Author Index / Subject Index

학회자료 대한전해질학회(구 대한전해질,혈압학회) 2005 Electrolytes & Blood Pressure Vol.3 No.2

Original Investigation : Importance of Residual Water Permeability on the Excretion of Water during Water Diuresis in Rats

( Surinder Cheema Dhadli ),( Chee Keong Chong ),( Namhee Kim ),( Kamel S Kamel ),( Mitchell L Halperin ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.1

When the concentration of sodium (Na+) in arterial plasma (PNa) declines sufficiently to inhibit the release of vasopressin, water will be excreted promptly when the vast majority of aquaporin 2 water channels (AQP2) have been removed from Luminal membranes of Late distal nephron segments. In this setting, the volume of filtrate delivered distally sets the upper Limit on the magnitude of the water diuresis. Since there is an unknown volume of water reabsorbed in the Late distal nephron, our objective was to provide a quantitative assessment of this parameter. Accordingly, rats were given a Large oral water Load, while minimizing non-osmotic stimuli for the release of vasopressin. The composition of plasma and urine were measured. The renal papilla was excised during the water diuresis to assess the osmotic driving force for water reabsorption in the inner medullary collecting duct. During water diuresis, the concentration of creatinine in the urine was 13-fold higher than in plasma, which implies that ~8% of filtered water was excreted. The papillary interstitial osmolality was 600 mOsm/L> the urine osmolality. Since 17% of filtered water is delivered to the earliest distal convoluted tubule micropuncture site, we conclude that half of the water delivered to the Late distal nephron is reabsorbed downstream during water diuresis. The enormous osmotic driving force for the reabsorption of water in the inner medullary collecting duct may play a role in this reabsorption of water. Possible clinical implications are illustrated in the discussion of a case example.

Review : Molecular Approach for Distal Renal Tubular Acidosis Associated AE1 Mutations

( Somkiat Vasuvattakul ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.1

The molecular approaches to distal renal tubular acidosis (dRTA) associated AE1 mutations Lead us to understand the genetic and pathophysiological aspects of the acidification defects. An unanticipated high value of the urine-blood (U-B) PCO2 after NaHCO3 Loading observed in a case of dRTA and southeast Asian ovalocytosis (SAO) might be from a mistarget of the AE1 to the Luminal membrane of type A intercalated cells. The mutations of the AE1 gene resulted in SAO and also affected renal acidification function. Notwithstanding, after the NH4Cl Loading in 20 individuals with SAO, the acidification in the distal nephron was normal. The presence of both SAO and G701D mutations of AE1 gene would explain the abnormal urinary acidification in the patients with the compound heterozogosity. In terms of the effect of the mutations on trafficking of AE1, truncated kidney isoform (kAE1) of wild-type showed a `dominant-positive effect` in rescuing the recessive mutant kAE1 (S773P or G701D) trafficking to the plasma membrane, in contrast with the dominant mutant kAE1 (R589H) resulting in a `dominantnegative effect` when heterodimerized with the wild-type kAE1. It is notable that the dominant mutants kAE1 (R901X or G609R) expression in MDCK cells clearly results in aberrant surface expression with some mutant protein appearing at the apical membrane. These might result in net bicarbonate secretion and increasing U-B PCO2 in the distal nephron. The molecular physiological and genetic approaches have permitted identification of the molecular defects, predominantly in transporter proteins, and should in turn prompt development of novel therapeutic strategies.

Review : A Practical Approach to Genetic Hypokalemia

( Shih Hua Lin ),( Sung Sen Yang ),( Tom Chau ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.1

Mutations in genes encoding ion channels, transporters, exchangers, and pumps in human tissues have been increasingly reported to cause hypokalemia. Assessment of history and blood pressure as well as the K+ excretion rate and blood acid-base status can help differentiate between acquired and inherited causes of hypokalemia. Familial periodic paralysis, Andersen`s syndrome, congenital chloride-losing diarrhea, and cystic fibrosis are genetic causes of hypokalemia with Low urine K+ excretion. With respect to a high rate of K+excretion associated with faster Na+ disorders (mineralocorticoid excess states), glucoricoid-remediable aldosteronism and congenital adrenal hyperplasia due to either 11β-hydroxylase and 17α-hydroxylase deficiencies in the adrenal gland, and Liddle`s syndrome and apparent mineralocorticoid excess in the kidney form the genetic causes. Among slow Cl- disorders (normal blood pressure, Low extracellular fluid volume), Bartter`s and Gitelman`s syndrome are most common with hypochloremic metabolic alkalosis. Renal tubular acidosis caused by mutations in the basolateral Na+/HCO3- cotransporter (NBC1) in the proximal tubules, apical H+-ATPase pump, and basolateral Cl-/HCO3- exchanger (anion exchanger 1, AE1) in the distal tubules and carbonic anhydroase II in both are genetic causes with hyperchloremic metabolic acidosis. Further work on genetic causes of hypokalemia will not only provide a much better understanding of the underlying mechanisms, but also set the stage for development of novel therapies in the future.

Review : Thiazide-Induced Hyponatremia

( Kyu Sig Hwang ),( Gheun Ho Kim ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.1

The importance of thiazide-induced hyponatremia (TIH) is reemerging because thiazide diuretic prescription seems to be increasing after the guidelines recommending thiazides as first-line treatment of essential hypertension have been introduced. Thiazide diuretics act by inhibiting reabsorption of Na+ and Cl- from the distal convoluted tubule by blocking the thiazide-sensitive Na+/Cl- cotransporter. Thus, they inhibit electrolyte transport in the diluting segment and may impair urinary dilution in some vulnerable groups. Risk factors predisposing to TIH are old age, women, reduced body masses, and concurrent use of other medications that impair water excretion. While taking thiazides, the elderly may have a greater defect in water excretion after a water Load compared with young subjects. Hyponatremia is usually induced within 2 weeks of starting the thiazide diuretic, but it can occur any time during thiazide therapy when subsequent contributory factors are complicated, such as reduction of renal function with aging, ingestion of other drugs that affect free water clearance, or changes in water or sodium intake. While some patients are volume depleted on presentation, most appear euvolemic. Notably serum Levels of uric acid, creatinine and urea nitrogen are usually normal or Low, suggestive of syndrome of inappropriate secretion of antidiuretic hormone. Despite numerous studies, the pathophysiological mechanisms underlying TIH are unclear. Although the traditional view is that diuretic-induced sodium or volume Loss results in vasopressin-induced water retention, the following 3 main factors are implicated in TIH: stimulation of vasopressin secretion, reduced free-water clearance, and increased water intake. These factors will be discussed in this review.

Review : Recent Advances of Oral Rehydration Therapy (ORT)

( Jin Soon Suh ),( Won Ho Hahn ),( Byoung Soo Cho ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2

Diarrheal disease is one of the leading causes of worldwide morbidity and mortality, especially in children. It causes loss of body fluid, which may lead to severe dehydration, electrolyte imbalance, shock and even to death. The mortality rate from acute diarrhea has decreased over the last few decades. This decline, especially in developing countries is largely due to the implantation of the standard World Health Organization-oral rehydration solution (WHOORS). However, the use of standard ORS has been limited by its inability to reduce fecal volume or diarrhea duration. Subsequently, this has led to various attempts to modify its compositions. And these modifications include the use of reduced osmolarity ORS, polymer-based ORS and zinc supplementation. Some of these variations have been successful and others are still under investigation. Therefore, further trials are needed to progress toward the ideal ORS. In this article, we briefly reviewed the pathophysiologic basis of the ORS, followed by the standard WHO-ORS and several modifications to improve the ORS.

Clinical Usefulness of the Serum Anion Gap

( Sik Lee ),( Kyung Pyo Kang ),( Sung Kyew Kang ) 대한전해질학회(구 대한전해질,혈압학회) 2006 Electrolytes & Blood Pressure Vol.4 No.1

The anion gap in the serum is useful in the interpretation of acid-base disorders and in the diagnosis of other conditions. In the early 1980s, ion-selective electrodes for specific ionic species were introduced for the measurement of serum electrolytes. This new method has caused a shift of the anion gap from 12±4 mEq/L down 6±3 mEq/L. It is worthy for clinicians to understand the range of normal anion gap and the measuring methods for serum sodium and chloride in the laboratories that support their practice. While an increase in the anion gap is almost always caused by retained unmeasured anions, a decrease in the anion gap can be generated by multiple mechanisms.

Molecular Physiology in Renal Water, Sodium and Acid-base Metabolism

Tae Hwan Kwon,Young Hee Kim 대한전해질학회 2003 대한전해질대사연구회지 Vol.1 No.1

고장성 자극에 대한 신장의 적응기전-TonEBP Transcriptional Activator의 기능

Na Gi Yeong 대한전해질학회 2004 대한전해질대사연구회지 Vol.2 No.1

신장 및 신장 질환에서 Heme Oxygenase의 역할

Jang Se Ho 대한전해질학회 2004 대한전해질대사연구회지 Vol.2 No.1