• Clinical and Experimental Pediatrics
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• v.49 no.5
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• pp.470-474
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• 2006

Hypokalemia and hyperkalemia are the most commonly encountered electrolyte abnormalities in hospitalized patients. Because untreated hypokalemia or hyperkalemia is associated with high morbidity and mortality, it is important to recognize and treat them immediately. Hypokalemia and hyperkalemia can result from disruptions in transcellular homeostasis or in the renal regulation of $K^+$ excretion. Although the recognition is simple, appropriate management requires an understanding of normal $K^+$ homeostasis and pathophysiology. In this article, normal $K^+$ homeostasis, pathophysiology, diagnosis and management of hypokalemia and hypokalemia are discussed.

• Childhood Kidney Diseases
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• v.18 no.2
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• pp.111-115
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• 2014

Hyperkalemia is often detected in young infants, particularly in association with acute pyelonephritis or a urinary tract anomaly. Cases of hyperkalemia in this population may also be due to transient pseudohypoaldosteronism, or immaturity of renal tubules in handling potassium excretion. Symptoms of hyperkalemia are non-specific, but are predominantly related to skeletal or cardiac muscle dysfunction, and can be fatal. Therefore, treatment has to be initiated immediately. Administration of fludrocortisone for hyperkalemia is appropriate in cases with hypoaldosteronism, but is challenging in young infants with hyperkalemia due to renal tubular immaturity, without pseudohypoaldosteronism. We report the case of a 25-day-old male presenting with persistent hyperkalemia with normal serum aldosterone, who was admitted with a first episode of pyelonephritis and unilateral high-grade vesicoureteral reflux. The patient was treated successfully with fludrocortisone.

• The Journal of Internal Korean Medicine
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• v.27 no.3
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• pp.745-750
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• 2006

Spironolactone reduces potassium excretion in renal collecting ducts and causes hyperkalemia. A 66-year-old female with urinary incontinence had to discontinue diuretics for hyperkalemia. After treatment with Jesaengsinkihwan-gagambang. she reduced urinary incontinence and her total urine volume was increased. BUN decreased from 32.2 to 16 and creatinine decreased from 1.5 th 0.9. So. we report one case of urinary incontinence with discontinuance of diuretics for hyperkalemia treated with Jesaengsinkihwan-gagambang.

• Acute and Critical Care
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• v.33 no.4
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• pp.271-275
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• 2018

We experienced a case of severe intraoperative hyperkalemia during laparoscopic radical nephrectomy in a 60-year-old male patient with renal insufficiency, whose hypertension had been managed by preoperative angiotensin II receptor blocker (ARB) and adrenergic beta-antagonist. After renal vessel ligation, his intraoperative potassium concentration suddenly increased to 7.0 mEq/L, but his electrocardiography (ECG) did not show any significant change. While preoperative ARB therapy has been regarded as a contributing factor for further aggravation of underlying renal insufficiency, we assumed that nephrectomy itself and rhabdomyolysis caused by surgical trauma also aggravated the underlying renal dysfunction and resulted in sudden hyperkalemia. Hyperkalemia was managed successfully with calcium gluconate, insulin, furosemide and crystalloid loading during the intraoperative and immediate postoperative periods, and potassium concentration decreased to 5.0 mEq/L at 8 hours after the operation. The patient's hospital course was uncomplicated, but his renal function deteriorated further.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.123-129
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• 1990

A comparative study of acid-base balance has been made between acidemia-induced hyperkalemia and hyperkalemia-induced acidemia. A group of rabbits was infused 0.1 N hydrochloric acid solution and metabolic acidosis was induced. Another group was administered 20 mM potassium chloride solution and hyperkalemia was induced. The third group was infused 0.1 N hydrochloric acid and 20 mM potassium chloride solution, simultaneously. Acid-base data and plasma potassium ion concentration were monitored every thirty minutes in these three groups of rabbits. Following results were obtained: 1 ) Along with the infusion of hydrochloric acid, acute metabolic acidosis was induced in the rabbits. Plasma bicarbonate ion concentration decreased primarily in this group. As a respiratory compensation, there was a tendency of reduction of arterial $Pco_{2}$. The alteration of data became larger along with the amount of administration and the time elapsed. However, hyperkalemia was not so severe compared with the second group. 2) In potassium chloride infused group, plasma potassium ion concentration increased along with the time elapsed and the amount of infusion. And the alteration of acid-base data was parrallel to the level of potassium ion concentration, above all depression of pH was prominent. 3) Above data suggest that when acute metabolic acidosis was induced, exchange of intracellular potassium ion with extracellular hydrogen ion seems significant for the regulation of extracellular acid-base balance. And when hyperkalemia was induced with the infusion of potassium chloride solution, the exchange of intracellular hydrogen ion with extracellular potassium ion also seems significant for the regulation of extracellular potassium balance. 4) In the group of rabbits infused hydrochloric acid and potassium simultaneously, disturbances of acid-base balance and potassium balance were much more severe than two other groups. In these mixed disturbances, the process of compensatory mechanism might be inhibited and one disturbance might aggregate each other. 5) Through above data it has been postulated that in acid-base disturbance potassium balance can be sacrificed as a compensatory mechanism, and vice versa in disturbance of potassium balance. And our data also suggest that hydrogen ion and potassium ion are compensatory pair, one another.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

• Korean Journal of Veterinary Research
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• v.62 no.2
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• pp.12.1-12.4
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• 2022

A 16-year-old, 7.4 kg, castrated male Cocker Spaniel presenting anorexia and weight loss was referred due to a splenic mass, and total splenectomy was performed to resolve clinical signs. Following surgery, the dog developed mild hyperkalemia (6.27 mmol/L) without any clinical symptoms. Further investigations were conducted to determine the cause of hyperkalemia. The serum-plasma potassium difference was measured (1.05 mmol/L), and pseudohyperkalemia was diagnosed. The cause of pseudohyperkalemia was considered as thrombocytosis after splenectomy. The dog did not receive any specific treatment to lower blood potassium. To our knowledge, we report the first case of post-splenectomy pseudohyperkalemia in a dog.

• Journal of Veterinary Science
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• v.24 no.5
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• pp.62.1-62.7
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• 2023

This case report describes the hematological and radiological examination of urinary bladder rupture and complete urethral obstruction. associated with urolithiasis in Hanwoo. Hyponatremia, hypochloremia, azotemia, and hyperglycemia were observed in both urethral obstruction and urinary bladder rupture. However, cattle with urethral obstruction showed hyperkalemia and mild hyperglycemia, whereas cattle with bladder rupture showed marked hyperglycemia and normal potassium levels. In ultrasonography, the urethral obstruction showed a dilated bladder with a thick bladder wall. In contrast to previous literature, in this study, severe electrolyte changes such as severe hyponatremia, hypochloremia, and hyperkalemia occurred in a case of complete urethral obstruction.

• Journal of Korean Neurosurgical Society
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• v.57 no.3
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• pp.197-203
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• 2015

Objective : The potassium disturbance associated with thiopental continuous infusion in neurosurgical patients is well known. However, the effect of propofol continuous infusion on serum potassium levels has not been investigated extensively. Methods : We reviewed the medical records of 60 consecutive patients who received coma therapy or deep sedation for intracranial pressure control using either thiopental or propofol between January 2010 and January 2012. Results : The overall incidence of hypokalemia (K<3.5 mmol/L) was comparable between thiopental and propofol groups (89.2% vs. 82.6%). But, the incidence of moderate to severe hypokalemia (K<3.0 mmol/L) was significantly higher in thiopental group (51.4% vs. 13.0%, p=0.003). The lowest potassium level (2.9 mmol/L vs. 3.2 mmol/L, p=0.020) was lower in thiopental group. The patients in the thiopental group required greater potassium replacement than the propofol group patients (0.08 mmol/kg/h vs. 0.02 mmol/kg/h, p<0.001). On multivariate analysis, thiopental [odds ratio, 95% confidence interval, 7.31 (1.78-27.81); p=0.005] was associated with moderate to severe hypokalemia during continuous infusion. The incidence of rebound hyperkalemia (K>5.0 mmol/L, 32.4% vs. 4.3%, p=0.010) and the peak potassium concentration (4.8 mmol/L vs. 4.2 mmol/L, p=0.037) after the cessation of therapy were higher in thiopental group. On multivariate analysis, thiopental [8.82 (1.00-77.81); p=0.049] and duration of continuous infusion [1.02 (1.00-1.04); p=0.016] were associated with rebound hyperkalemia once therapy was discontinued. Conclusion : Propofol was less frequently associated with moderate to severe hypokalemia after induction and rebound hyperkalemia following the cessation of continuous infusion than thiopental.

• Clinical and Experimental Pediatrics
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• v.56 no.7
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• pp.308-311
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• 2013

In this report, we present a pediatric case of severe symptomatic hypermagnesemia resulting from the use of magnesium oxide as a laxative in a child undergoing continuous cyclic peritoneal dialysis for end-stage renal disease. The patient showed abnormal electrocardiography (ECG) findings, such as tall T waves, a widened QRS complex, and irregular conduction, which were initially misdiagnosed as hyperkalemia; later, the correct diagnosis of hypermagnesemia was obtained. Emergent hemodialysis successfully returned the serum magnesium concentration to normal without complications. When abnormal ECG changes are detected in patients with renal failure, hypermagnesemia should be considered.