Changes In Sodium Concentration Research Articles

Bone marrow as multidimensional orbit oscillator after autologous bone marrow transplantation.

The local renin-angiotensin system (RAS) in bone marrow is probably involved in the control of hematopoiesis. Earlier observations suggest the relationship between the frequency of sodium and potassium concentration changes in urine and bone marrow recovery after chemotherapy. The purpose of this study was to prove the relationship between sodium and potassium excretion changes in urine and granulocyte counts in peripheral blood after autologous bone marrow and peripheral blood stem cell transplantation. The correlation between amplitude maximum FFmax of F=d[Na]/d[K], where d[Na] and d[K] are changes of sodium and potassium excretions in 24 h, and granulocytes, recorded k days later, was found in 12 patients with autologous bone marrow transplantation (BMT) and/or PBSCT. In patients with successful engraftment, k ranged from 4 to 7 days. In the patient with unsuccessful BMT, k was 12 days. The results imply the interaction between systemic and bone marrow RAS.

Osmoregulatory control of renal sodium excretion after sodium loading in humans.

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by approximately 4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 +/- 8 vs. 110 +/- 17 micromol/min). However, after HiNa+ the corresponding natriureses were identical (135 +/- 33 vs. 139 +/- 39 micromol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23-52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

Ethanol exhalation as a predictor of dilution hyponatraemia during endometrial ablation

This study investigated the effectiveness of ethanol as an early indicator of resorption during transcervical endometrium resection (TCRE). Ethanol was added as a marker and exhaled alcohol concentrations were measured with an Alcomed test. Ninety‐three patients underwent endometrial ablation under general anaesthesia and exhaled ethanol levels and blood sodium concentrations were monitored simultaneously every 3 minutes. In 23% of the cases the Alcomed test was the first indicator of absorption. Relevant changes in blood sodium concentrations appeared later in 9% of the cases and gives a positive Alcomed test. The predictive exhaled ethanol value for preventing the transurethral prostate resection (TUR) syndrome is 1.5 promille. A marked difference in fluid resorption during hysteroscopic myomectomy was observed (400–1000 ml during TCRE and myomectomy vs. 100–300 ml TCRE only). Of 83 TCRE patients, 23 had a positive Alcomed test. Ten patients underwent a hysteroscopic myomectomy. Sensitivity and specificity were determined for a decrease of more than 5 mmol l−1 in blood sodium and for several ethanol levels. The sensitivity was 100% for an ethanol level of at least 0.05 promille. The specificity was 90.9% and the positive predictive value 41.7%. All patients with a decrease of more than 5 mmol l−1 in blood sodium concentration were detected using a threshold of 0.05 promille exhaled ethanol and nine out of 10 patients with a blood sodium decrease of at least 5 mmol l−1 also had an ethanol level of at least 0.05 promille. Unfortunately a positive Alcomed test has a poor prognostic value.

EDS of thin Biological Specimen in the Study of Time-Dependent Physiological Processes

Abstract The contraction of muscle depends on the ability of intracellular organelles to rapidly release and take up large amounts of activator calcium. In cardiac muscle the intracellular sodium concentration is known to also modulate this Ca2+ release: Na+-Ca2+ exchange creates narrow cytosolic microdomains just internal to the sarcolemma (approximately 20 nm wide) with locally elevated concentrations of Ca2+ and Na+. The existence of such “functional” compartments with transient high ionic concentrations has been postulated for explaining the nigh efficiency of signal transmission during excitation-contraction coupling. We present results showing that electron probe microanalysis (EPMA) at the high spatial resolution of scanning transmission electron microscopy (STEM) can detect changes in sodium and calcium concentration of membrane-limited organelles and functional microdomains provided the cardiac myocytes are rapidly frozen at defined times during activation of contraction.

Alpha-Adrenergic effects on Na+-K+ pump current in guinea-pig ventricular myocytes.

1. The whole-cell patch clamp was employed to study Na+-K+ pump current (Ip) in acutely isolated myocytes. alpha-Adrenergic receptors were activated with noradrenaline (NA) after blocking beta-adrenergic receptors with propranolol. Ip was measured as the current blocked by strophanthidin (Str). 2. Activation of alpha-receptors by NA increased Ip in a concentration-dependent manner. The K0.5 depended on intracellular calcium ([Ca2+]i), however maximal stimulation did not. At 15 nM [Ca2+]i the K0.5 was 219 nM NA whereas at 1.4 microM [Ca2+]i it was 3 nM. 3. The voltage dependence of Ip was not shifted by NA at either high or low [Ca2+]i. At each voltage, maximal stimulation of Ip was 14-15 %. 4. Staurosporine (St), an inhibitor of protein kinase C (PKC), eliminated the alpha-receptor-mediated stimulation of Ip at either high or low[Ca2+]i. 5. The stimulation of Ip was independent of changes in intracellular sodium or external potassium concentrations, and did not reflect a change in affinity for Str. 6. Phenylephrine, methoxamine and metaraminol, three selective alpha1-adrenergic agonists, stimulate Ip in a similar manner to NA. Stimulation of Ip by NA was eliminated by prazosin, an alpha1-antagonist, but was unaffected by yohimbine, an alpha2-antagonist. 7. We conclude noradrenaline activates ventricular alpha1-receptors, which are specifically coupled via PKC to increase Na+-K+ pump current. The sensitivity of the coupling is [Ca2+]i dependent, however the maximal increase in pump current is [Ca2+]i and voltage independent.

Changes in osmotic and ionic concentrations in the hemolymph of Macrobrachium rosenbergii exposed to varying salinities and correlation to ionic and crystalline composition of the cuticle

Osmotic and ionic regulatory ability were examined in the giant freshwater prawn, Macrobrachium rosenbergii in response to varying salinities. In freshwater, and under conditions of low salinity, hemolymph osmolality was maintained around 450 mOsm. Under high salinity, osmolality values increased in a time-wise manner until reaching levels of the surrounding rearing water. Changes in sodium concentration generally paralleled osmotic change, and potassium and magnesium concentrations increased upon exposure to extremely high salinity. In contrast, total calcium concentration was maintained at high levels regardless of salinity treatment. Examination of crystalline structure and ionic composition of the cuticle revealed that it was comprised principally of an α-chitin-like material, and calcite (calcium carbonate). Calcite accounted for 25% of total bulk weight in freshwater, while sodium, potassium and magnesium constituents combined comprised less than 2.5% of this total. Although sodium, potassium and magnesium contents increased nearly 2-fold in response to changing salinity, calcium levels remained relatively constant.

Maturation of Rabbit Proximal Straight Tubule NaCl Transport † 1833

The present in vitro microperfusion study compared the mechanism and rates of NaCl transport in neonatal and adult rabbit proximal straight tubules. In proximal straight tubules perfused with a late proximal tubular fluid and bathed in a serum-like albumin solution, the rate of volume absorption(Jv) was 0.54±0.10 and 0.12±0.05 nl/mm·min in adults and neonates, respectively (p<0.05). With the addition of 10-5M bath ouabain, Jv decreased to 0.27±0.07 and-0.03±0.04 nl/mm·min in adult and neonatal tubules, respectively(p<0.05), consistent with lower rates of active and passive NaCl transport in the neonatal proximal straight tubule. The rate of change of intracellular pH (pHi) in response to a change in luminal sodium and chloride concentration was used to assess the relative rates of Na+/H+ and Cl-/base exchange, respectively. The rates of Na+/H+ antiporter activity was 37.7±4.9 and 206.1±25.2 pmol/mm·min (p<0.01) in neonatal and adult proximal straight tubules, respectively. Cl-/base exchange was 6.0±1.2 and 45.7±6.6 pmol/mm·min (p<0.01) in neonatal and adult proximal straight tubules, respectively. In both neonatal and adult proximal straight tubules the rate of Cl-/base exchange was not affected by formate, bicarbonate, or cyanide and acetazolamide, but was inhibited by DIDS, consistent with Cl-/OH- exchange. These data demonstrate an increase in both active and passive proximal straight tubule NaCl transport during postnatal renal development. The increase in active NaCl transport is due to increases in both Na+/H+ antiporter and Cl-/OH- exchange activity.

Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage?

Animal studies indicate that elevated extracellular sodium can increase glutamate-induced excitotoxicity. Therefore, we investigated the relationship between sodium and glutamate and the effect of changes in sodium concentrations on the outcome of head-injured patients. Thirty-four (34) patients were selected for this study and divided into a group of patients having episodes (> or = 30-min) of high sodium in dialysates (> or = 200 mM; HIGH, n = 11) and a group of patients having no such episodes (NORMAL, n = 23). Levels for sodium (226 +/- 5.7 mM), glutamate (12.53 +/- 2.2 microM) and ICP (32.2 +/- 4.0 mm Hg,) were relatively high during the high sodium episodes. Overall, mean values for glutamate, ICP and outcome did not differ amono both groups. The mean dialysate sodium concentration, however, was significantly higher in the HIGH (178 +/- 6 mM) compared to the NORMAL group (158 +/- 3 mM; p < 0.01). Spearman rank correlation between sodium and glutamate or ICP were not significant. The HIGH sodium group did not have significantly more patients with poor outcome than the NORMAL group. The results indicated sodium concentrations did not affect the outcome of head-injured patients. However, other sodium monitoring techniques are desirable to elucidate these apparent potentially major sodium transients, which we have observed in the human cortex, after severe head injury.

A simulation of the effects of changes in the Na and K content of milk during mastitis on the growth ofStaphylococcus aureus,Streptococcus uberisandEscherichia coli

In a mastitic event damage to the epithelial tissue of the mammary gland, and in particular an increase in paracellular permeability allows sodium to enter the milk from the blood (Schaar and Funke, 1986). Normally there is a stepwise gradient of declining sodium concentration from the interstitial fluid to the epithelial cells to the milk (Berga and Neville, 1985). Milk potassium content is reduced in milk of cows with mastitis, but the proportional change is less than that of sodium (Wegner and Stull, 1978). An experiment was conducted to investigate the response of three mastitis pathogens to the changes in sodium and potassium concentrations in their growth media that are typical of the changes occurring during a mastitic event.

Measurement of polyamine transport. Adherent cells.

Most cells can take up polyamines, and some polyamine analogs, by a process that is independent of amino acid transport systems (,), and that, in certain circumstances, can substitute for synthesis de novo. In some cells polyamines are taken up by both saturable and nonsaturable systems. Uptake by saturable systems is energy-requiring, temperature-dependent, carrier-mediated, and operates against a substantial concentration gradient (,). In many cells putrescine and, often, spermidine transport is sodium-sensitive (the term sodium-sensitive is preferable to the more frequently used sodium-dependent, because removal of extracellular sodium reduces, but often does not abolish, uptake). In contrast, spermine transport in most cells is not affected by changes in extracellular sodium concentrations. The number of carriers in the polyamine transport system varies with cell type. In human umbilical vein endothelial cells there are apparently two carriers, one shared by spermine and spermidine, and one capable of transporting all three polyamines (). In contrast, porcine aortic endothelial cells appear to possess three carriers, one for each polyamine (). Multiple carriers are not uncommon, although many cell types appear to possess a single polyamine carrier able to transport putrescine, spermidine, and spermine, although with differing affinities ().

A simulation of the effects of changes in the Na and K content of milk during mastitis on the growth of Staphylococcus aureus, Streptococcus uberis and Escherichia coli

In a mastitic event damage to the epithelial tissue of the mammary gland, and in particular an increase in paracellular permeability allows sodium to enter the milk from the blood (Schaar and Funke, 1986). Normally there is a stepwise gradient of declining sodium concentration from the interstitial fluid to the epithelial cells to the milk (Berga and Neville, 1985). Milk potassium content is reduced in milk of cows with mastitis, but the proportional change is less than that of sodium (Wegner and Stull, 1978). An experiment was conducted to investigate the response of three mastitis pathogens to the changes in sodium and potassium concentrations in their growth media that are typical of the changes occurring during a mastitic event.

Changes in subsarcolemmal sodium concentration measured by Na-Ca exchanger activity during Na-pump inhibition and beta-adrenergic stimulation in guinea-pig ventricular myocytes.

Measurement of Na-Ca exchange activity was used to examine subsarcolemmal sodium levels ([Na+]s) in single, voltage-clamped guinea-pig cardiac myocytes while Na-K pump activity was modulated pharmacologically. Changes in Nas were evaluated from phase-plane analysis of the changes in intracellular calcium, measured using the fluorescent indicators Fura-red and Fluo-3. Activation of beta-adrenoceptors with 1 microM isoprenaline resulted in activation of the cAMP-dependent chloride current, but had no effect on the calcium transient mediated via the Na-Ca exchanger, regardless of whether the Na-K pump was active or inhibited (with strophanthidin). The ability of Na-Ca exchange activity to report [Na+]s was demonstrated by the effect of changing the extracellular rubidium concentration from 1 to 5.4 mM to modulate Na-K pump activity. We suggest that beta-adrenergic stimulation does not directly affect either the Na-K pump or the Na-Ca exchanger and that the Na-Ca exchanger can be used as a sensitive indicator of changes in [Na+]s and Na-K pump activity.

Spatial distribution of synaptically activated sodium concentration changes in cerebellar Purkinje neurons.

The spatial distribution of Na(+)-dependent events in guinea pig Purkinje cells was studied with a combination of high-speed imaging and simultaneous intracellular recording. Individual Purkinje cells in sagittal cerebellar slices were loaded with either fura-2 or the Na+ indicator sodium binding benzofuran isophthalate (SBFI) with sharp electrodes or patch electrodes on the soma or dendrites. [Na+]i changes were detected in response to climbing fiber and parallel fiber stimulation. These changes were located both at the anatomically expected sites of synaptic contact in the dendrites and in the somatic region. The variation in time course of these [Na+]i changes in different locations implies that Na+ enters at the synapse and diffuses rapidly to locations of lower initial [Na+]i. The synaptically activated somatic [Na+]i changes probably reflect Na+ entry through voltage-sensitive Na+ channels because they were detected only when regenerative potentials were recorded in the soma. [Na+]i changes in response to antidromically or intrasomatically evoked Na+ action potentials also were confined to the cell body. These observations are in agreement with other evidence that Na+ spikes are generated in the somatic region of the Purkinje neuron and spread passively into the dendrites. Plateau potentials, evoked by depolarizing pulses to the soma or dendrites, caused [Na+]i changes only in the soma, indicating that the noninactivating Na+ channels contributing to this potential also were concentrated in this region. The climbing fiber-activated [Na+]i changes were blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, indicating that these changes were not due to direct stimulation of the Purkinje neuron or activation of metabotropic receptors. Direct depolarization of the soma or dendrites never caused dendritic [Na+]i increases, suggesting that the climbing fiber-activated [Na+]i changes in the dendrites are due to Na+ entry through ligand-gated channels. A climbing fiber-like regenerative potential could be recorded in the soma after anode break stimulation, parallel fiber activation, or depolarizing pulses to the soma. The [Na+]i changes evoked by all of these potentials were confined to the cell body region of the Purkinje cell. [Ca2+]i changes in the dendrites evoked by the anode break potential were small relative to climbing fiber-activated changes, suggesting that a Ca2+ spike was not evoked by this response. The anode break and directly responses were blocked by tetrodotoxin. These results suggest that the somatically recorded climbing fiber response is predominantly a Na(+)-dependent event, consisting of a few fast action potentials and a slower regenerative response activating the same channels as the Na+ plateau potential.

Medullary pathways mediating depressor responses from Na(+)-sensitive sites in nucleus of the solitary tract.

Two series of experiments were done in male Wistar rats to investigate the medullary pathways that mediate the depressor responses from sodium-sensitive sites in the nucleus of the solitary tract (NTS). In the first series, the anterograde tract tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoresed unilaterally at sites in the NTS at which microinjections (20 nl) of a 154-175 mM NaCl solution elicited depressor responses. PHA-L injection sites were found to be localized within the medial subnucleus of the NTS (Sm). In the medulla, PHA-L-labeled fibers and presumptive terminal boutons were observed bilaterally, but with an ipsilateral predominance, throughout the rostrocaudal extent of the NTS the dorsal motor nucleus of the vagus, area postrema, the ventrolateral medulla (VLM), and nucleus ambiguus. The pontine region, containing the A5 catecholaminergic cell group and the parabrachial nucleus, also received projections from Sm. In the second series of experiments, the effect of blocking synaptic transmission in VLM with cobalt chloride (CoCl2; 5 mM, 100 nl) on the cardiovascular response elicited by microinjection (20 nl) of hypertonic saline (154-175 mM) into the ipsilateral Sm was investigated in the alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rat. Microinjection of CoCl2 into VLM, at sites shown in the previous study to receive efferent projections from Sm, significantly attenuated the depressor (60%) and bradycardic (80%) responses to stimulation of Sm. These data indicate that the sodium-sensitive region of the caudal Sm innervates VLM neurons and suggest that these VLM neurons are involved in mediating the depressor and bradycardic responses elicited by changes in the extracellular concentration of sodium.

Role of arginine vasopressin in the regulation of extracellular fluid volume.

The Henry-Gauer hypothesis postulates that changes in left atrial pressure induce changes in the release of arginine vasopressin (AVP), which subsequently modulates the renal output of fluid. Results of the past decades indicate that this hypothesis is too simplistic in explaining the complexity of extracellular fluid volume (ECFV) regulation in humans. Factors controlling renal sodium excretion are the primary modulators of ECFV. AVP is probably important in the related adjustments of renal water excretion whereby changes in plasma sodium concentration induce changes in plasma osmolality and, subsequently, in release of AVP. Evidence has accrued that changes in arterial variables, e.g., arterial pulse pressure, induce changes in the release of AVP during acute changes in central blood volume. Thus, arterial baroreflex regulation of AVP release might constitute one of several pathways of ECFV regulation. Recent results from the D2-Spacelab mission on ECFV regulation are surprising. Following an isotonic saline infusion, renal sodium and fluid output were lower than expected from results of simulation experiments, and venous plasma NE and renin higher. Since plasma AVP was low, high levels of this variable cannot constitute an explanation for the attenuated renal output of fluid during flight. Thus, the currently used models (in particular head-down bed rest) for simulating microgravity should be critically reevaluated. In addition, the relationship between central cardiovascular variables, endocrine mediators, and renal function during microgravity should be a focus of future research.

Effect of lesions of forebrain circumventricular organs on c-fos expression in the central nervous system to plasma hypernatremia

Experiments were carried out on conscious adult male Wistar rats to investigate the effect of selective ablation of the subfornical organ (SFO), and/or the anteroventral third ventricular (AV3V) region on the induction of Fos in central structures in response to plasma hypernatremia. Fos induction, detected immunohistochemically, was used as a marker for neuronal activation. Intravenous infusions of hypertonic saline resulted in dense Fos-like immunoreactivity in several forebrain (paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), median preoptic nucleus (MnPO), medial preoptic nucleus, organum vasculosum of the laminae terminalis and SFO) and brainstem (nucleus of the solitary tract, ventrolateral medulla, and parabrachial nucleus) structures. Intravenous infusions of the hypertonic saline solution into animals with lesions of either the SFO, the AV3V or both resulted in a decreased number of Fos-like immunoreactive neurons in the MnPO, PVH and SON. In addition, the number of Fos-labeled neurons in the SON after lesions of both the SFO and the AV3V was significantly greater than that observed in isotonic saline infused controls. Finally, lesions of the forebrain circumventricular structures did not alter the Fos labeling in brainstem structures as a result of the infusion of the hypertonic solution. These data suggest that changes in plasma osmolality and/or concentration of sodium alter the activity of SON and brainstem neurons in the absence of afferent inputs from the SFO and AV3V.

Osmolality and electrolytes in cerebrospinal fluid and serum of febrile children with and without seizures.

During acute febrile diseases mild disturbances of water and electrolyte balance occur frequently. It has been suggested that changes in electrolyte balance, in particular hyponatraemia, might predispose a child to convulsions during febrile illness; however, the changes of electrolytes in the CSF are not known. We have studied the effects of fever and convulsions on water and electrolyte balance in CSF and serum by measuring osmolality and electrolyte concentrations in children. The febrile population consisted of 60 children, 36 of whom had seizures during fever. Twenty-one children without convulsions and nine children with epileptic symptoms were nonfebrile controls. We noticed that CSF is subject to changes in osmolality and electrolyte concentration during fever, while convulsions do not exhibit such changes. CSF osmolality and sodium concentrations were lower in febrile children than in nonfebrile controls. The osmolality in febrile children with convulsions was 3.8% (P < 0.01) and without seizures 3.5% (P < 0.01) lower than in nonfebrile nonconvulsive children. The changes in CSF sodium concentration, and to a lesser extent potassium and chloride concentrations, paralleled those of CSF osmolality. A positive correlation was observed between the CSF and serum osmolatities (r = 0.73, P < 0.0001), and sodium concentrations (r = 0.63, P < 0.0001). A negative correlation between the body temperature and both CSF osmolality (r = -0.66, P < 0.0001) and sodium concentration (r = -0.59, P < 0.0001) exhibits also the important regulative role of increased body temperature. Fever is an important factor for disturbances in fluid and electrolyte balance. The alterations in CSF osmolality and sodium concentration do not, however, give an unambiguous explanation for the susceptibility to simple febrile seizures.

Changes in sodium, calcium and magnesium ion concentrations in sturgeon (Huso huso) urine and in kidney morphology

During adaptation to brackish water the young great sturgeon Huso huso is able to regulate its serum osmolarity and ion concentrations. After transfer from fresh water to brackish water the ion concentrations in the urine increase and the urine becomes isoosmotic to the blood serum after 24h. The Na+ and K+ concentrations in the urine increase during the first 12 h by 4.4 and 7.7 times, respectively, later decreasing again. The Mg2+ and Ca2+ concentrations in the urine increase by 3.4 and 14 times during the first 72h in brackish water and remain high thereafter. These results suggest that the kidneys play an important part in the regulation of serum osmolarity and in the removal of Ca2+; however, in contrast to teleosts, Mg2+ must be removed extrarenally. During adaptation to a hyperosmotic medium the diameters of the Malpighian bodies, the glomeruli and the diameter of the tubules initially all decrease, but the distal tubules become morphologically differentiated into two regions and the diameter of the distal section later increases again. It is suggested that this is the site of Ca2+ secretion into the urine.

Urea, sodium, and water changes in profiling dialysis

Control of osmolarity, as well as sodium, urea, and water balance in anuric patients under intermittent haemodialysis therapy is fundamentally different from subjects with normal kidney function. Whereas in subjects with normal kidney function excretion of solutes and water is performed continuously, during dialysis, within a short period of time most sodium and only a small amount of urea are removed convectively with the ultrafiltration of water (1 litre of ultrafiltrate = 8.5 g sodium chloride and about 1.5 g urea). On the other hand most urea and a small amount of sodium is removed by diffusion, depending on the dialyser clearance and the difference in concentration between plasma and dialysis fluid. The relatively short period of treatment induces acute changes in fluid volume, urea, and sodium concentration as well as in plasma osmolarity, which in healthy subjects never happen. The consequence are side-effects of dialysis therapy such as osmotic dysequilibrium syndrome, muscle cramps, symptomatic hypotension, and thirst. Having no mechanism to excrete sodium during the long period between two dialyses, the anuric patient only has the possibility to dilute a high sodium concentration by drinking or to minimize sodium ingestion. Consequently the amount of fluid ingestion depends on the amount of sodium chloride ingestion by eating and probably on an increase in sodium concentration due to dialysis treatment itself. Among other methods profiling of ultrafiltration and sodium concentration in dialysis fluid has been proposed to optimize dialysis therapy. To evaluate the benefit of profiling to the patient the basic conditions of water and solute distribution and exchange in dialysis therapy have to be considered.

Ultrafiltration and solute kinetics using low sodium peritoneal dialysate

Low sodium peritoneal dialysate has been reported to enhance sodium loss and alleviate signs of fluid overload in continuous ambulatory peritoneal dialysis patients. To elucidate the mechanisms involved, we compared ultrafiltration and solute kinetics using low sodium dialysate (LNaD; 105 mEq/liter sodium, 2.5% glucose, 348 mOsm/liter), conventional dialysate with equal osmolality (CD1.5; 132 mEq/liter sodium, 1.5% glucose, 348 mOsm/liter) and conventional dialysate with equal glucose concentration (CD2.5; 132 mEq/liter sodium, 2.5% glucose, 403 mOsm/liter). A 2 liter, six hour exchange of each dialysate was performed on separate days in 10 chronic peritoneal dialysis patients. Transperitoneal solute diffusion was assessed by calculating the permeability-area product (PA) of the peritoneal membrane from the dependence of plasma and dialysate solute concentrations on tie. Net fluid removed using LNaD of 190 +/- 90 (SEM) ml was similar to that using CD2.5 (250 +/- 90 ml) but higher (P < 0.01) than that using CD1.5 (-200 +/- 60 ml). Sodium loss was higher using LNaD (72 +/- 11 mEq, P < 0.01) and CD2.5 (41 +/- 12 mEq, P < 0.05) than using CD1.5 (-18 +/- 8 mEq). Changes in plasma sodium concentration were small during each dwell and were not different among the study dialysates. PA values for urea (23.4 +/- 1.6 ml/min), creatinine (10.0 +/- 1.0 ml/min), and glucose (10.3 +/- 1.3 ml/min) were similar when determined in each dialysate. The PA value for sodium (7.6 +/- 1.5 ml/min) could only be accurately determined in LNaD. We conclude that: (1) net fluid removed is greater using LNaD than CD1.5 despite similar osmolalities because LNaD has a higher glucose concentration and glucose is a more effective osmotic solute than sodium; (2) sodium loss when using LNaD is enhanced by both diffusion and convection; and (3) sodium diffuses across the peritoneum slower than urea, creatinine and glucose. These data suggest that LNaD alleviates signs of fluid overload by increasing net fluid removal and enhancing sodium loss.