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Biomedical subjects

Minhtri K Nguyen

Publications and source records attributed to Minhtri K Nguyen.

18 recordsLinked to original sources
PubMed2006

Is the osmotically inactive sodium storage pool fixed or variable?

Recently, there is renewed interest in the role of osmotically inactive Na(+) storage during Na(+) retention. Although it is well accepted that a portion of the total exchangeable Na(+) reservoir is osmotically inactive, there is current controversy as to whether the osmotically inactive Na(+) storage pool is fixed or variable during Na(+) retention. In this article, we analyze the current scientific evidence to assess whether the osmotically inactive Na(+) storage pool can be dynamically regulated. Our analysis supports the assertion that the osmotically inactive Na(+) storage pool is fixed rather than variable.

Animals↗
PubMed2006

Whole-body electrolyte-free water clearance: derivation and clinical utility in analyzing the pathogenesis of the dysnatremias.

The total exchangeable sodium (Na(e)), total exchangeable potassium (K(e)), and total body water (TBW) are the major determinants of the plasma water sodium concentration ([Na(+)](pw)). The relationship between [Na(+)](pw) and Na(e), K(e), and TBW was empirically determined by Edelman et al., where: [Na(+)](pw) = 1.11(Na(e) + K(e))/TBW - 25.6 (Eq. 1). According to Eq. 1, changes in the mass balance of Na(+), K(+), and H(2)O will therefore result in changes in the [Na(+)](pw). Historically, in evaluating the pathogenesis of the dysnatremias, free water clearance (FWC) and electrolyte-free water clearance (EFWC) have been used to evaluate the pathophysiology of the dysnatremias. However, such analyses are only valid when there is no concomitant input and non-renal output of Na(+), K(+), and H(2)O. Since the classic FWC and EFWC formulas fail to account for the input and non-renal output of Na(+), K(+), and H(2)O, these formulas cannot be used to evaluate the pathogenesis of the dysnatremias or to predict the directional change in the [Na(+)](pw). In this article, we have addressed this limitation by deriving a new formula, termed whole-body electrolyte-free water clearance (WB-EFWC), which calculates whole-body electrolyte-free water clearance for a given mass balance of Na(+), K(+), and H(2)O, rather than simply the urinary component (FWC, EFWC formulas). Unlike previous formulas, which consider only the renal component of electrolyte-free water clearance, WB-EFWC accounts for all sources of input and output of Na(+), K(+), and H(2)O, and will therefore be helpful in conceptually understanding the basis for changes in the [Na(+)](pw) in patients with the dysnatremias.

Body Water↗
PubMed2006

True hyponatremia secondary to intravenous immunoglobulin.

Hyponatremia is characterized as either "true hyponatremia," which represents a decrease in the Na(+) concentration in the water phase of plasma, or "pseudohyponatremia," which is due to an increased percentage of protein or lipid in plasma, with a normal plasma water Na(+) concentration ([Na(+)]). Pseudohyponatremia is a known complication of intravenous immunoglobulin (IVIG). Because IVIG has been reported to result in post-infusional hyperproteinemia, IVIG-induced hyponatremia has been attributed to pseudohyponatremia. In this case report, we demonstrate that IVIG therapy can result in true hyponatremia, resulting from sucrose-induced translocation of water from the intracellular compartment (ICF) to the extracellular compartment (ECF), as well as the infusion of a large volume of dilute fluid, in patients with an underlying defect in urinary free water excretion.

Adult↗
PubMed2006

Fatal hyponatremia in a young woman after ecstasy ingestion.

BACKGROUND: A 20-year old, otherwise healthy, female college student presented in an unresponsive state with respiratory distress after ingesting ecstasy (3,4-methylenedioxymethamphetamine). She had initial plasma sodium concentration of 117 mmol/l. INVESTIGATIONS: Physical examination, blood chemistry panel, urinary osmolality and electrolytes, arterial blood gas, chest X-ray, and CT scan of the brain. DIAGNOSIS: Hyponatremia associated with noncardiogenic pulmonary edema and cerebral edema. MANAGEMENT: Administration of a total of 6.8 l of isotonic saline and 0.245 l of 3% hypertonic saline with sporadic administration of intravenous furosemide. The patient died approximately 12 h after admission.

Adult↗
PubMed2005

Quantitative interrelationship between Gibbs-Donnan equilibrium, osmolality of body fluid compartments, and plasma water sodium concentration.

The presence of negatively charged, impermeant proteins in the plasma space alters the distribution of diffusible ions in the plasma and interstitial fluid (ISF) compartments to preserve electroneutrality. We have derived a new mathematical model to define the quantitative interrelationship between the Gibbs-Donnan equilibrium, the osmolality of body fluid compartments, and the plasma water Na+ concentration ([Na+]pw) and validated the model using empirical data from the literature. The new model can account for the alterations in all ionic concentrations (Na+ and non-Na+ ions) between the plasma and ISF due to Gibbs-Donnan equilibrium. In addition to the effect of Gibbs-Donnan equilibrium on Na+ distribution between plasma and ISF, our model predicts that the altered distribution of osmotically active non-Na+ ions will also have a modulating effect on the [Na+]pw by affecting the distribution of H2O between the plasma and ISF. The new physiological insights provided by this model can for the first time provide a basis for understanding quantitatively how changes in the plasma protein concentration modulate the [Na+]pw. Moreover, this model defines all known physiological factors that may modulate the [Na+]pw and is especially helpful in conceptually understanding the pathophysiological basis of the dysnatremias.

Blood Proteins↗
PubMed2005

Evolving concepts in the quantitative analysis of the determinants of the plasma water sodium concentration and the pathophysiology and treatment of the dysnatremias.

The physiologic and clinical implications of the empirical formula originally discovered by Edelman et al [J Clin Invest 37:1236-1256, 1958] relating the plasma water sodium concentration ([Na(+)](pw)) to the total exchangeable sodium (Na(e)), total exchangeable potassium (K(e)), and total body water (TBW) have recently been elucidated. It is quite remarkable that the full significance of the Edelman equation discovered almost 50 years ago had remained unrecognized by clinicians and physiologists until recently. Although Edelman and colleagues had shown that the [Na(+)](pw) is proportional to the magnitude of (Na(e)+ K(e))/TBW, the linear equation relating [Na(+)](pw) to (Na(e)+ K(e))/TBW had a slope greater than unity of 1.11, and a non-zero y intercept of -25.6 whose significance was unrecognized and more often than not ignored. It has recently been demonstrated that the slope and y intercept in this equation are quantitatively determined by several additional physiologic parameters, which in addition to (Na(e)+ K(e))/TBW, play a role both in modulating the [Na(+)](pw) and in the generation of the dysnatremias. Even more remarkably, based only on the theoretical principles of Gibbs-Donnan and osmotic equilibrium, all the physiologic parameters that determine the magnitude of the [Na(+)](pw) can be incorporated into a simple conceptual and mathematical framework that sheds light on a broad of range of seemingly unrelated topics that have heretofore been treated separately clinically, including (1) effect of changes in the mass balance of Na(+), K(+), and H(2)O on the [Na(+)](pw); (2) modulation of [Na(+)](pw) in hyperglycemic states; (3) definition of an isonatric solution; (4) current formulas used to quantitate electrolyte-free water excretion; (5) complex role of K(+) in modulating the [Na(+)](pw); and (6) quantitative analysis of the generation and treatment of the dysnatremias. Moreover, this analysis has also proven to be an indispensable tool for deriving new formulas to aid the clinician in both interpreting the pathogenesis and treating the dysnatremias.

Humans↗
PubMed2004

A new formula for predicting alterations in plasma sodium concentration in peritoneal dialysis.

Alterations in the plasma water sodium concentration ([Na+]pw) result from changes in the total exchangeable sodium (Na e), total exchangeable potassium (K e), and total body water (TBW). The empirical relationship between the [Na+]pw and Na e, K e, and TBW was originally demonstrated (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958), where [Na+]pw = 1.11(Na e + K e)/TBW - 25.6 (Eq. 1). Based on Eq. 1, alterations in the [Na+]pw can be predicted by considering changes in the mass balance of Na+, K+, and H2O. In accounting for the mass balance of Na+, K+, and H2O in patients on peritoneal dialysis, considerations must also be taken to determine the modulating effect of dialysate clearance of Na+ and K+ and fluid changes resulting from this therapeutic modality on the [Na+]pw. In this article, we derive a new formula for predicting alterations in the plasma Na+ concentration ([Na+]p) in patients on peritoneal dialysis, taking into consideration the empirical relationship between the [Na+]pw and Na e, K e, and TBW (Eq. 1) as well as changes in mass balance of Na+ + K+ and H2O.

Humans↗
PubMed2004

Derivation of a new formula for calculating urinary electrolyte-free water clearance based on the Edelman equation.

In evaluating the renal mechanisms responsible for the generation of the dysnatremias, an analysis of free water clearance (FWC) and electrolyte-free water clearance (EFWC) is often utilized to characterize the rate of urinary free water excretion in these disorders. Previous analyses of FWC and EFWC have failed to consider the relationship among plasma water Na(+) concentration ([Na(+)](pw)), total exchangeable Na(+) (Na(e)), total exchangeable K(+) (K(e)), and total body water (TBW); (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958). In their derivations, the classic FWC and EFWC formulas fail to consider the quantitative and physiological significance of the slope and y-intercept in this equation. Consequently, previous EFWC formulas incorrectly assume that urine is isonatric when [Na(+) + K(+)](urine) = [Na(+)](p) or [Na(+) + K(+)](urine) = [Na(+)](p) + [K(+)](p) (where [Na(+)](p) and [K(+)](p) represent plasma Na(+) and K(+) concentrations, respectively). Moreover, previous formulas cannot be utilized in the setting of hyperglycemia. In this article, we have derived a new formula termed modified electrolyte-free water clearance (MEFWC) for determining the electrolyte-free water clearance, taking into consideration the empirical relationship between the [Na(+)](pw) and Na(e), K(e), and TBW: MEFWC = V [1 - 1.03[Na(+) + K(+)](urine)/([Na(+)](p) + 23.8)]. MEFWC, unlike previous formulas, is derived based on the requirement of the Edelman equation that urine is isonatric only when [Na(+) + K(+)](urine) = (Na(e) + K(e))/TBW = 0.97[Na(+)](p) + 23.1. Furthermore, since we have shown that the y-intercept in the Edelman equation varies directly with the plasma glucose concentration, in patients with hyperglycemia, MEFWC = V [1 - 1.03[Na(+) + K(+)](urine)/{[Na(+)](p) + 23.8 + (1.6/100)([glucose](p) - 120)}]. The MEFWC formula will be especially useful in assessing the renal contribution to the generation of the dysnatremias.

Animals↗
PubMed2004

Determinants of plasma water sodium concentration as reflected in the Edelman equation: role of osmotic and Gibbs-Donnan equilibrium.

Edelman et al. have empirically shown that plasma water sodium concentration ([Na(+)](pw)) is equal to 1.11(Na(e) + K(e))/TBW - 25.6 (Edelman IS, Leibman J, O'Meara MP, Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958). However, the physiological significance of the slope and y-intercept in this equation has not been previously considered. Our analysis demonstrates that there are several clinically relevant parameters determining the magnitude of the y-intercept that independently alter [Na(+)](pw):1) osmotically inactive exchangeable Na(+) and K(+); 2) plasma water K(+) concentration; and 3) osmotically active non-Na(+) and non-K(+) osmoles. In addition, we demonstrate quantitatively the physiological significance of the slope in the Edelman equation and its role in modulating [Na(+)](pw). The slope of 1.11 in this equation which Edelman et al. determined empirically can be theoretically predicted by considering the combined effect of the osmotic coefficient of Na(+) salts at physiological concentrations and Gibbs-Donnan equilibrium. In addition, our results demonstrate that the slope has an independent quantitative impact on the magnitude of the y-intercept in the Edelman equation. From a physiological standpoint, the components of both the slope and the y-intercept need to be addressed when considering the factors that modulate [Na(+)](pw).

Animals↗
PubMed2004

Role of potassium in hypokalemia-induced hyponatremia: lessons learned from the Edelman equation.

It is well known that changes in the mass balance of K+ can lead to an alteration in the plasma water sodium concentration ([Na+]pw). We have recently shown that based on the Edelman equation, the [Na+]pw is determined by the total exchangeable Na+ (Nae), total exchangeable K+ (Ke), total body water (TBW), osmotically inactive Nae and Ke, plasma water [K+], intracellular and extracellular osmotically active non-Na+ and non-K+ osmoles, and plasma osmotically active non-Na+ and non-K+ osmoles. In light of these findings, a re-analysis of the role of K+ in modulating the [Na+]pw is required in understanding the pathophysiology of hypokalemia-induced hyponatremia. In this article, we characterize the complex role of K+ in the pathogenesis of hypokalemia-induced hyponatremia using a three-compartment model and the known parameters in the Edelman equation. Our analysis indicates that K+ modulates the [Na+]pw by changing Ke in addition to the parameters in the y-intercept of the Edelman equation. Moreover, the magnitude of potassium-induced changes in the [Na+]pw is determined by the pathophysiologic mechanisms by which changes in Ke occur.

Humans↗
PubMed2004

New insights into the pathophysiology of the dysnatremias: a quantitative analysis.

Recent theoretical considerations have played an important role in advancing our understanding of the physiological mechanisms responsible for perturbing the plasma water sodium concentration ([Na(+)](pw)) in health and disease. Central to these considerations is the original empirical relationship between the [Na(+)](pw) and total exchangeable sodium (Na(e)), total exchangeable potassium (K(e)), and total body water (TBW) initially discovered by Edelman and colleagues (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958). The non-zero values of the slope and y-intercept in the Edelman equation are a consequence of the effects of the osmotic coefficient of Na(+) salts at physiological concentrations and Gibbs-Donnan and osmotic equilibrium. Moreover, in addition to Na(e), K(e), and TBW, the physiological components of the y-intercept in this equation play a role in modulating the [Na(+)](pw) and in the generation of the dysnatremias. In this review, the pathophysiological mechanisms underlying the generation and treatment of the dysnatremias are analyzed theoretically and quantitatively. Importantly, the non-zero values of both the slope and y-intercept in the Edelman equation result in several theoretical predictions that can be tested experimentally and have been mathematically incorporated into recently derived equations used to analyze both the generation and the optimal treatment of the dysnatremias. In addition, we review current concepts regarding 1) the role of Gibbs-Donnan and osmotic equilibrium in the determination of the [Na(+)](pw); 2) the modulating effect of osmotically inactive exchangeable Na(+) and K(+) on the [Na(+)](pw); 3) the effect of glucose on the [Na(+)](pw) as reflected by changes in Na(e), K(e), and TBW as well as changes in several components of the y-intercept resulting from the hyperglycemia; and 4) the complex role of K(+) in modulating the [Na(+)](pw).

Body Water↗
PubMed2003

A new quantitative approach to the treatment of the dysnatremias.

Rapid correction of the dysnatremias can result in significant patient morbidity and mortality. To avoid overly rapid correction of the dysnatremias, the sodium deficit equation, water deficit equation, and Adrogue-Madias equation are frequently utilized to predict the change in plasma sodium concentration (Delta[Na+]p) following a therapeutic maneuver. However, there are significant limitations inherent in these equations. Specifically, the sodium deficit equation assumes that total body water (TBW) remains unchanged. Similarly, when using the Adrogue-Madias equation, the volume of infusate required to induce a given Delta[Na+]p is determined by dividing the target Delta[Na+]p by the result of this formula. This calculation also assumes that TBW remains constant. In addition, neither of these equations are applicable in the management of symptomatic syndrome of inappropriate antidiuretic hormone secretion (SIADH) because they fail to consider the subsequent increase in sodium excretion following the administration of infusate. Furthermore, in the treatment of hypernatremia, the water deficit equation is only applicable if the hypernatremia is caused by pure water loss. In hypernatremia caused by hypotonic fluid losses, the water deficit equation does not provide any information on the differential effect of infusates of variable [Na+] and [K+] on the [Na+]p. Finally, all these equations fail to consider any ongoing Na+, K+, or H2O losses. Taking all these limitations into consideration, we have derived two new equations which determine the volume of a given infusate required to induce a target Delta[Na+]p. These equations consider the mass balance of Na+, K+, and H2O, as well as therapy-induced changes in TBW. The first equation is applicable to both hypernatremia and hyponatremia. The second equation is applicable to the management of severe symptomatic SIADH requiring intravenous therapy.

Adult↗
PubMed2003

A simple quantitative approach to analyzing the generation of the dysnatremias.

BACKGROUND: Although the dysnatremias are the most common electrolyte disorders in hospitalized patients, the complexity of the parameters normally used to explain their generation mechanistically is often bewildering to medical students and experts alike. A number of methods have been utilized clinically to analyze retrospectively and predict prospectively the pathogenesis of these disorders. These approaches include the measurements of plasma and urine osmolality, free water clearance, electrolyte free water clearance, and tonicity balance. METHODS: All previous analyses are problematic in that they fail to incorporate mathematically in a single equation the known factors that account quantitatively for changes in the plasma water sodium concentration. In this paper, we have derived a simple formula for use at the bedside based on all known factors that can generate the dysnatremias. The formula incorporates (1) the known empirical relationship between the plasma water Na+ concentration, total body water (TBW), and exchangeable Na+ (Na+(e)) and K+ (K+(e)); (2) changes in mass balance of H2O (VMB) and Na+ + K+ (EMB); and (3) the effect of hyperglycemia. RESULTS: This new equation, unlike all previous qualitative and quantitative approaches, can account mathematically for the simultaneous effects of TBW, Na(e), K(e), EMB, VMB, and the plasma glucose on the plasma water sodium concentration. Clinical examples are provided that demonstrate the utility of this new equation in analyzing the pathogenesis of the dysnatremias. CONCLUSION: The conceptual simplification resulting from the use of this formula should significantly improve the current approaches used in analyzing the generation of the dysnatremias.

Adolescent↗
PubMed2003

Molecular pathogenesis of nephrogenic diabetes insipidus.

There have been significant advances recently in the understanding of the molecular causes of nephrogenic diabetes insipidus. The resistance of the collecting duct to the action of vasopressin in this disorder results from abnormalities in several of the intricate steps that mediate the increase in principal cell hydraulic conductivity in response to the hormone. In this article, we review the current understanding of the known genetic causes of nephrogenic diabetes insipidus that affect the binding of vasopressin to the V2 receptor and subsequent intracellular signaling events, as well as the translocation of aquaporin-2 water channels to the apical membrane. In addition, genetic diseases, which decrease collecting-duct water absorption by diminishing the interstitial medullary osmolarity, are discussed.

Animals↗