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Electrolytes & Blood Pressure update

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수록정보
수록범위 : 3권1호(2005)~18권1호(2020) |수록논문 수 : 175
Electrolytes & Blood Pressure
18권1호(2020년 06월) 수록논문
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KCI등재 SCOPUS

1Urinary Concentration Defect and Renal Glycosuria in Cyclosporine-treated Rats

저자 : Jun Han Lee , Su A Kim , Chor Ho Jo , Chang Hwa Lee , Gheun-ho Kim

발행기관 : 대한전해질학회 간행물 : Electrolytes & Blood Pressure 18권 1호 발행 연도 : 2020 페이지 : pp. 1-9 (9 pages)

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Background: Urinary concentration impairment is a major feature of cyclosporine nephrotoxicity.
Methods: We explored two possible mechanisms that may underlie cyclosporine-induced polyuria; water, and/or osmotic diuresis. Cyclosporine was subcutaneously injected to normal salt-fed Sprague-Dawley rats at a daily dose of 25mg/kg for 2 weeks (Experiment I) and 7.5mg/kg for 6 weeks (Experiment II).
Results: In Experiment I, cyclosporine treatment caused an increase in urine volume (2.7±0.5 vs. 10.3±1.13mL/d/100 g BW, p<0.001) and a decrease in urine osmolality (2,831±554 vs. 1,379±478mOsm/kg H2O, p<0.05). Aquaporin-2 (AQP2) protein expression decreased in cyclosporine-treated rat kidneys (cortex, 78±8%, p<0.05; medulla, 80±1%, p<0.05). Experiment II also showed that urine volume was increased by cyclosporine treatment (4.97±0.66 vs. 9.65±1.76mL/d/100 g BW, p<0.05). Whereas urine osmolality was not affected, urinary excretion of osmoles was increased (7.5±0.4 vs. 14.9±1.4mosmoles/d/100 g BW, p<0.005). Notably, urinary excretion of glucose increased in cyclosporine-treated rats (7±1 vs. 10,932±2,462 mg/d/100 g BW, p<0.005) without a significant elevation in plasma glucose. In both Experiment I and II, GLUT2 protein expression in the renal cortex was decreased by cyclosporine treatment (Experiment I, 55±6%, p<0.005; Experiment II, 88 ±3%, p<0.05).
Conclusion: Both water diuresis and osmotic diuresis are induced by cyclosporine nephrotoxicity. AQP2 and GLUT2 downregulation may underlie water and osmotic diuresis, respectively.

KCI등재 SCOPUS

2Voriconazole-induced Severe Hyperkalemia Precipitated by Multiple Drug Interactions

저자 : Jae Young Choi , Seong Geun Cho , Ki-seok Jang , Gheun-ho Kim

발행기관 : 대한전해질학회 간행물 : Electrolytes & Blood Pressure 18권 1호 발행 연도 : 2020 페이지 : pp. 10-15 (6 pages)

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Voriconazole, a triazole antifungal agent used to treat serious fungal infections, has a pharmacokinetic characteristic of undergoing hepatic metabolism by the cytochrome P450 system. Few cases of hyperkalemia have been reported, which presented only when the serum voriconazole level was exceptionally elevated by drugdrug interactions. Additionally, azole antifungals may interfere with the biosynthesis of adrenal steroids and therefore can predispose patients to aldosterone deficiency. However, it is unclear whether voriconazole itself can induce hypoaldosteronism or hyperkalemia. Here, we report a case of voriconazole-induced hyperkalemia in a patient administered concurrent medications to treat comorbidities. Voriconazole was orally administered for pulmonary aspergillosis, and three episodes of severe hyperkalemia recurred, which improved with emergency treatment. In the first episode, renin-angiotensin-aldosterone system inhibitors were associated. We found that dronedarone might have increased the voriconazole level in the second episode. At that time, severe hypercalcemia was concurrent, which improved with acute hemodialysis and eliminating dronedarone. Finally, severe hyperkalemia recurred without concurrent medications known to interact with voriconazole. Upon switching from voriconazole to itraconazole, the hyperkalemia was resolved. Drug level monitoring is necessary when voriconazole is used. Genetic susceptibility, such as through CYP2C19 polymorphism, may be investigated for patients with adverse reactions to voriconazole.

KCI등재 SCOPUS

3Extremely Severe Hypernatremia Caused by Wrong Belief in a Patient with Cervical Cancer

저자 : Myeong Su Park , Hyuk Jin Park , Hong Sang Choi , Chang Seong Kim , Eun Hui Bae , Seong Kwon Ma , Soo Wan Kim , Minah Kim

발행기관 : 대한전해질학회 간행물 : Electrolytes & Blood Pressure 18권 1호 발행 연도 : 2020 페이지 : pp. 16-18 (3 pages)

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A 56-year old female patient who was undergoing follow-up for cervical cancer in our oncology center was presented to the emergency center with anxiety and excessive thirst. The initial serum sodium level of the patient exceeded 200mEq/L, rising up to 238mEq/L during hospitalization. The extremely severe hypernatremia was caused by patient's wrong belief that bay salt would cure the cancer. The patient was treated with hypotonic solution and finally with appropriate hydration, she was fully recovered without any neurological complications.

KCI등재 SCOPUS

4Recurrent Severe Hyponatremia in a Patient with Sjögren's Syndrome

저자 : Hyung Duk Kim , Jennifer Lee , Byung Ha Chung , Chul Woo Yang , Yong-soo Kim , Cheol Whee Park

발행기관 : 대한전해질학회 간행물 : Electrolytes & Blood Pressure 18권 1호 발행 연도 : 2020 페이지 : pp. 19-22 (4 pages)

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Sjögren's syndrome (SS) is an autoimmune disease that presents with exocrine gland dysfunction. Renal involvement is common in SS and often results in tubu-lointerstitial nephritis, renal tubular acidosis, and Fanconi's syndrome. Electrolyte imbalances are commonly the first symptom of renal involvement of SS. The most common feature of dysnatremia in SS is hypernatremia with diabetes insipidus. However, cases of hyponatremia with syndrome of inappropriate antidiuretic hormone secretion (SIADH) are rarely reported in patients with SS. Herein, we report a case of recurrent severe SIADH in a patient with SS.

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