month before ambulatory monitoring, OBP values were recorded at the beginning of each HD session by expert dialysis technicians. Each value was derived from the mean of three consecutive measurements. The mean of 12 such values, monitoring a period of 1 month, was designated as OBP.

Ambulatory blood pressure measurement (ABPM)
ABPM was recorded on inter-HD days using an A&D Takeda TM2421 (A&D, Tokyo, Japan) [7]. BP readings were taken at 15 min intervals from 7 a.m. to 10 p.m. for awake BP and at 30 min intervals from 10 p.m. to 7 a.m. for asleep BP. ABPM recordings having >10% of values missing were excluded from the study. Dipper patients were classified as having night-time systolic BP (SBP) decreases of at least 10% compared to the daytime values. The SBP night/day (N/D) ratio was also calculated.

Echocardiography
Standard two-dimensional and two-dimensional-guided M-mode echocardiography was performed with a Sonolayer {alpha} SSA-270 (Toshiba, Nasu, Japan) using a 3.75 MHz transducer. Echocardiograms were taken according to the American Society of Echocardiography guidelines on inter-HD midweek days. We measured left ventricle internal diastolic diameter (LViDD), diastolic posterior wall thickness (PWT) and interventricular septum thickness (IVS).

LVM was calculated using the Devereux formula [8]: LVM (g) = 0.8 x 1.04 x [(LviDD + IVS + PWT)3 – LviDD3] + 0.6. LVMi was calculated by dividing LVM by body surface area. Sex-specific criteria were used to determine the presence of LVH (males, LVMi >= 131 g/m2; females, LVMi >=100 g/m2) [9].

Relative wall thickness (RWT) was calculated using the following formula: RWT = (2 x PWT)/LViDD; values of >0.45 in the presence of LVH suggested left ventricular concentric hypertrophy. Fractional shortening (FS%), a measure of left ventricle function, was calculated as follows: FS% = [LViDD – LViSD (left ventricle internal systolic diameter)] x 100/LViDD. Systolic dysfunction was defined as FS < 25%.

Bioimpedance measurements
Impedance measurements were performed at the bedside according to standard, tetrapolar, whole-body (hand–foot) techniques using a single-frequency (50 kHz) analyser (BIA-101; Akern–RJL Systems, Florence, Italy). Although there may be differences between multi-frequency and single-frequency BIA determinations of total body water (TBW) and related parameters [10], previous studies failed to detect significant improvements from single to multiple frequency (5, 50, 100, 500 and 1000 kHz) analysers in the measurement of total body resistance (R) and reactance (Xc) [11,12]. Therefore, we performed single-frequency measurements with the same operator at 20 min after midweek HD. R and Xc values were collected and used in specific formulas supplied by the manufacturer [1315] to determine TBW, body cell mass (BCM) and ECW, which was reported as a percentage of TBW. In order reveal any potential flaws associated with the equations, we also reported R, Xc and PA (the arc tangent of the Xc/R ratio). When using a 50 kHz fixed-frequency BIA device, R is related to TBW, and Xc is related to ECW [16]; a decrease in PA, which captures the relative contribution of Xc and R, is the consequence of cell membrane reduction [17].

Statistical analysis
Results are expressed as means ± SD. Unpaired Student’s t-tests and Mann–Whitney tests were used when applicable to investigate differences between hypertensive and normotensive patients and between patients with and without LVH. The {chi}2 test was used to analyse non-parametric data. Pearson’s correlation coefficients and multiple linear regression analysis were used to identify the possible determinants of hypertension and LVMi. Multiple stepwise linear regression was performed using LVMi as the dependent variable and gender, age, HD age, Kt/V, haemoglobin, 24 h SBP and ECW% as independent variables. The variables entered in multiple linear regression to predict LVMi were tested after studying simple regression analysis. Two-tailed P-values of <0.05 were considered to be significant.



   Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
A total of 110 patients (67 male and 43 female, age 55.6 ± 17.2 years, HD age 30.2 ± 40.4 months) satisfied the inclusion criteria; the other 10 patients were excluded because of very low PAs (<3°). Hypertension was present in 74.5% of the patients (52 males, 30 females). Diabetes mellitus was present in 13.6% of the patients, ischaemic heart disease in 30% and previous history of myocardial infarction in 5.5%. There were no differences between hypertensive and normotensive patients for age (56.7 ± 16.7 vs 52.5 ± 18.4 years), spKt/V (1.31 ± 0.25 vs 1.39 ± 0.26), haemoglobin (10.4 ± 1.4 vs 10.9 ± 1.6 g/dl) or residual renal function (0.97 ± 1.7 vs 1.07 ± 1.6 ml/min). Normotensive patients were on HD for a longer period than hypertensives (46.5 ± 69.6 vs 24.5 ± 21.3 months, P = 0.01). Hypertensive patients showed higher BP values than normotensives in spite of antihypertensive treatments [systolic OBP, 148.3 ± 13.5 vs 125.5 ±15.5 mmHg, P < 0.001; diastolic OBP, 81.6 ± 8.1 vs 71.9 ± 7.2 mmHg, P < 0.001; 24 h SBP, 146.2 ± 16.8 vs 119.5 ± 11.1 mmHg, P < 0.001; 24 h diastolic BP (DBP), 80.6 ± 10.9 vs 69.9 ± 7.1 mmHg, P < 0.001; 24 h pulse pressure (PP), 65.7 ± 17.8 vs 49.5 ±9.6 mmHg, P < 0.001]. More hypertensive patients were non-dippers compared with normotensives (72 vs 50%; {chi}2 = 4.5, P = 0.03; SBP N/D ratio, 0.96 ± 0.1 vs 0.91 ± 0.6, P = 0.01).

Of the hypertensive patients, 20.7% were kept off pharmacological treatment, 24.5% were treated with only one drug, and the remaining patients were given a combination of antihypertensive drugs. Angiotensin-converting enzyme inhibitors were prescribed to 22% of patients, calcium channel blockers to 52.4%, ß-adrenergic-receptor blockers to 15.9%, {alpha}-ß-adrenergic blockers to 18.8%, central {alpha}-agonists to 34.1% and direct vasodilators to 3.7%. There were no differences in epoeitin treatment between hypertensive and normotensive patients (84.5 ± 79 vs 83.1 ± 72.6 IU/kg/week). BIA revealed that Xc was lower in hypertensive patients than in normotensives (49.5 ± 12 vs 57 ± 16.3 {Omega}, P = 0.01), whereas ECW% was higher in hypertensives (46.5 ± 7.7 vs 43 ± 7.2, P = 0.02). We found no differences for TBW% (hypertensives, 55.9 ± 6.4; normotensives, 55.6 ± 6.1) or BCM% (hypertensives, 33.8 ± 7.8; normotensives, 35.5 ± 6.9). dBw and inter-HD body weight increases ({triangleup}Bw) did not differ between hypertensive and normotensive patients (dBw, 65.5 ± 11.7 vs 61.1 ± 13.4 kg; {triangleup}Bw, 2.63 ± 1.02 vs 2.64 ± 1.26 kg). ECW was correlated with the age of patients (r = 0.29, P < 0.01), SBP (r = 0.35, P < 0.01) and PP (r = 0.34, P < 0.001).

LVH was present in 61.8% of patients, 37 male and 31 female (Table 1). The pattern of LVH was eccentric in 73.5% of cases. The length of HD treatment, in months, did not differ between patients with (+) or without (–) LVH (29.3 ± 43.8 vs 31.6 ± 34.5 months). There were no differences between LVH+ and LVH– patients for residual renal function (LVH+, 0.87 ± 1.77 ml/min; LVH–, 1.18 ± 1.51 ml/min), spKt/V, haemoglobin, or uric acid (Table 2). SBP, DBP, PP and the SBP N/D ratio were significantly higher in LVH+ patients (Table 3). BIA revealed decreases in Xc and PA and an increase in ECW% in LVH+ patients (Table 4). The two groups were not different for dBw (LVH+, 63.1 ± 11.9 kg; LVH–, 66.4 ± 12.5 kg) or {triangleup}Bw (LVH+, 2.57 ±1.14 kg; LVH–, 2.73 ± 0.97 kg).


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Table 1. Echocardiographic parameters in 110 patients with (+) or without (–) LVH

 

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Table 2. Clinical and blood chemistries in patients with (+) or without (–) LVH

 

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Table 3. Twenty-four hour ambulatory BP monitoring in patients with (+) or without (–) LVH

 

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Table 4. BIA in patients with (+) or without (–) LVH

 
LVMi was significantly correlated with asleep SBP (r = 0.50, P < 0.001), PP (r = 0.34, P < 0.001), age (r = 0.21, P = 0.03), Xc (–0.51, P < 0.001), PA (–0.37, P < 0.001) and ECW% (r = 0.49, P < 0.001) (Figure 1). A stepwise multiple linear regression model revealed that LVMig/sqm was significantly correlated with ECW%, SBP and male gender (r = 0.65, P < 0.001) (Table 5).



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Fig. 1. Correlation between left ventricular mass index (LVMi) and ECW (%) or reactance in 110 HD patients.

 

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Table 5. Stepwise linear regression with left ventricular mass index as the dependent variable

 


   Discussion
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Large epidemiological studies have consistently demonstrated that cardiovascular diseases are the main cause of mortality in HD patients (http://www.usrds.org/2001pdf/h.pdf, http://www.sin-ridt.org/). The large majority of patients with chronic renal failure are hypertensive, and the initiation of dialysis does not correct the high BP levels in most of these patients. Hypertension has been correlated with left ventricular dysfunction and hypertrophy. Other specific causes of LVH in HD patients include anaemia, hyperkinetic flow induced by arteriovenous fistulas, hyperparathyroidism, hyper-homocysteinaemia and retention of advanced glycated end-products. It is also well known that the causality of hypertension in the general population may be different from that in HD patients, which probably includes fluid overload [3]. Our study examined potential relationships between hypertension, LVH and fluid overload, which was measured by BIA as ECW. From this study, we found a strong association between fluid overload and hypertension and, more importantly, a correlation between ECW and LVMi.

Several studies with renal patients have investigated the relationship between hypertension and fluid or salt overload. Blumberg et al. [18], >30 years ago, realized that there was a strong association between fluid overload and hypertension. Since then, a large number of studies have examined this topic. Özkahya et al. [19] demonstrated that narrow control of sodium intake combined with strict ultrafiltration produced reductions in dBw, in BP and, consequently, in the need for antihypertensive drugs. Rahman et al. [20] reported that high interdialytic weight gains were correlated with high BP. Chen et al. [21], while measuring ECW%, observed that hypertensive HD patients had higher levels of ECW compared with their normotensive counterparts and that a reduction of ECW performed in a restricted group of over-hydrated hypertensive patients was accompanied by a decrease in BP. Other studies seem to confirm the observation that a reduction in ECW causes normalization of BP in HD patients, or at least a better control of BP. The long HD sessions used by Charra et al. [22] appeared, at least in part, to produce optimal BP control as a consequence of fluid overload reduction. Katzarski et al. [23] studied hypertensive and normotensive patients on standard (4 h thrice-weekly) and long-term (8 h thrice-weekly) HD while using BIA and measuring inferior vena cava diameters. Hypertensive patients on standard HD showed increases in ECW compared with their normotensive counterparts and with patients on long-term HD; the same pattern of results was demonstrated for inferior vena cava diameters. In another study, short daily HD sessions normalized BP in >90% of patients, and the reductions in BP and LVMi were closely correlated with reductions in fluid overload measured by BIA as ECW [24]. Therefore, since reductions in fluid overload appear to be crucial for the control of cardiovascular complications in HD patients, instruments are needed that could allow assessment of true dBw. Clinical approaches for estimating dry weight are often unsatisfatory, because many factors can induce measurement errors such as lean body mass reduction, intra-HD hypotension due to cardiac dysfunction, or altered increases in total peripheral resistance and venous capacity [25]. Spiegel et al. [26], using BIA in patients that achieved clinically determined ideal dBw, observed that 50% of these showed increased volumes. This observation indicates that HD patients frequently do not reach a physiologic dBw and that methods other than clinical determination are needed to assess fluid overload. Although biochemical markers, such as atrial natriuretic peptide or cyclic guanidine monophosphate, represent a sensible method for assessing overload, there are specific limitations, such as congestive heart failure, tricuspid and mitral valve disease and altered left atrial haemodynamics. In addition, these markers require a sophisticated and expensive technology available to only a few centres, making their determination unsuitable for routine clinical use. The measurement of inferior vena cava, although widely available, is affected by inter-operator error and shows large variability [27].

BIA of body composition may provide an easy, cheap and a widely distributed tool for the study of fluid overload in HD patients. This technology is based on the assumption that the conduction of current through the human body is characterized by two components: R due to water and ions and Xc due to the capacitor property of cellular membranes. BIA seems to be useful in the assessment of dBw in HD patients. ECW reduction during HD sessions correlates significantly with ultrafiltrate removal and changes in body weight [21]. A recent study by Cooper et al. [6] demonstrated that TBW estimated by BIA did not differ significantly from estimations using D2O dilution, which is the gold standard for water measurements.

Our study, by using BIA determinations of ECW, confirmed previous reports of an association between fluid load and hypertension, supporting the hypothesis that hypertension is strongly associated with ECW increases in HD patients. The prevalence of hypertension in our patients was not different from that generally observed in HD populations, and our patients had high BP values even though they were treated with antihypertensive drugs. With the increase in HD age, we observed a tendency for better BP control, which may be explained by progressive reductions in fluid overload or decreases in left ventricular function.

We found that volume overload was linked not only with hypertension but also with LVH. This link with ventricular hypertrophy is a novel finding and is consistent with the observation that LVMi was correlated not only with BP but also with ECW. The finding that LVH was eccentric in the majority of patients confirms that the increase in LVMi was related to volume overload, which itself is the cause of both hypertension and LVH. This observation is in line with the findings of Hart et al. [28], who assessed the role of volume overload in the aetiopathogenesis of early LVH in the general population. In contrast to what was observed for BP values, we do not report a correlation between LVMi and dialysis history, which is in line with the observations of Foley et al. [29], who observed a progressive cardiac enlargement and LVH after dialysis onset, particularly during the first year of HD therapy.

We also analysed haemoglobin to assess the role of this risk factor in the development of LVH. We found that anaemia was not a relevant risk factor for LVH, which may be due to haemoglobin levels that were corrected to a target range resulting in no difference between the normotensive and hypertensive groups. However, there is controversy over the role of anaemia in LVH. For example, Foley et al. [30] failed to find a regression with LVH after correction of anaemia with epoietin {alpha}.

In conclusion, our study confirmed the association between ECW, a derived parameter of BIA measurements, and BP. More importantly, we also found that fluid load was associated with left ventricular mass in HD patients. BIA may thus be considered a useful tool that is inexpensive and simple to use for the clinical diagnosis of fluid overload in HD patients.



   Acknowledgments
 
The authors would like to thank Dr Alberto Andreaux for language revision.

Conflict of interest statement. None declared.



   References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 

  1. Middleton RJ, Parfrey PS, Foley RN. Left ventricular hypertrophy in the renal patient. J Am Soc Nephrol 2001; 12: 1079–1084[Free Full Text]
  2. Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC, Barre PE. Serial change in echocardiographic parameters and cardiac failure in end-stage renal disease. J Am Soc Nephrol 2000; 11: 912–916[Abstract/Free Full Text]
  3. Horl MP, Horl WH. Hemodialysis-associated hypertension: pathophysiology and therapy. Am J Kidney Dis 2002; 39: 227–244[CrossRef][ISI][Medline]
  4. Lewin NW, Zhu F, Keen M. Interdialytic weight gain and dry weight. Blood Purif 2001; 19: 217–221[CrossRef][ISI][Medline]
  5. Chertow GM, Lowrie EG, Wilmore DW et al. Nutritional assessment with bioelectrical impedance analysis in maintenance hemodialysis. J Am Soc Nephrol 1995; 6: 75–81[Abstract]
  6. Cooper BA, Aslani A, Ryan M et al. Comparing different methods of assessing body composition in end stage renal failure. Kidney Int 2000; 58: 408–416[CrossRef][ISI][Medline]
  7. Imai Y, Sasaki S, Minami N et al. The accuracy and performance of the A&D TM2421, a new ambulatory blood pressure device based on the cuff-oscillometric method and the Korotoff sound technique. Am J Hypertension 1992; 5: 719–726[ISI][Medline]
  8. Ganau A, Devereux RB, Roman JM et al. Patterns of left ventricular hypertrophy and geometry remodelling in essential hypertension. J Am Coll Cardiol 1992; 19: 1550–1558[ISI][Medline]
  9. Levi D, Savage DD, Garrison RJ, Anderson KM, Kannel WB, Castelli WP. Echocardiographic criteria for the left ventricular hypertrophy: the Framingham study. Am J Cardiol 1987; 59: 956–960[ISI][Medline]
  10. Cornish BH, Thomas BJ, Ward LC. Improved prediction of extracellular and total body water us impedance loci generated by multiple frequency bioelectrical impedance analysis. Phys Med Biol 1993; 38: 337–346[CrossRef][ISI][Medline]
  11. Hannan WJ, Cowen SJ, Fearon KCH, Plester CE, Falconer JS, Richardson RA. Evaluation of multi-frequency bio-impedance analysis for the assessment of extracellular and total body water in surgical patients. Clin Sci 1994; 86: 479–485[ISI][Medline]
  12. Piccoli A, Rossi B, Pillon L. Is the 50-kHz the optimal frequency in routine estimation of body water by bio-impedance analysis? Am J Clin Nutr 1992; 56: 1069
  13. Lukaski HC, Bolonchuk WW. Estimation of body fluid volume using tetrapolar bioelectric impedance measurements. Aviat Space Environ Med 1998; 59: 1163–1169
  14. Snel YE, Brummer RJM, Doerga ME, Zelissen PMJ, Koppeschaar HPF. Validation of extracellular water determination by bioelectric impedance analysis in growth hormone-deficient adults. Ann Nutr Metab 1995; 39: 242–250[CrossRef][ISI][Medline]
  15. Kotler DP, Burastero S, Wang J, Pierson RN Jr. Prediction of body cell mass, fat-free mass, total body water with bioelectrical impedance analysis: effects of race, sex, and disease. Am J Clin Nutr 1996; 64 (Suppl 3): S489–S497[Abstract]
  16. Pencharz PB, Azcue M. Use of bioelectrical impedance analysis measurements in the clinical management of malnutrition. Am J Clin Nutr 1996; 64 (Suppl 3): S485–S488[Abstract]
  17. Chertow GM, Lazarus JM, Lew NL, Ma L, Lowrie EG. Bioimpedance norms for the hemodialysis population. Kidney Int 1997; 52: 1617–1621[ISI][Medline]
  18. Blumberg A, Nelp WB, Hegstrom RM, Scribner BH. Extacellular volume in patients with chronic renal disease treated for hypertension by sodium restriction. The Lancet 1967; 2: 69–73[Medline]
  19. Özkahya M, Töz H, Ünsal A et al. Treatment of hypertension in dialysis patients by ultrafiltration: role of cardiac dilatation and time factor. Am J Kidney Dis 1999; 34: 218–221[ISI][Medline]
  20. Rahman M, Fu P, Sehgal AR, Smith MC. Interdialytic weight gain, compliance with dialysis regimen, and age are independent predictors of blood pressure in hemodialysis patients. Am J Kidney Dis 2000; 35: 257–265[ISI][Medline]
  21. Chen YC, Chen HH, Yeh JC, Chen SY. Adjusting dry weight by extracellular volume and body composition in hemodialysis patients. Nephron 2002; 92: 91–96[CrossRef][ISI][Medline]
  22. Charra B, Chazot C, Jean G, Laurent G. Long, slow dialysis. Miner Electrolyte Metab 1999; 25: 391–396[CrossRef][ISI][Medline]
  23. Katzarski KS, Charra B, Luik AJ et al. Fluid state and blood pressure control in patients treated with long and short hemodialysis. Nephrol Dial Transplant 1999; 14: 369–375[Abstract]
  24. Fagugli RM, Reboldi G, Quintaliani G et al. Short daily haemodialysis: blood pressure control and left ventricular mass reduction in hypertensive haemodialysis patients. Am J Kid Dis 2001; 38: 371–376[ISI][Medline]
  25. Cavalcanti S, Cavani S, Santoro A. Role of short-term regulatory mechanism on pressure response to hemodialysis-induced hypovelemia. Kidney Int 2002; 61: 228–238[CrossRef][ISI][Medline]
  26. Spiegel DM, Bashir K, Fisch B. Bioimpedance resistance ratios for the evaluation of dry weight in hemodialysis. Clin Nephrol 2000; 53: 108–114[ISI][Medline]
  27. Jaeger JQ, Mehta RL. Assessment of dry weight in hemodialysis: an overview. J Am Soc Nephrol 1999; 10: 392–403[Abstract/Free Full Text]
  28. Hart CY, Meyer DM, Tazelaar HD et al. Load versus humoral activation in the genesis of early hypertensive heart disease. Circulation 2001; 104: 215–220[Abstract/Free Full Text]
  29. Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC, Barre PE. Long-term evolution of cardiomyopathy in dialysis patients. Kidney Int 1998; 54: 1720–1725[CrossRef][ISI][Medline]
  30. Foley RN, Parfrey PS, Morgan J et al. Effect of hemoglobin levels in hemodialysis patients with asymptomatic cardiomyopathy. Kidney Int 2000; 58: 1325–1335[CrossRef][ISI][Medline]
Received for publication: 8.11.02
Accepted in revised form: 9. 4.03





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