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Long-term Follow up of Congenital Adrenal Hyperplasia Patients with Hyponatremia.

Jun Hyuk SONG ; Kyu Ha LEE ; Sung Do KIM ; Byoung Soo CHO

Electrolytes & Blood Pressure.2007;5(2):140-146. doi:10.5049/EBP.2007.5.2.140

Congenital adrenal hyperplasia (CAH) caused by 21-hydroxylase deficiency is an autosomal recessive disease, which leads to cortisol and aldosterone deficiency and hyperandrogenism. Typical medical treatment includes oral glucocorticoid and mineralocorticoid administration to suppress adrenal androgens and to compensate for adrenal steroid deficiencies. Usually, they have been managed with hydrocortisone (cortisone) and fludrocortisone (florinef). However, some patients stopped taking medicine without the doctor's consent. Among these patients, four cases of CAH patients showing the presence of hyponatremia as an initial electrolyte disorder were found with adrenal adenoma discovered by abdominal computerized tomography scan. Hypersecretion of adrenocorticotrophic hormone may play a role in the development of adrenal tumor and chronic poor compliance to therapy appears to be associated with development of the tumor. Two cases were managed with adrenalectomy because of increasing adrenal tumor size and virilization. Whereas the other two cases did not increase in size and were observed without adrenalectomy. Therefore, it is important that patients with CAH maintain steroid medication to avoid the appearance of adrenal tumor.
Adenoma ; Adrenal Hyperplasia, Congenital* ; Adrenalectomy ; Adrenocorticotropic Hormone ; Aldosterone ; Androgens ; Compliance ; Fludrocortisone ; Follow-Up Studies* ; Humans ; Hydrocortisone ; Hyperandrogenism ; Hyponatremia* ; Steroid 21-Hydroxylase ; Virilism

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Renal Subcapsular Hematoma: A Consequence of Reperfusion Injury of Long Standing Renal Artery Stenosis.

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

Electrolytes & Blood Pressure.2007;5(2):136-139. doi:10.5049/EBP.2007.5.2.136

Renal artery stenosis is a cause of secondary hypertension which can be cured by surgical or radiological intervention such as percutaneous transluminal renal artery stent placement. In this case we present a subcapsular hematoma of the kidney, a complication following percutaneous transluminal stent placement in the renal artery. Reperfusion injury to the kidney may be a possible mechanism of subcapsular hematoma of the kidney. Long standing severe renal artery stenosis and high pre- and post- procedure pressure gradient might contribute to the complication.
Angioplasty ; Hematoma* ; Hypertension ; Hypertension, Renovascular ; Kidney ; Renal Artery Obstruction* ; Renal Artery* ; Reperfusion Injury* ; Reperfusion* ; Stents

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Pseudohyperphosphatemia in a Patient with Multiple Myeloma.

Yonggu LEE ; Taiyon KOO ; Joo Hark YI ; Jung Hye CHOI ; Sang Woong HAN ; Ile Kyu PARK ; Ho Jung KIM

Electrolytes & Blood Pressure.2007;5(2):131-135. doi:10.5049/EBP.2007.5.2.131

Hyperphosphatemia is an unusual manifestation in patients with multiple myeloma without a significantly reduced glomerular filtration rate. Serum phosphate may be falsely elevated when a large amount of paraproteins is present in the serum, because ultraviolet light absorbance is elevated with the phosphomolybdate ultraviolet assay, which is most commonly used for serum phosphate measurement. This pseudohyperphosphatemia can be confirmed by deproteinization of the serum of patients. We report a case of multiple myeloma presenting with spurious hyperphosphatemia revealing pseudohyperphosphatemia by deproteinization of serum using sulfosalicylic acid.
Glomerular Filtration Rate ; Humans ; Hyperphosphatemia ; Multiple Myeloma* ; Paraproteinemias ; Paraproteins ; Ultraviolet Rays

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Electrolyte and Acid-Base Disturbances Induced by Clacineurin Inhibitors.

Chang Hwa LEE ; Gheun Ho KIM

Electrolytes & Blood Pressure.2007;5(2):126-130. doi:10.5049/EBP.2007.5.2.126

Nephrotoxicity is the most common and clinically significant adverse effect of calcineurin inhibitors. Cyclosporine and tacrolimus nephrotoxicity is manifested by both acute azotemia and chronic progressive renal disease and tubular zdysfunction. An elevation in the plasma potassium concentration due to reduced efficiency of urinary potassium excretion is common in cyclosporine-treated patients; it may be severe and potentially life-threatening with concurrent administration of an angiotensin converting enzyme inhibitor, which diminishes aldosterone release. Tubular injury induced by cyclosporine can also impair acid excretion. This may be presented as a hyperchloremic metabolic acidosis associated with decreased aldosterone activity and suppression of ammonium excretion by hyperkalemia. Some patients treated with cyclosporine develop hypophosphatemia due to urinary phosphate wasting. Renal magnesium wasting is also common presumably due to drug effects on magnesium reabsorption. Hypomagnesemia has also been implicated as a contributor to the nephrotoxicity associated with cyclosporine. Both cyclosporine and tacrolimus are associated with hypercalciuria. Attention must be paid to drug dose, side effects, and drug interactions to minimize toxicity and maximize efficacy.
Acidosis ; Aldosterone ; Ammonium Compounds ; Azotemia ; Calcineurin ; Cyclosporine ; Drug Interactions ; Humans ; Hypercalciuria ; Hyperkalemia ; Hypophosphatemia ; Magnesium ; Peptidyl-Dipeptidase A ; Plasma ; Potassium ; Tacrolimus

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Electrolyte and Acid-Base Disturbances Associated with Non-Steroidal Anti-Inflammatory Drugs.

Sejoong KIM ; Kwon Wook JOO

Electrolytes & Blood Pressure.2007;5(2):116-125. doi:10.5049/EBP.2007.5.2.116

Inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention (edema, hypertension), hyponatremia, hyperkalemia, and decreased renal function. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the effects of antihypertensive agents, and rarely aggravation of congestive heart failure. Although rare, NSAIDs can cause hyponatremia by reducing renal free water clearance. Hyperkalemia could occur to a degree sufficient to cause cardiac arrhythmias. Renal function can decline sufficiently enough to cause acute renal failure. NSAIDs associated electrolyte and acid-base disturbances are not uncommon in some clinical situations. Adverse renal effects of NSAIDs are generally associated with prostaglandin dependent states such as volume-contracted states, low cardiac output, or other conditions that tend to compromise renal perfusion. All NSAIDs seem to share these adverse effects. In view of many NSAIDs users' susceptibility to renal adverse effects due to their underlying disease or condition, physicians should be cautious in prescribing NSAIDs to susceptible patients.
Acidosis, Renal Tubular ; Acute Kidney Injury ; Anti-Inflammatory Agents, Non-Steroidal ; Antihypertensive Agents ; Arrhythmias, Cardiac ; Cardiac Output, Low ; Edema ; Heart Failure ; Humans ; Hyperkalemia ; Hyponatremia ; Perfusion ; Sodium ; Water ; Weight Gain

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Antimicrobial-induced Electrolyte and Acid-Base Disturbances.

Yang Wook KIM

Electrolytes & Blood Pressure.2007;5(2):111-115. doi:10.5049/EBP.2007.5.2.111

Antimicrobials are one of the most widely prescribed classes of therapeutic agents. Although adverse effects of antimicrobials are generally minimal and reversible, serious sequelae can sometimes remain, such as unusual forms of renal failure, acid base disturbance and electrolyte abnormalities. Many antimicrobials, especially vancomycin or aminoglycosides, are associated with development of acute renal failure caused by acute tubular necrosis, allergic acute interstitial nephritis, or vasculitis. Besides, some antimicrobial agents can cause serious fluid and electrolyte imbalance. To prevent these serious consequences, early recognition and correction of their harmful renal and electrolyte effects are required.
Acute Kidney Injury ; Aminoglycosides ; Anti-Infective Agents ; Necrosis ; Nephritis, Interstitial ; Renal Insufficiency ; Vancomycin ; Vasculitis

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Factors associated with Hypokalemia in Continuous Ambulatory Peritoneal Dialysis Patients.

Hyun Wook KIM ; Jae Hyun CHANG ; Sun Young PARK ; Sung Jin MOON ; Dong Ki KIM ; Jung Eun LEE ; Seung Hyeok HAN ; Beum Seok KIM ; Shin Wook KANG ; Kyu Hun CHOI ; Ho Young LEE ; Dae Suk HAN

Electrolytes & Blood Pressure.2007;5(2):102-110. doi:10.5049/EBP.2007.5.2.102

Hypokalemia is a frequent problem in patients on continuous ambulatory peritoneal dialysis (CAPD) and is affected by multiple factors. To evaluate factors associated with hypokalemia, we studied 68 patients on maintenance CAPD treatment for at least six months. In univariate analysis, patients with hypokalemia were associated with older age and the presence of diabetes mellitus. Serum albumin, calcium-phosphate product, triglyceride, body mass index, protein nitrogen appearance, and lean body mass assessed by creatinine kinetics were significantly lower as compared to those without hypokalemia. Serum C-reactive protein was significantly higher in the patients with hypokalemia. Multivariate stepwise linear regression analysis revealed that the serum albumin level and the ultrafiltration volume at the peritoneal equilibration test were independent factors associated with hypokalemia. This suggests that the serum potassium level may be an important nutritional marker in CAPD patients. Further longitudinal investigation is needed to clarify this relationship.
Body Mass Index ; C-Reactive Protein ; Creatinine ; Diabetes Mellitus ; Humans ; Hypokalemia* ; Kinetics ; Linear Models ; Nitrogen ; Nutritional Status ; Peritoneal Dialysis, Continuous Ambulatory* ; Potassium ; Serum Albumin ; Triglycerides ; Ultrafiltration

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Varying Dialysate Bicarbonate Concentrations in Maintenance Hemodialysis Patients Affect Post-dialysis Alkalosis but not Pre-dialysis Acidosis.

U Seok NOH ; Joo Hark YI ; Sang Woong HAN ; Ho Jung KIM

Electrolytes & Blood Pressure.2007;5(2):95-101. doi:10.5049/EBP.2007.5.2.95

This study aimed to assess the effects of different dialysate bicarbonate concentrations in correcting acid-base imbalance in 53 stable hemodialysis patients in a university-hemodialysis unit. Three different bicarbonate concentrations were assigned, i.e. 25 mEq/L in 10, 30 mEq/L in 30, and 35 mEq/L in 13 patients. Blood gas analyses from arterial line blood samples before and after dialysis in the mid-week were performed for the determination of pH and serum bicarbonate concentration ([HCO3-]). The mean values of predialysis arterial [HCO3-] were mildly acidotic in all 3 groups, but not significantly different among them, whereas those of post-dialysis arterial [HCO3-] were alkalotic, especially in the group of 35 mEq/L as compared with the other two groups. The mean blood pH was not significantly different among the 3 groups. As expected, there was a positive correlation between pre-dialysis pH and post-dialysis pH (r=0.45, p=0.001), and pre-dialysis [HCO3-] and post-dialysis [HCO3-] (r=0.58, p=0.000), but with a negative correlation between pre-dialysis [HCO3-] and the increment of intradialytic [HCO3-] following hemodialysis (r=-0.46, p=0.001). In conclusion, this study shows that the impact of conventional dialysate bicarbonate concentrations ranging from 25 to 35 mEq/L is not quite different on the mild degree of predialysis acidemia, but the degree of postdialysis alkalemia is more prominent in higher bicarbonate concentrations. Base supply by hemodialysis alone does not seem to be the main factor to determine the predialysis acidosis in end-stage renal disease patients on chronic maintenance hemodialysis.
Acid-Base Imbalance ; Acidosis* ; Alkalosis* ; Blood Gas Analysis ; Dialysis ; Humans ; Hydrogen-Ion Concentration ; Kidney Failure, Chronic ; Renal Dialysis* ; Vascular Access Devices

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Altered Regulation of 11beta-hydroxysteroid Dehydrogenase II in the Kidney of Rats with Experimental Hypertension.

Seong Su KANG ; Soo Wan KIM ; Jong Un LEE

Electrolytes & Blood Pressure.2007;5(2):89-94. doi:10.5049/EBP.2007.5.2.89

The present study was aimed at investigating the role of type II 11beta-hydroxysteroid dehydrogenase (IIbeta- HSD II) in the development of hypertension. Two-kidney, one-clip (2K1C), deoxycorticosterone acetate (DOCA)/salt, or NG-nitro-L-arginine methyl ester (L-NAME) hypertension was induced in male Sprague- Dawley rats. Four weeks later, the expression of 11beta-HSD II mRNA was determined in the kidney by Northern blot analysis. The plasma level of aldosterone was measured by radioimmunoassay. In 2K1C hypertension, the expression of 11beta-HSD II was decreased in the clipped kidney and increased in the non-clipped kidney. The expression was increased in the remnant kidney of DOCA/salt hypertension, while decreased in the kidneys of L-NAME hypertension. The plasma level of aldosterone was increased, decreased, and remained unchanged in 2K1C, DOCA/salt, and L-NAME hypertension, respectively. The down-regulation of 11beta-HSD II may contribute to the sodium retention, thereby increasing the blood pressure in 2K1C and L-NAME hypertension. On the contrary, the up-regulation in DOCA/salt hypertension may play a compensatory role to dissipate the sodium retention.
11-beta-Hydroxysteroid Dehydrogenases* ; Aldosterone ; Animals ; Blood Pressure ; Blotting, Northern ; Desoxycorticosterone ; Down-Regulation ; Humans ; Hypertension* ; Kidney* ; Male ; NG-Nitroarginine Methyl Ester ; Plasma ; Radioimmunoassay ; Rats* ; RNA, Messenger ; Sodium ; Up-Regulation

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Immunolocalization of Protein Kinase C Isoenzymes alpha, betaI, betaII and gamma in Adult and Developing Rat Kidney.

Wan Young KIM ; Gye Sil LEE ; Young Hee KIM ; Eun Young PARK ; Jin Sun HWANG ; Hyang KIM ; Jin KIM

Electrolytes & Blood Pressure.2007;5(2):75-88. doi:10.5049/EBP.2007.5.2.75

Protein kinase C (PKC) plays an important role not only in signal transduction mechanisms in various biological processes, but also in the regulation of growth and differentiation during development. We studied the classical PKC alpha, betaI, betaII and gamma, with regard to their expression in adult and developing rat kidney. PKCalpha appeared in the ureteric bud at embryonic day (E) 16, and the proximal and distal anlage at E18. After birth, the immunoreactivity of PKCalpha gradually decreased. In adult, PKCalpha was expressed intensely in the connecting tubule (CNT), the collecting ducts (CD) and the renal corpuscle, and weakly in the proximal and distal tubules. PKCbetaI appeared in the ureteric bud at E16, and the proximal anlage at E18. After birth, the immunoreactivity of PKCbetaI gradually disappeared from the CD and proximal tubule. In adult, PKCbetaI was expressed in the intercalated cells of the CNT and cortical CD, the proximal straight tubule, and the renal corpuscle. PKCbII appeared in distal anlage at E18, and increased markedly after birth. In the CD, PKCbetaII immunoreactivity appeared after birth. In adult, PKCbetaII was expressed in the distal tubule, the CNT and the CD. The immunoreactivity for PKCgamma appeared only in the proximal anlage at E18, and increased temporally around the time of birth. However, no immunoreactivity for PKCgamma was observed in adult rat kidney. These results indicate that classical PKC isoforms appear to play a role in the regulation of various renal functions and differentiation within specific functional units of the uriniferous tubule in rat kidney.
Adult* ; Animals ; Biological Processes ; Humans ; Kidney* ; Parturition ; Protein Isoforms ; Protein Kinase C beta ; Protein Kinase C* ; Protein Kinases* ; Rats* ; Signal Transduction ; Ureter

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