Author Index / Subject Index

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

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 : 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 : Uncoventional Views on Certain Aspects of Toxin-Induced Metabolic Acidosis

( Man S. Oh ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.1

This discussion will highlight the following 9 specific points that related to metabolic acidosis caused by various toxins. The current recommendation suggests that alcohol dehydrogenase inhibitor fomepizole is preferred to ethanol in treatment of methanol and ethylene glycol poisoning, but analysis of the enzyme kinetics indicates that ethanol is a better alternative. In the presence of a modest increase in serum osmolal gap (<30 mOsm/L), the starting dose of ethanol should be far Less than the usual recommended dose. One can take advantage of the high vapor pressure of methanol in the treatment of methanol poisoning when hemodialysis is not readily available. Profuse sweating with increased water ingestion can be highly effective in reducing methanol Levels. Impaired production of ammonia by the proximal tubule of the kidney plays a major role in the development of metabolic acidosis in pyroglutamic acidosis. Glycine, not oxalate, is the main final end product of ethylene glycol metabolism. Metabolism of ethylene glycol to oxalate, albeit important clinically, represents Less than 1% of ethylene glycol disposal. Urine osmolal gap would be useful in the diagnosis of ethylene glycol poisoning, but not in methanol poisoning. Hemodialysis is important in the treatment of methanol poisoning and ethylene glycol poisoning with renal impairment, with or without fomepizole or ethanol treatment. Severe Leucocytosis is a highly sensitive indicator of ethylene glycol poisoning. Uncoupling of oxidative phosphorylation by salicylate can explain most of the manifestations of salicylate poisoning.

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.

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.

Case Report : Hypercalcemia Associated with Acute Kidney Injury and Metabolic Alkalosis

( Jong Hyeok Jeong ),( Eun Hui Bae ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2

Most cases of hypercalcaemia are secondary to malignancy or primary hyperparathyroidism. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis, and renal failure secondary to treatment of iatrogenic hypoparathyroidism and osteoporosis. Persistent ingestion of calcium carbonate and vitamin D caused milk-alkali syndrome. The patient was managed with intravenous fluids and withdrawal of calcium carbonate and vitamin D. She responded well to the treatment and the calcium concentration, renal function and metabolic alkalosis were normalized. Milk-alkali syndrome may be important as a reemerging cause of hypercalcemia.

Review : Atherosclerotic Renovascular Hypertension: Lessons from Recent Clinical Studies

( Woo Kyung Chung ),( Se Joong Kim ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2

Atherosclerotic renovascular hypertension is a form of secondary hypertension due to renal artery stenosis. After the introduction of medical therapy such as with statins and angiotensin blocking agents, it has been considered a very slowly progressive disease. In the 1990s, surgical methods were compared to radiological intervention and showed no additional benefits. Recent clinical data also demonstrate that in cases of relatively stable atherosclerotic renovascular disease, medical therapy is as effective as other interventions with regard to patient outcomes. In this paper the recent clinical outcomes are reviewed.

Review : Fluid and Electrolyte Disturbances in Critically Ill Patients

( Jay Wook Lee ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2

Disturbances in fluid and electrolytes are among the most common clinical problems encountered in the intensive care unit (ICU). Recent studies have reported that fluid and electrolyte imbalances are associated with increased morbidity and mortality among critically ill patients. To provide optimal care, health care providers should be familiar with the principles and practice of fluid and electrolyte physiology and pathophysiology. Fluid resuscitation should be aimed at restoration of normal hemodynamics and tissue perfusion. Early goaldirected therapy has been shown to be effective in patients with severe sepsis or septic shock. On the other hand, liberal fluid administration is associated with adverse outcomes such as prolonged stay in the ICU, higher cost of care, and increased mortality. Development of hyponatremia in critically ill patients is associated with disturbances in the renal mechanism of urinary dilution. Removal of nonosmotic stimuli for vasopressin secretion, judicious use of hypertonic saline, and close monitoring of plasma and urine electrolytes are essential components of therapy. Hypernatremia is associated with cellular dehydration and central nervous system damage. Water deficit should be corrected with hypotonic fluid, and ongoing water loss should be taken into account. Cardiac manifestations should be identified and treated before initiating stepwise diagnostic evaluation of dyskalemias. Divalent ion deficiencies such as hypocalcemia, hypomagnesemia and hypophosphatemia should be identified and corrected, since they are associated with increased adverse events among critically ill patients.

Review : Acid-Base Disorders in ICU Patients

( Yun Kyu Oh ) 대한전해질학회(구 대한전해질,혈압학회) 2010 Electrolytes & Blood Pressure Vol.8 No.2

Metabolic acid-base disorders are comnom clinical problems in ICU patients. Arterial blood gas analysis and anion gap (AG) are important laboratory data in approaching acid-base interpretation. When measuring the AG, several factors such as albumin have influence on unmeasured anions and unmeasured cations. If a patient has hypoalbuminemia, the AG should be adjusted according to the albumin level. High AG metabolic acidoses including lactic acidosis, ketoacidosis, and ingestion of toxic alcohols are common in ICU patients. The treatment target of lactic acidosis and ketoacidosis is not the acidosis, but the underlying condition causing acidosis. Gastric acid loss, diuretics, volume depletion, renal compensation for respiratory acidosis, hypokalemia, and mineralocorticoid excess are common causes of metaboic alkalosis. In chloride responsive metaboic alkalosis, volume and potassium repletion are mandatory.