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A Case of Isolated Glycosuria Mediated by an SLC5A2 Gene Mutation and Characterized by Postprandial Heavy Glycosuria Without Salt Wasting.

Kyeong Min KIM ; Soon Kil KWON ; Hye Young KIM

Electrolytes & Blood Pressure.2016;14(2):35-37. doi:10.5049/EBP.2016.14.2.35

Familial renal glycosuria (FRG) is an inherited disorder characterized by persistent glycosuria in the absence of hyperglycemia. It is caused by mutations in the sodium-glucose co-transporter, leading to increase in the renal excretion of glucose and sodium. However, there have been no studies on the role of fasting and postprandial changes in the urinary sodium excretion in patients with FRG. We report a case of renal glycosuria, which was confirmed by a SLC5A2 mutation via gene sequencing, and compared the postprandial urinary glucose and sodium excretion. A 26-year-old man sometimes experienced glycosuria on routine screening; however, other laboratory findings were normal. His fasting and postprandial urinary glucose excretion levels were 295mg/dL and 2,170mg/dL, respectively. The fasting and postprandial urinary sodium excretion levels were 200mEq/L and 89mEq/L, respectively. In patients with FRG, excessive diuresis might be prevented by a compensatory mechanism that reduces postprandial sodium excretion.
Adult ; Diuresis ; Fasting ; Glucose ; Glycosuria* ; Glycosuria, Renal ; Humans ; Hyperglycemia ; Mass Screening ; Renal Elimination ; Sodium ; Sodium-Glucose Transport Proteins

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A Case Report of Syndrome of Inappropriate Antidiuretic Hormone Induced by Pregabalin.

Youn Joo JUNG ; Dong Young LEE ; Hae Won KIM ; Hyun Sun PARK ; Beom KIM

Electrolytes & Blood Pressure.2016;14(2):31-34. doi:10.5049/EBP.2016.14.2.31

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of euvolemic hyponatremia, and many medications have been associated with SIADH. Pregabalin is a drug used for the treatment of neuropathic pain, though common adverse effects include central nervous system disturbance, peripheral edema, and weight gain. However, hyponatremia caused by pregabalin has been rarely reported. Here we report a patient with pregabalin-induced hyponatremia who met the criteria for SIADH; after discontinuation of the drug, his condition rapidly improved. This case can help clinicians diagnose and treat new-onset hyponatremia in patients who recently initiated pregabalin therapy.
Central Nervous System ; Edema ; Humans ; Hyponatremia ; Inappropriate ADH Syndrome ; Neuralgia ; Pregabalin* ; Weight Gain

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Severe Hypernatremia Caused by Acute Exogenous Salt Intake Combined with Primary Hypothyroidism.

Woo Jin JUNG ; Su Min PARK ; Jong Man PARK ; Harin RHEE ; Il Young KIM ; Dong Won LEE ; Soo Bong LEE ; Eun Young SEONG ; Ihm Soo KWAK ; Sang Heon SONG

Electrolytes & Blood Pressure.2016;14(2):27-30. doi:10.5049/EBP.2016.14.2.27

This report describes a case of severe hypernatremia with a serum sodium concentration of 188.1mmol/L caused by exogenous salt intake. A 26-year-old man diagnosed with Crohn's disease 5 years previously visited our clinic due to generalized edema and personality changes, with aggressive behavior. He had compulsively consumed salts, ingesting approximately 154 g of salt over the last 4 days. Despite careful fluid management that included not only hypotonic fluid therapy for 8 hours but also hypertonic saline administration, his serum sodium level decreased sharply at 40.6 mmol/L; however, it returned to normal within 72-hour of treatment without any neurological deficits. Primary hypothyroidism was also diagnosed. He was discharged after 9 days from admission, with a stable serum sodium level. We have described the possibility of successful treatment in a patient with hypernatremia caused by acute salt intoxication without sustained hypotonic fluid therapy.
Adult ; Crohn Disease ; Edema ; Fluid Therapy ; Humans ; Hypernatremia* ; Hypothyroidism* ; Salts ; Sodium

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Genetic Variations of Tyrosine Hydroxylase in the Pathogenesis of Hypertension.

Yu Ho LEE ; Yang Gyun KIM ; Ju Young MOON ; Jin Sug KIM ; Kyung Hwan JEONG ; Tae Won LEE ; Chun Gyoo IHM ; Sang Ho LEE

Electrolytes & Blood Pressure.2016;14(2):21-26. doi:10.5049/EBP.2016.14.2.21

One of the major pathophysiological features of primary hypertension is an inappropriate activation of the sympathetic nervous system, which is mediated by excessive synthesis and secretion of catecholamine into the blood. Tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of catecholamine, has been highlighted because genetic variations of TH could alter the activity of the sympathetic nervous system activity and subsequently contribute to the pathogenesis of hypertension. Here, we discuss the role of TH as a regulator of sympathetic activity and review several studies that investigated the relationship between genetic variations of TH and hypertension.
Genetic Variation* ; Hypertension* ; Polymorphism, Single Nucleotide ; Sympathetic Nervous System ; Tyrosine 3-Monooxygenase* ; Tyrosine*

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Two Cases of Severe Hyperkalemia with Atypical Electrocardiographic Manifestations.

Sik LEE ; Min Hee LEE ; Kyung Pyo KANG ; Won KIM ; Sung Kwang PARK ; Sung Kyew KANG

Electrolytes & Blood Pressure.2005;3(1):52-54.

No abstract available.
Electrocardiography* ; Hyperkalemia*

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Hypertension in Renal Diseases.

Kwon Wook JOO

Electrolytes & Blood Pressure.2005;3(1):44-51.

Renal disease is closely associated with hypertension. Hypertension belongs to the clinical picture of chronic kidney disease (CKD). Hypertension associated with renal diseases occurs as a complication of various glomerular and interstitial diseases and may accelerate the decline of renal function if inadequately controlled. The pathophysiology through which the kidney raises blood pressure have been considerably clarified in recent years and it could be shown that "hypertension goes with the kidney" in experimental and clinical studies. The combined interactions of multiple independent mechanisms are thought to be involved in the development of hypertension. Impaired renal sodium handling leads to volume expansion. There is inappropriate activation of the renin-angiotensin system. As only recently documented in detail, renal injury raises the sympathetic tone, even when whole kidney glomerular filtration rate (GFR) is unchanged. This results from stimulating afferent signals coming from the kidney. There also is an evidence of impaired endothelial cell dependent vasodilatation even in very early stages of renal dysfunction. And other factors including uric acid, parathyoid hormone (PTH), and calcium may play a role in concert with other factors in the development of hypertension of renal diseases. Understanding these pathophysiologies is important for appropriate antihypertensive treatment.
Blood Pressure ; Calcium ; Endothelial Cells ; Glomerular Filtration Rate ; Hypertension* ; Kidney ; Kidney Failure, Chronic ; Renal Insufficiency, Chronic ; Renin-Angiotensin System ; Sodium ; Uric Acid ; Vasodilation

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Dietary Salt and Potassium Intake and Hypertension.

Seung Hun LEE ; Yoon Sik CHANG

Electrolytes & Blood Pressure.2005;3(1):36-43.

Evidence for a relationship between high sodium intake and high blood pressure comes from animal experimental studies, controlled clinical trials, and epidemiologic studies. Aanalyses from the International Co-Operative Study of Salt and Blood Pressure found estimates of systolic and diastolic blood pressure lower by 3 to 6 mmHg and 0 to 3 mmHg, respectively, for each lower daily sodium intake; the Dietary Approaches to Stop Hypertension-Sodium feeding trial showed that lower versus higher sodium reduced systolic blood pressure and diastolic blood pressure by 6.7 and 3.5 mmHg, respectively. Lowered sodium intake may help lower blood pressure and reduce or obviate the need for antihypertensive drugs. Most of studies suggest that potassium intake has inverse relationship on systolic and diastolic blood pressure; dietary potassium deficiency induces a salt sensitivity in the high incidence and prevalence of hypertension in African-Americans. Increased potassium intake reduces systolic and diastolic blood pressure; this effect is more enhanced in hypertensives compared to normotensives, and in those consuming a high intake of sodium. Increased potassium intake in combination with sodium restriction may provide the optimal means for prevention and treatment of hypertension. Increased potassium intake may reduce the risk of stroke independent of its effects on blood pressure
Animal Experimentation ; Antihypertensive Agents ; Blood Pressure ; Diet ; Hypertension* ; Incidence ; Potassium* ; Potassium, Dietary ; Prevalence ; Sodium ; Stroke

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Renal Sodium Handling and Hypertension.

Yang Wook KIM

Electrolytes & Blood Pressure.2005;3(1):32-35.

Renal sodium handling is known as an important function that maintains both body fluid volume and blood pressure regulation. Recently, advances in molecular biology have led that alterations of tubular sodium handling are closely related to changes of blood pressure. Also, tubular sodium uptakes are controlled by any protein participating in its reabsorption and regulation, which are influenced by genetic, nutritional, metabolic and neurohormonal factors. All of these factors, alone or combination, may be able to impair the normal renal tubular sodium handling and develop high blood pressure. The investigations about the role of kidney in hypertension are shifting toward inherited as well as acquired tubular defects and further studies about renal sodium handling based on sodium transporters on the tubular segments will be needed. This review will discuss the relationship between renal sodium handling and hypertension.
Blood Pressure ; Body Fluids ; Hypertension* ; Kidney ; Molecular Biology ; Sodium*

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Adrenomedullin and The Kidney.

Won KIM

Electrolytes & Blood Pressure.2005;3(1):24-31.

Adrenomedullin (AM) is a multi-functional peptide discovered in human pheochromocytoma. Initially, it was suggested that AM was synthesized only by tumor cells, however, subsequent studies revealed that it was produced also by normal adrenal medulla as well as by many other tissues. Now it is well established that AM functions as a circulating hormone and local paracrine mediator with multiple biological activities. AM stimulated cAMP production in human platelets and exerted potent and long-lasting hypotensive activity in the rat. AM is a physiologically relevant regulator in fluid and electrolyte homeostasis; inhibition both water and salt intake, increase renal blood flow, and cause diuresis and natriuresis. The up-regulation of cardiac AM system in hypertension may be a protective mechanism decreasing myocardial overload due to vasodilatory and natriuretic properties of AM, as well as limiting further myocardial hypertrophy and remodeling. AM may protect the kidney against ischemia-reperfusion injury. AM is also suggested as antiapoptotic, anti-inflammatory and angiogenic factor. In this review, I offer a review of our current knowledge on AM and give the putative role of AM in water-electrolyte balance, hypertension and kidney disease.
Adrenal Medulla ; Adrenomedullin* ; Angiogenesis Inducing Agents ; Animals ; Diuresis ; Homeostasis ; Humans ; Hypertension ; Hypertrophy ; Kidney Diseases ; Kidney* ; Natriuresis ; Pheochromocytoma ; Rats ; Renal Circulation ; Reperfusion Injury ; Up-Regulation ; Water-Electrolyte Balance

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Blood Pressure Regulation by Vasoactive Peptide Genes: Transgenic And Knockout Animal Models.

Dowhan AHN

Electrolytes & Blood Pressure.2005;3(1):14-23.

Hypertension is a polygenic and multifactorial disease and is intimately related to salt homeostasis. Four important vasoactive peptide systems participate in regulating blood pressure and salt homeostasis. Their interplay is indispensible in many physiologic and pathologic conditions. While the renin-angiotensin and the endothelin systems raise blood pressure by inducing vasoconstriction and sodium retention (or excretion), the kallikrein-kinin and the natriuretic peptide systems reduce blood pressure by eliciting vasodilatation and natriuresis. Gene targeting as well as transgenesis have provided us a lot of information on the biological functions of the genes of these systems. Animal models from these technologies are discussed in relation to blood pressure regulation.
Angiotensins ; Animals* ; Blood Pressure* ; Endothelins ; Gene Targeting ; Gene Transfer Techniques ; Homeostasis ; Hypertension ; Models, Animal* ; Natriuresis ; Sodium ; Vasoconstriction ; Vasodilation

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