Extracellular Fluid Expansion Research Articles

Salt-sensitive trait of normotensive individuals is associated with altered autonomous cardiac regulation: a randomized controlled intervention study.

Blood pressure (BP) responses to sodium intake show great variation, discriminating salt-sensitive (SS) from salt-resistant (SR) individuals. The pathophysiology behind salt sensitivity is still not fully elucidated. We aimed to investigate salt-induced effects on body fluid, vascular tone, and autonomic cardiac response with regard to BP change in healthy normotensive individuals. We performed a randomized crossover study in 51 normotensive individuals with normal body mass index and estimated glomerular filtration rate. Subjects followed both a low-Na+ diet (LSD, <50 mmol/day) and a high-Na+ diet (HSD, >200 mmol/day). Cardiac output, systemic vascular resistance (SVR), and cardiac autonomous activity, through heart rate variability and cross-correlation baroreflex sensitivity (xBRS), were assessed with noninvasive continuous finger BP measurements. In a subset, extracellular volume (ECV) was assessed by iohexol measurements. Subjects were characterized as SS if mean arterial pressure (MAP) increased ≥3 mmHg after HSD. After HSD, SS subjects (25%) showed a 6.1-mmHg (SD 1.9) increase in MAP. No differences between SS and SR in body weight, cardiac output, or ECV were found. SVR was positively correlated with Delta BP (r = 0.31, P = 0.03). xBRS and heart rate variability were significantly higher in SS participants compared to SR participants after both HSD and LSD. Sodium loading did not alter heart rate variability within groups. Salt sensitivity in normotensive individuals is associated with an inability to decrease SVR upon high salt intake that is accompanied by alterations in autonomous cardiac regulation, as reflected by decreased xBRS and heart rate variability. No discriminatory changes upon high salt were observed among salt-sensitive individuals in body weight and ECV.NEW & NOTEWORTHY Extracellular fluid expansion in normotensive individuals after salt loading is present in both salt-sensitive and salt-resistant individuals and is not discriminatory to the blood pressure response to sodium loading in a steady-state measurement. In normotensive subjects, the ability to sufficiently vasodilate seems to play a pivotal role in salt sensitivity. In a normotensive cohort, differences in sympathovagal balance are also present in low-salt conditions rather than being affected by salt loading. Whereas treatment and prevention of salt-sensitive blood pressure increase are mostly focused on renal sodium handling and extracellular volume regulation, our study suggests that an inability to adequately vasodilate and altered autonomous cardiac functioning are additional key players in the pathophysiology of salt-sensitive blood pressure increase.

Determinants of hypokalemia following hypertonic sodium bicarbonate infusion.

The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, - 0.16 to - 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses.

EFFECT OF MALARIA INFECTION ON HEPATIC AND RENAL FUNCTIONS IN PREGNANT WOMEN ATTENDING ANTENATAL CLINIC AT GENERAL HOSPITAL DUTSE, JIGAWA-NIGERIA

The effect of malaria infection on hepatic and renal functions in pregnancywas investigated. Three malarious and non-malarious pregnant women of age ranges 15 to 40 years with a mean (SD) of 23.5 (6.6) years and a median (IQR) of 20.5 (18.3 to 27) years were enrolled. Liver enzymes (AST, ALT and ALP) and Kidney (UCE) functions were determined using Randox standard assay kits. The levels of alkaline phosphatase (ALP) and albumin were significant as malaria infected pregnant women had significantly lowered levels of ALP and albumin compared to controls (21.3 vs 26.1 IU/L, P = 0.03 and 4.8 vs 6.0 g/dl P = 0.02). There was no significant difference between malaria infected pregnant women and their non-malarious counterparts (P &gt; 0.05) in their renal functions. There was no significant difference in mean concentrations of urea, creatinine, sodium, potassium and chloride regardless of the severity of malaria. Usually in pregnancy markers of liver function decrease due to expansion of extracellular fluid except alkaline phosphatase which is elevated due to its placental origin. Results of this study showed decreased level of ALP which could possibly be an indication that the parasite has not reached its hepatic stage. The severity of gestational malaria depends on the initial immunity of the pregnant woman. The impact of malaria on pregnancy and conversely, the impact of pregnancy on malaria, are two factors which must be put into consideration during gestational malaria

Potential Novel Benefits of Sodium Restriction in Chronic Kidney Disease.

Chronic kidney disease is a global public health issue, and it has been considered as the epidemic of the 21st century. Therefore, all initiatives addressed to slow down the evolution and complications of this condition should be well received. While the effects of salt reduction on cardiovascular disease have some controversial issues, in chronic kidney disease, such a policy is beneficial in multiple aspects. In chronic kidney disease patients, dietary sodium restriction is regularly recommended to control extracellular fluid expansion, hypertension and cardiovascular risk. Instead, the effects of sodium reduction on chronic kidney disease progression are still controversial. In the last years, potentially beneficial effects of a low sodium diet on chronic kidney disease evolution have emerged. Firstly, recent magnetic resonance-based findings of increased Na depots in skin and muscle associated with renal function, ageing and sodium intake open a vast body of investigation as a potential tool for monitoring effects of sodium restriction. In this narrative review, we also discussed novel aspects of sodium restriction in chronic kidney disease to manage metabolic acidosis as well as renal effects on fibroblast growth factor 23 or gut microbiota. Beyond current evidence, these approaches showed that common findings of kidney failure environment such as sodium -sensitivity, micro-inflammation, arterial stiffness metabolic acidosis and sarcopenia could be delayed controlling dietary sodium. Additional studies are now needed in populations with chronic kidney disease to confirm these new findings, addressed to slow down the evolution and complications of this condition.

Renin Activity in Heart Failure with Reduced Systolic Function-New Insights.

Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin–angiotensin–aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). Here, we review the role of active renin, a crucial, upstream enzymatic regulator of the RAAS, as a prognostic and diagnostic plasma biomarker of heart failure with reduced ejection fraction (HFrEF) progression; we also discuss its potential as a pharmacological bio-target in HF therapy. Clinical and experimental studies indicate that plasma renin activity is elevated with symptomatic HFrEF with edema in patients, as well as in companion animals and experimental models of HF. Plasma renin activity levels are also reported to be elevated in patients and animals with rEF before the development of symptomatic HF. Modulation of renin activity in experimental HF significantly reduces edema formation and the progression of systolic dysfunction and improves survival. Thus, specific assessment and targeting of elevated renin activity may enhance diagnostic and therapeutic precision to improve outcomes in appropriate patients with HFrEF.

Extracellular Fluid/Intracellular Fluid Volume Ratio as a Novel Risk Indicator for All-Cause Mortality and Cardiovascular Disease in Hemodialysis Patients.

BackgroundIn hemodialysis patients, fluid overload and malnutrition are accompanied by extracellular fluid (ECF) expansion and intracellular fluid (ICF) depletion, respectively. We investigated the relationship between ECF/ICF ratio (as an integrated marker reflecting both fluid overload and malnutrition) and survival and cardiovascular disease (CVD) in the context of malnutrition-inflammation-arteriosclerosis (MIA) complex.MethodsSeventy-seven patients from a single hemodialysis unit were prospectively enrolled. The ECF/ICF volume was measured by segmental multi-frequency bioimpedance analysis. MIA and volume status were measured by serum albumin, C-reactive protein (CRP), pulse wave velocity (PWV) and plasma B-type natriuretic peptide (BNP), respectively.ResultsThe mean ECF/ICF ratio was 0.56±0.06 and the cut-off value for maximum discrimination of survival was 0.57. Compared with the low ECF/ICF group, the high ECF/ICF group (ratio≥0.57, 42%) had higher all-cause mortality, CVD, CRP, PWV, and BNP, but lower serum albumin. During the 5-year follow-up, 24 all-cause mortality and 38 CVD occurred (18 and 24, respectively, in the high ECF/ICF group versus 6 and 14 respectively in the low ECF/ICF group, P<0.001). In the adjusted Cox analysis, the ECF/ICF ratio nullifies the effects of the MIA and volume status on survival and CVD and was an independent predictor of all-cause mortality and CVD: hazard ratio (95% confidence interval); 1.12 (1.01–1.25) and 1.09 (1.01–1.18) for a 0.01 increase in the ECF/ICF ratio. The degree of malnutrition (albumin), inflammation (CRP), arteriosclerosis (PWV), and fluid overload (BNP) were correlated well with the ECF/ICF ratio.ConclusionsHemodialysis patients with high ECF/ICF ratio are not only fluid overloaded, but malnourished and have stiff artery with more inflammation. The ECF/ICF ratio is highly related to the MIA complex, and is a major risk indicator for all-cause mortality and CVD.

G380(P) Hyponatremia – cerebral salt wasting

Setting PICU Consultant and PICU registrar Problem 4 year old child transferred to PICU after space occupying lesion cranial surgery. On day 2 post operatively was noted to have very high urine output with falling serum sodium. His urine output was very variable and ranged from 3 ml/kg/hour to 17 ml/kg/hour. He had very high urinary sodium content. Clinical context Falling sodium High urine output Low plasma osmolality Assessment of problem and analysis of its causes Hyponatremia in Patients with Neurologic Disorders Inappropriate secretion of antidiuretic hormone (SIADH) Cerebral salt wasting (CSW) syndrome The distinction between these two conditions is important because their treatments are different. It is not possible to distinguish CSW from SIADH based on serum and urine laboratory findings alone, because their associated abnormalities are identical. For this reason, accurate determination of the patient’s volume status is the key to differentiating these syndromes. Fundamental difference between the two processes is extracellular fluid volume status. Patients with CSW have hypovolemia compared with patients with SIADH, who have euvolemic or mild extra cellular fluid expansion. The mainstay of therapy for CSW is replacement of the sodium and water that is lost as a result of pathologic natriuresis and diuresis. This is in direct contrast to the treatment of SIADH, the crux of which is free water restriction. CVP-directed treatment of hyponatremia and volume status in such patients is effective. Intervention New guidelines for cerebral salt wasting introduced in PICU guidelines. Lessons learnt Consider CSW in children with low sodium and high urine output, measure volume status, in PICU setting with CVP measurement

Role of intestinal Na(+)/H(+) exchanger inhibition in the prevention of cardiovascular and kidney disease.

The expansion of extracellular fluid (ECF) volume increases the plasma volume, which consequently increases blood pressure and episodes of heart failure and chronic kidney disease (1). In the ECF, sodium chloride is the most abundant salt, and ECF volume increases linearly as the dietary intake of sodium increases (2). Furthermore, a normal sodium intake can also increase ECF volume in the end-stage renal disease patients (3). Thus, sodium balance is an important factor in the normal physiological functions of cardiovascular and renal system.

Biofeedback dialysis for hypotension and hypervolemia: a systematic review and meta-analysis

Intradialytic hypotension (IDH) is associated with morbidity and mortality. We conducted a systematic review to determine whether biofeedback hemodialysis (HD) can improve IDH and other outcomes, compared with HD without biofeedback. Data sources included the Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE and ISI Web of Science. We included randomized trials that enrolled adult patients (>18 years) with IDH or extracellular fluid expansion and that used biofeedback to guide ultrafiltration and/or dialysate conductivity. Two authors assessed trial quality and independently extracted data in duplicate. We assessed heterogeneity using I(2). We applied the GRADE framework for rating the quality of evidence. We found two parallel-arm randomized controlled clinical trials and six randomized crossover trials meeting inclusion criteria. All trials were open-label and at least four were industry-sponsored. Studies were small (median n = 27). No study evaluated hospitalization and the evidence for effect on mortality was of very low quality. Three studies assessed quality of life (QoL); none demonstrated benefit or harm, and quality of evidence was very low. Biofeedback significantly reduced IDH (risk ratio 0.61, 95% confidence interval 0.44-0.86; I(2)= 0%). Quality of evidence for this outcome was low due to risk of bias and potential publication bias. Biofeedback dialysis significantly reduces the frequency of IDH. Large and well-designed randomized trials are needed to assess the effects on survival, hospitalization and QoL.

About uses of magnesium during perioperative period

About uses of magnesium during perioperative period

Diagnostic Value of Urinary Sodium, Chloride, Urea, and Flow

Up to 30% of hospitalized critically ill patients may have a rise in serum creatinine concentration. In addition to history and physical examination, there is diagnostic value in assessing urinary electrolytes, solute excretion, and urine flow in these patients. The correct interpretation of these urinary parameters can avoid unnecessary volume overload and mechanical ventilation, risk factors for increased mortality in patients with rising serum creatinine. The present article also discusses the role of arterial underfilling in causing prerenal azotemia in the presence of an increase in total body sodium and extracellular fluid expansion. As with extracellular fluid volume depletion, arterial underfilling secondary to impaired cardiac function or primary arterial vasodilation can delay or prevent recovery from ischemic or toxic acute tubular necrosis. The present brief review discusses the various aspects of the correct interpretation of urinary electrolytes, solute excretion, and urine flow in the setting of a rising serum creatinine concentration.

SALT RETENTION IN HEART FAILURE IS ASSOCIATED WITH UPREGULATION OF NHE3 IN RENAL PROXIMAL TUBULE

Heart failure (HF) is associated with sodium and water retention and extracellular fluid expansion. A principal site of renal salt and water reabsorption is the proximal tubule (PT). We therefore hypothesized that NHE3, the major apical transcellular pathway for sodium reabsorption in the PT, is upregulated in an experimental model of HF. HF was induced in male rats by left ventricle radio-frequency ablation. Sham-operated (SO) rats were used as controls. Six weeks after surgery, HF rats had high left ventricular end-diastolic pressure (> 15 mmHg) and low stroke work and displayed lower urinary flow and sodium excretion than SO controls. Stationary in vivo microperfusion revealed that PT-bicarbonate reabsorption was significantly higher in HF than in SO rats (2.71 ± 0.34 vs. 1.90 ± 0.11 nmol/cm2/s). NHE3 expression in renal cortex was significantly higher in HF than in SO rats at both protein (46 ± 4%) and mRNA levels (225 ±31%). Additionally, the phosphorylation ratio PS552-NHE3/NHE3 was 37 ± 2% lower in HF rats as compared to SO controls. These data strongly suggest that NHE3 is upregulated in HF at both transcriptional and post-translational levels. Altered PT NHE3 modulation may play a role in the renal sodium and water retention observed in HF.

Hypertension in kidney transplant recipients

Arterial hypertension is frequently observed in renal transplant recipients. Its pathogenesis is multifactorial in most cases. Calcineurin inhibitors (CNI) can increase peripheral vascular resistance by inducing arteriolar vasoconstriction and can cause extracellular fluid expansion by reducing the glomerular filtration rate (GFR), activating the renin-angiotensin system (RAS), and by inactivating the atrial natriuretic peptide. Glucocorticoids can impair urinary water and salt excretion. Poor graft function can lead to increased extracellular volume and inappropriate production of renin. Native kidneys, older age of the donor and transplant renal artery stenosis (TRAS) may also contribute to the development of hypertension. Arterial hypertension not only can increases the risk for cardiovascular events but can also deteriorate renal allograft function. A number of studies have shown that the higher the levels of blood pressure are, the higher is the risk of graft failure. On the other hand, a good control of blood pressure may prevent many cardiovascular and renal complications. Appropriate lifestyle modification is the first step for treating hypertension. Calcium channel blockers (CCB) and renin-angiotensin system (RAS) inhibitors are the most frequently used antihypertensive agents, but in many cases, a combination of these and other drugs is required to obtain good control of hypertension.

Lowering Postdialysis Plasma Sodium (Conductivity) to Increase Sodium Removal in Volume-Expanded Hemodialysis Patients: A Pilot Study Using a Biofeedback Software System

Extracellular fluid expansion is common in hemodialysis patients. Aggressive fluid removal may lead to intradialytic complications. High dialysate sodium concentrations may lessen complications, but may increase extracellular volume. We hypothesized that decreasing plasma sodium concentration during dialysis will increase sodium removal and decrease extracellular volume. Pilot clinical trial. 16 patients with end-stage kidney disease treated using thrice-weekly hemodialysis at a university teaching hospital hemodialysis unit. Stepwise decrease in postdialysis plasma sodium level (calculated as end-of-session plasma conductivity) over 4 phases effected by dialysate conductivity measurement cells and a biofeedback software system (Diacontrol; Hospal, www.hospal.it) that allowed alteration of dialysate inlet conductivity and calculation of plasma conductivity. Decrease in postdialysis plasma sodium (conductivity) levels, sodium removal, redistribution of body water, and effect of these on interdialytic weight gain and blood pressure. Plasma sodium and conductivity values (the latter measured in millisiemens per centimeter); ionic mass balance (sodium removal); bioelectrical impedance analysis measurements of body-water compartments and phase angle; interdialytic weight gain; and blood pressure. Plasma sodium concentrations at the end of dialysis were decreased from 137.8 (phase 1) to 135.6 mmol/L (phase 4) and end-of-session plasma conductivity values were decreased from 14.0 (phase 1) to 13.5 mS/cm (phase 4; all mean values). Ionic mass balance increased from 383 to 480 mmol. Extracellular water was significantly decreased, phase angle was increased, and blood pressure and interdialytic weight gain were decreased. Plasma sodium levels correlated significantly with plasma conductivity; thus, changes in postdialysis plasma sodium levels can be inferred from changes in end-of-session plasma conductivity values. Small number of patients. No information for dietary sodium intake. To decrease extracellular volume, it may be necessary to add diffusive to convective sodium losses.

Clinical aspect of recent progress in phosphate metabolism. Management of hyperphosphagtemia

In spite of various cause of hyperphosphatemia, there is a limited number of modality which include restriction of phosphate intake, phosphate binder, extra cellular fluid expansion and blood purification. Each therapy has certain deficit but combination of those may get preferable consequence. Now various new phosphate binders and the inhibitors of sodium-dependent phosphate transporters are being developed. Those agents might promise a better outcome of the treatment of hyperphosphatemia.

Recognition and treatment of anemia in the setting of heart failure due to systolic left ventricular dysfunction

Anemia is increasingly recognized as a common, important and treatable condition in patients with congestive heart failure. Despite increasing knowledge of anemia, as well as its coassociation with chronic renal disease, advanced New York Heart Association class and worse prognosis, there are very few evidence-based recommendations for treatment. The use of supplemental iron, especially intravenous forms, for the treatment of iron-deficiency anemia in heart failure patients is associated with improved symptoms, cardiac size and function, and possibly improved outcomes. However, many patients with heart failure suffer from anemia due to other causes, including renal failure (so-called cardiorenal syndrome), erythropoietin resistance, possible ACE inhibitor use and extracellular fluid expansion. The association between anemia and adequate iron stores has led to interest in the use of erythrocyte-stimulating agents, such as erythropoietin and darbepoetin. While early data are promising, recent evidence in non-heart failure trials has led to caution in their use and given way to anticipation of results of ongoing definitive randomized trials of this therapy, such as the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT) and Reduction of Events with Darbepoetin-α in Heart Failure (RED-HF) studies.

Salt: Its Role in Chronic Kidney Disease

Few controversies in medicine have such a long history as that of whether salt is identifiably dangerous or not dangerous. The most common reported association between excess dietary salt intake and clinical outcome has been in the field of hypertension, but dietary sodium intake mediates effects that go far beyond, and are independent of, extracellular fluid expansion and elevation in blood pressure. For nephrologists, clinical trials that demonstrate no negative outcome of a high salt diet in the general population are thus not particularly assuasive, because patients with chronic kidney disease (CKD) represent an entity that is by no means comparable to the general population. This review takes a look at the challenges associated with salt balance in CKD patients (particularly at K/DOQI stage 5), followed by a summary of current concepts believed to play a part in salt-mediated pathophysiology, and the conclusion, based on the present state of scientific knowledge, that it appears advisable to advocate low dietary salt intake in this patient population.

Neurogenic pulmonary oedema post-haemodialysis.

Pulmonary oedema can develop due to many causes (Table 1). In the patient with renal failure, pulmonary oedema typically occurs in the setting of raised pulmonary arterial pressure due to extracellular fluid expansion, due to a combination of excessive inter-dialytic weight gain and failure to achieve ‘dry’ or ‘post-dialysis target’ weight, often associated with cardiac dysfunction. However, increased lung interstitial fluid can also occur in conditions, typified by normal pulmonary arterial pressures. Pulmonary complications are well recognized in both acute and chronic liver failure. Excessive pulmonary vasodilatation, in combination with high levels of vasopressin, catecholamines and sympathetic nervous system activity, leads to shunting, with increased V/Q mismatch, termed the hepatopulmonary syndrome [1]. In addition, increased circulating endotoxin and pro-inflammatory cytokines lead to increased pulmonary endothelial activation and increased pulmonary interstitial fluid formation [2]. This can be exacerbated by a concomitant reduction in plasma colloid oncotic pressure. In cases of neurogenic pulmonary oedema, pulmonary hydrostatic pressure and endothelial activation combine to increase lung interstitial water [3]. A case of acute pulmonary oedema occurring after intermittent haemodialysis treatment is reported in a patient, 9 days after paracetamol (acetaminophen) self-poisoning, due to neurogenic pulmonary oedema.

Pathophysiological Mechanisms of Salt-Dependent Hypertension

Changes in salt intake are associated in general with corresponding changes in arterial blood pressure. An exaggerated increment in blood pressure driven by a salt load is characteristic of salt-sensitive hypertension, a condition affecting more than two thirds of individuals with essential hypertension who are older than 60 years. In the last decade, significant insight was gained about the role of the kidney in the increment in blood pressure induced by sodium retention. The present review focuses on the pathophysiological characteristics of the blood pressure increase driven by expansion of extracellular fluid and the increment in plasma sodium concentration. In addition, we discuss systemic and renal conditions that result in decreased urinary sodium excretion and were implicated in the development of salt-sensitive hypertension.

Extravascular Lung Water and Peripheral Volume Status in Hemodialysis Patients With and Without a History of Heart Failure

Determining volume status in hemodialysis patients with a history of congestive heart failure (CHF) is difficult. Extravascular lung water (EVLW) may be derived from blood ultrasound velocity changes following injections of 0.9% and 5% saline. Bioimpedance spectroscopy can measure total body water (TBW) and its intracellular fluid (ICF) and extracellular fluid (ECF) compartments. We studied 29 clinically euvolemic hemodialysis patients, 12 of whom had a history of CHF. The ECF and ICF were measured before dialysis, and EVLW was measured during dialysis. Values of EVLW were similar between patients without CHF and those with CHF (3.55 ml/kg +/- 0.94 SD versus 3.88 ml/kg +/- 0.82 SD, respectively; p = NS). The ECF/ICF ratio was higher among patients with a history of CHF (1.27 +/- 0.29) than among those without such a history (1.04 +/- 0.04; p < 0.05), indicating that ECF volume overload was present in both groups, but was higher in those with a CHF history. There was a positive correlation between EVLW and ECF/ICF ratios (r = 0.54, p < 0.01). Measurements of EVLW were higher in two pulmonary edema patients ((7.95 ml/kg and 5.95 ml/kg; p < 0.05). The results of this study suggest that 1) hemodialysis patients with a history of CHF have more ECF volume overloaded than those without such a history; 2) the degree of ECF expansion is associated with increasing EVLW volume, even in patients without pulmonary edema; and 3) ECF volume expansion eventually exceeds limits and pulmonary edema occurs. These developing technologies of volume measurement may be of value in this challenging clinical area.