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ACE2 and Angiotensin-(1-7) in Hypertensive Renal Disease.

Electrolytes & Blood Pressure.2011;9(2):41-44. doi:10.5049/EBP.2011.9.2.41

The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-[Angiotensin-(1-7)(Ang-(1-7)]-Mas receptor axis has an opposing function to that of the ACE-Angiotensin II (Ang II)-Angiotensin type 1 (AT1) receptor axis. Ang-(1-7) is present in the kidneys at concentrations comparable to those of Ang II and is associated with vasodilation, modulation of sodium and water transport, and stimulation of nitric oxide (NO) synthase. Ang-(1-7) also acts as a physiological antagonist of Ang II by counterbalancing the Ang II-mediated intracellular signaling pathway. In a hypertensive model, increased ACE and decreased ACE2 along with a higher ACE/ACE2 ratio in hypertensive kidneys appeared to favor Ang II generation, leading to hypertensive renal damage. In addition, the administration of a selective Ang-(1-7) receptor blocker or an ACE2 inhibitor was associated with worsening of hypertension and renal function. Ang-(1-7)-mediated increases in renal blood flow were abolished by blockade of the Mas receptor and by inhibition of prostaglandin release and NO in spontaneously hypertensive rats and in Wistar-Kyoto controls. Further research on the function of the ACE2-Ang-(1-7)-Mas receptor axis could lead to a novel target for inhibiting kidney disease progression.
Angiotensin I ; Angiotensin II ; Hypertension ; Kidney ; Kidney Diseases ; Nitric Oxide ; Peptide Fragments ; Peptidyl-Dipeptidase A ; Rats, Inbred SHR ; Renal Circulation ; Sodium ; Vasodilation ; Water ; Axis, Cervical Vertebra

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Volume Control by Using the Body Composition Monitor in a Puerperal Patient on Hemodialysis.

Wookyung CHUNG ; Shung Han CHOI ; Jiyoon SUNG ; Eul Sik JUNG ; Dong Su SHIN ; Ji Yong JUNG ; Jae Hyun CHANG ; Hyun Hee LEE ; Seung Ho LEE ; Sejoong KIM

Electrolytes & Blood Pressure.2011;9(2):63-66. doi:10.5049/EBP.2011.9.2.63

Accurate measurement of the volume status in hemodialysis patients is important as it can affect mortality. However, no studies have been conducted regarding volume management in cases where a sudden change of body fluid occurs, such as during puerperium in hemodialysis patients. This report presents a case in which the patient was monitored for her body composition and her volume status was controlled using a body composition monitor (BCM) during the puerperal period. This case suggests that using a BCM for volume management may help maintain hemodynamic stability in patients with a rapidly changing volume status for a short term period, such as during puerperium.
Body Composition ; Body Fluids ; Hemodynamics ; Humans ; Organothiophosphorus Compounds ; Postpartum Period ; Renal Dialysis

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Effects of Dietary Salt Restriction on Puromycin Aminonucleoside Nephrosis: Preliminary Data.

Chor Ho JO ; Sua KIM ; Joon Sung PARK ; Gheun Ho KIM

Electrolytes & Blood Pressure.2011;9(2):55-62. doi:10.5049/EBP.2011.9.2.55

Proteinuria is a major promoter that induces tubulointerstitial injury in glomerulopathy. Dietary salt restriction may reduce proteinuria, although the mechanism is not clear. We investigated the effects of dietary salt restriction on rat kidneys in an animal model of glomerular proteinuria. Male Sprague-Dawley rats were used and divided into 3 groups: vehicle-treated normal-salt controls, puromycin aminonucleoside (PA)-treated normal-salt rats, and PA-treated low-salt rats. PA was given at a dose of 150 mg/kg BW at time 0, followed by 50 mg/kg BW on days 28, 35, and 42. Sodium-deficient rodent diet with and without additional NaCl (0.5%) were provided for normal-salt rats and low-salt rats, respectively. On day 63, kidneys were harvested for histopathologic examination and immunohistochemistry. PA treatment produced overt proteinuria and renal damage. Dietary salt restriction insignificantly reduced proteinuria in PA-treated rats, and PA-treated low-salt rats had lower urine output and lower creatinine clearance than vehicle-treated normal-salt controls. When tubulointerstitial injury was semiquantitatively evaluated, it had a positive correlation with proteinuria. The tubulointerstitial injury score was significantly increased by PA treatment and relieved by low-salt diet. ED1-positive infiltrating cells and immunostaining for interstitial collagen III were significantly increased by PA treatment. These changes appeared to be less common in PA-treated low-salt rats, although the differences in PA-treated normal-salt versus low-salt rats did not reach statistical significance. Our results suggest that renal histopathology in PA nephrosis may potentially be improved by dietary salt restriction. Non-hemodynamic mechanisms induced by low-sodium diet might contribute to renoprotection.
Animals ; Collagen ; Creatinine ; Diet ; Diet, Sodium-Restricted ; Humans ; Immunohistochemistry ; Kidney ; Male ; Models, Animal ; Nephrosis ; Proteinuria ; Puromycin ; Puromycin Aminonucleoside ; Rats ; Rats, Sprague-Dawley ; Rodentia

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V2 Receptor Antagonist; Tolvaptan.

Joo Hark YI ; Hyun Jong SHIN ; Ho Jung KIM

Electrolytes & Blood Pressure.2011;9(2):50-54. doi:10.5049/EBP.2011.9.2.50

Hyponatremia is the most common electrolyte disorder in hospitalized patients. Many studies documented that it was related to increased morbidity and mortality in patients with congestive heart failure, liver cirrhosis, and neurologic diseases. Although knowledge of hyponatremia has been cumulated, the optimal management of hyponatremia remains incompletely established in clinical practice because of the diversity of underlying disease states, and its multiple causes with differing pathophysiologic mechanisms. Since vasopressin receptor antagonists have unique aquaretic effect to selectively increase electrolytes-free water excretion, clinicians could apply a more effective method to treat hyponatremia. Tolvaptan has significant evidence that it improves serum sodium levels in patients with euvolemic or hypervolemic hyponatremia related with heart failure, cirrhosis or syndrome of inappropriate anti-diuretic hormone. Tolvaptan has acceptable safety and tolerability for long-term usage in chronic hyponatremia, and the beneficial effects on serum Na+ occurred in patients with both mild and marked hyponatremia.
Benzazepines ; Fibrosis ; Heart Failure ; Humans ; Hyponatremia ; Liver Cirrhosis ; Receptors, Vasopressin ; Sodium ; Water

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Mechanisms of the Effects of Acidosis and Hypokalemia on Renal Ammonia Metabolism.

Ki Hwan HAN

Electrolytes & Blood Pressure.2011;9(2):45-49. doi:10.5049/EBP.2011.9.2.45

Renal ammonia metabolism is the predominant component of net acid excretion and new bicarbonate generation. Renal ammonia metabolism is regulated by acid-base balance. Both acute and chronic acid loads enhance ammonia production in the proximal tubule and secretion into the urine. In contrast, alkalosis reduces ammoniagenesis. Hypokalemia is a common electrolyte disorder that significantly increases renal ammonia production and excretion, despite causing metabolic alkalosis. Although the net effects of hypokalemia are similar to metabolic acidosis, molecular mechanisms of renal ammonia production and transport have not been well understood. This mini review summarizes recent findings regarding renal ammonia metabolism in response to chronic hypokalemia.
Acid-Base Equilibrium ; Acidosis ; Alkalosis ; Ammonia ; Hypokalemia ; Kidney

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Water Intoxication Following Low-Dose Intravenous Cyclophosphamide.

Tai Yeon KOO ; Sang Cheol BAE ; Joon Sung PARK ; Chang Hwa LEE ; Moon Hyang PARK ; Chong Myung KANG ; Gheun Ho KIM

Electrolytes & Blood Pressure.2007;5(1):50-54. doi:10.5049/EBP.2007.5.1.50

Cyclophosphamide is frequently used for the treatment of severe lupus nephritis, but is very rarely associated with dilutional hyponatremia. Recently we experienced a case of water intoxication following low-dose intravenous cyclophosphamide. Five hours after one dose of intravenous pulse cyclophosphamide 750 mg, the patient developed nausea, vomiting, and general weakness. Serum sodium concentration revealed 114 mEq/L and her hyponatremia was initially treated with hypertonic saline infusion. Then her serum sodium concentration rapidly recovered to normal with water restriction alone. During the course of intravenous pulse cyclophosphamide therapy, one must be aware of the possibility of significant water retention.
Cyclophosphamide* ; Humans ; Hyponatremia ; Lupus Nephritis ; Nausea ; Sodium ; Vomiting ; Water Intoxication*

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SIADH Associated with Prostate Cancer.

Kyun Sang LEE ; Taek Won KANG ; Seong Kwon MA ; Soo Wan KIM ; Nam Ho KIM ; Ki Chul CHOI

Electrolytes & Blood Pressure.2007;5(1):47-49. doi:10.5049/EBP.2007.5.1.47

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common disease leading to hyponatremia, and it is characterized by an inappropriately elevated serum ADH level relative to serum osmolality. This syndrome may occur in a variety of clinical settings including malignancies. However, it is rarely observed in association with prostate cancer. Moreover, its pathogenesis and clinical characteristics have not been completely understood. We report a case of SIADH associated with prostate cancer in a 64-year-old male patient with a literature review.
Humans ; Hyponatremia ; Inappropriate ADH Syndrome* ; Male ; Middle Aged ; Osmolar Concentration ; Prostate* ; Prostatic Neoplasms*

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Metabolic Acidosis in Maintenance Hemodialysis Patients: Clinical Impact and Intervention.

Ho Jung KIM ; Sang Woong HAN

Electrolytes & Blood Pressure.2007;5(1):42-46. doi:10.5049/EBP.2007.5.1.42

Metabolic acidosis has been considered as one of the reverse epidemiologic factors for the morbidity and mortality in maintenance hemodialysis patients (MHP). Expectedly, in the recent large scale epidemiologic study (The Dialysis Outcome Practice Pattern Study, DOPPS), a mild to moderate degree of predialysis metabolic acidosis has shown better nutritional status and lower relative risk for mortality and hospitalization in MHP. Similarly, another recent study of the largest sample size of MHP of more than 55,000 revealed the lowest unadjusted mortality with mild to moderate degree of predialysis HCO3 levels (17 to 23 mEq/L). However, it was reversed after case-mix and multivariate adjustment, including the malnutrition-inflammation complex syndrome, so that predialysis HCO3 levels of more than 22 mEq/L had a lower death risk. On view of this up-to-date on-going controversy about the optimal acid-base status for MHP, this paper will review the historical and break-through data about the pros and cons of metabolic acidosis published in the clinical human studies of MHP, a special subgroup of chronic kidney disease patients. Based on these results, if possible, we would like to suggest the best practice guideline, particularly, for the optimal predialysis HCO3 level, dialysate HCO3 concentration, and dietary protein intake.
Acidosis* ; Dialysis ; Dietary Proteins ; Epidemiologic Factors ; Hospitalization ; Humans ; Mortality ; Nutritional Status ; Practice Guidelines as Topic ; Renal Dialysis* ; Renal Insufficiency, Chronic ; Sample Size

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Hypertensive Hypokalemic Disorders.

Kyu Bok CHOI

Electrolytes & Blood Pressure.2007;5(1):34-41. doi:10.5049/EBP.2007.5.1.34

Hypokalemia is a common clinical problem. The kidney is responsible for long term potassium homoeostasis, as well as the serum potassium concentration. The main nephron site where K secretion is regulated is the cortical collecting duct, mainly via the effects of aldosterone. Aldosterone interacts with the mineralocorticoid receptor to increase sodium reabsorption and potassium secretion; the removal of cationic sodium makes the lumen relatively electronegative, thereby promoting passive potassium secretion from the tubular cell into the lumen through apical potassium channels. As a result, any condition that decreases the activity of renal potassium channels results in hyperkalemia (for example, amiloride intake or aldosterone deficiency) whereas their increased activity results in hypokalemia (for example, primary aldosteronism or Liddle's syndrome). The cause of hypokalemia can usually be determined from the history. If there is no apparent cause, the initial step is to see if hypokalemia is in associated with systemic hypertension or not. In the former group hypokalaemia is associated with a high mineralocorticoid effect or hyperactive sodium channel as in Liddle's syndrome. In hypertensive hypokalemic patients, measurement of the renin, aldosterone, and cortisol concentrations would be of help in differential diagnosis.
Aldosterone ; Amiloride ; Diagnosis, Differential ; Humans ; Hydrocortisone ; Hyperaldosteronism ; Hyperkalemia ; Hypertension ; Hypokalemia ; Kidney ; Mineralocorticoids ; Nephrons ; Potassium ; Potassium Channels ; Receptors, Mineralocorticoid ; Renin ; Sodium ; Sodium Channels

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Regulation of Urea Transporters by Tonicity-responsive Enhancer Binding Protein.

Ju Young JUNG ; Moo KWON ; Jim KIM

Electrolytes & Blood Pressure.2007;5(1):28-33. doi:10.5049/EBP.2007.5.1.28

Urea accumulation in the renal inner medulla plays a key role in the maintenance of maximal urinary concentrating ability. Urea transport in the kidney is mediated by transporter proteins that include renal urea transporter (UT-A) and erythrocyte urea transporter (UT-B). UT-A1 and UT-A2 are produced from the same gene. There is an active tonicity-responsive enhancer (TonE) in the promoter of UT-A1, and the UT-A1 promoter is stimulated by hypertonicity via tonicity-responsive enhancer binding protein (TonEBP). The downregulation of UT-A2 raises the possibility that TonEBP also regulates its promoter. There is some evidence that TonEBP regulates expression of UT-A in vivo; (1) during the renal development of the urinary concentrating ability, expression of TonEBP precedes that of UT-A1; (2) in transgenic mice expressing a dominant negative form of TonEBP, expression of UT-A1 and UT-A2 is severely impaired; (3) in treatment with cyclosporine A, TonEBP was significantly downregulated after 28 days. This downregulation involves mRNA levels of UT-A2; (4) in hypokalemic animals, downregulation of TonEBP contributed to the down regulation of UT-A in the inner medulla. These data support that TonEBP directly contributes to the urinary concentration and renal urea recycling by the regulation of urea transporters.
Animals ; Carrier Proteins* ; Cyclosporine ; Down-Regulation ; Erythrocytes ; Kidney ; Mice ; Mice, Transgenic ; Recycling ; RNA, Messenger ; Urea*

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