Decrease In Serum Potassium Research Articles

Insulin Improves Survival in a Canine Model of Acute β-Blocker Toxicity

Study objective: To compare the efficacy of a novel antidote, insulin, with standard treatments, glucagon and epinephrine, in a canine model of acute β-blocker toxicity. Methods: Anesthetized dogs were fitted with instruments by means of thoracotomy and vascular cutdown for multiple cardiodynamic, hemodynamic, metabolic, and electrical measures. After basal measurements were taken, animals received intravenous propranolol (.25 mg/kg/minute) continuously for the remainder of the experiment. Toxicity was defined as a 25% decrease in the product of heart rate times mean blood pressure. Thirty minutes after the development of toxicity, toxic measures were taken (treatment 0 minutes), and then the animals (n=6 each group) received either sham (saline solution), insulin (4 IU/minute with glucose clamped), glucagon (50 μg/kg bolus, then 150 μg/kg/hour infusion), or epinephrine (1 μg/kg/minute). Animals were monitored until death or for 240 minutes. Results: Propranolol decreased contractility, left ventricular pressure, and systemic blood pressure, and resulted in death of all sham-treated animals by 150 minutes. Six of six insulin-treated, four of six glucagon-treated, and one of six epinephrine-treated animals survived. Survival was greater for insulin-treated animals, compared with either glucagon-treated ( P<.05) or epinephrine-treated animals ( P<.02) by the log-rank test. Insulin-treated animals were characterized by improved cardiodynamics and hemodynamics, increased myocardial glucose uptake, and decreased serum potassium. Conclusion: Conclusion: Insulin is a superior antidote compared with glucagon or epinephrine in an anesthetized canine model of acute β-blocker toxicity. [Kerns W, Schroeder D, Williams C, Tomaszewski C, Raymond W: Insulin improves survival in a canine model of acute β-blocker toxicity. Ann Emerg Med June 1997; 29:748-757.]

Effects of furosemide on hemorheologic alterations induced by incremental treadmill exercise in Thoroughbreds

Abstract Objective To determine whether furosemide treatment altered the blood flow properties and serum and RBC electrolyte concentrations of Thoroughbreds during submaximal treadmill exercise. Design Thoroughbreds were subjected to submaximal treadmill exercise with and without treatment with furosemide (1 mg/kg of body weight, IV). Animals 5 healthy Thoroughbreds that had raced within the past year and had no history of exercise-induced pulmonary hemorrhage. Procedure Venous blood samples were obtained before exercise, at treadmill speeds of 9 and 13 m/s, and 10 minutes after exercise, and hemorheologic and electrolyte test results were determined. Results Hemorheologic changes 60 minutes after furosemide administration included increased PCV, plasma total protein concentration, whole blood viscosity, mean RBC volume, and RBC potassium concentration, and decreased serum potassium concentration, serum chloride concentration, and RBC chloride concentration. Furosemide treatment attenuated the exercise-associated changes in RBC size, serum sodium concentration, serum potassium concentration, RBC potassium and chloride concentrations, and RBC density; exacerbated exercise-associated increases in whole blood viscosity; and had no effect on RBC filterability. Conclusions The hemorheologic effects of furosemide probably occurred secondary to total body and transmembrane fluid and electrolyte fluxes and would not improve blood flow properties. Clinical Relevance The beneficial effects of furosemide treatment in reducing the severity of bleeding in horses with exercise-induced pulmonary hemorrhage cannot be explained by improved blood flow properties. (Am J Vet Res 1996;57:891–895)

A randomized, double-masked comparison of the antihypertensive efficacy and safety of combination therapy with losartan and hydrochlorothiazide versus captopril and hydrochlorothiazide in elderly and younger patients

A multinational, randomized trial was conducted to compare the antihypertensive efficacy and safety of the combination therapy of the angiotensin II receptor antagonist losartan with hydrochlorothiazide (HCTZ) (fixed-dose tablet) with that of the angiotensin-converting enzyme inhibitor captopril with HCTZ (fixed-dose tablet) in elderly and younger patients with mild-to-moderate essential hypertension. The study consisted of a 4-week single-masked placebo baseline period followed by a 12-week double-masked, parallel comparison of once-daily administration of losartan 50 mg/HCTZ 12.5 mg or captopril 50 mg/HCTZ 25 mg (2:1 randomization ratio). Patients with a mean trough sitting diastolic blood pressure (SiDBP) of 95 to 115 mm Hg after the placebo baseline period were randomly assigned to receive losartan/HCTZ (n = 216) or captopril/HCTZ (n = 109). At each center, patients were stratified according to age (<65 and ⩾65 years). The primary efficacy variable was the mean change from baseline to week 12 in trough SiDBP. Safety was assessed by recording adverse experiences and clinical laboratory measurements. At week 12, mean reductions from baseline in trough sitting systolic blood pressure and SiDBP were comparable in the losartan/HCTZ (21.5 and 12.6 mm Hg, respectively) and captopril/HCTZ (20.6 and 13.4 mm Hg, respectively) groups. Both fixed-dose combinations had an equal response regardless of the age of the patient. At week 12, a similar percentage of patients in the losartan/HCTZ and captopril/HCTZ groups had a trough SiDBP less than 90 mm Hg or a 10 mm Hg or greater reduction from baseline (71% and 75%, respectively). Significantly fewer patients in the losartan/HCTZ group had clinical adverse experiences that were considered drug related by the investigator (9% vs 18%). The incidences of cough and headache also were much less in the losartan/HCTZ group. Captopril/HCTZ was associated with significantly greater mean elevations in serum creatinine and uric acid and mean decreases in serum potassium. We concluded that once-daily administration of losartan 50 mg and HCTZ 12.5 mg as a fixed-dose tablet is an effective regimen for both elderly and younger patients with mild-to-moderate essential hypertension. The antihypertensive efficacy of the losartan 50 mg/HCTZ 12.5 mg combination is comparable to that of the captopril 50 mg/HCTZ 25 mg combination, but losartan/HCTZ has a more favorable safety, tolerability, and metabolic profile.

Effect of prednisolone on amino acid-induced changes in renal haemodynamics and tubular function

The effect of oral prednisolone treatment on renal haemodynamics, tubular function and various hormones during amino acid infusion was studied in 14 normal men. A balanced amino acid solution was infused for 120 min, before and after 4 days of prednisolone treatment (40 mg day-1). During amino acid infusion before prednisolone glomerular filtration rate, renal plasma flow, urinary sodium excretion, fractional excretion of sodium, lithium clearance, fractional excretion of lithium, serum insulin (s-insulin), plasma glucagon (p-glucagon) and s-growth hormone increased, whereas p-atrial natriuretic peptide, p-aldosterone, p-vasopressin and s-insulin-like growth factor 1 were unchanged, and potassium excretion and fractional excretion of potassium fell. After prednisolone treatment the most important differences during amino acid infusion were a significantly lower fractional excretion of sodium after 120 min (before prednisolone 26%; after prednisolone-7%; p < 0.05), a more pronounced increase in s-insulin after 120 min (before 118%; after 200%; p < 0.05) and a lower s-potassium. In conclusion, amino acid infusion increased fractional sodium excretion in healthy men, and this increase was reduced by prednisolone due to increased reabsorption in the distal tubules. It is suggested that the more pronounced the increases in plasma insulin and the decrease in serum potassium are mediators of the increased distal tubular sodium reabsorption during amino acid infusion during prednisolone treatment.

Some sodium, potassium and water changes in the elderly and their treatment

Creatinine clearance decreases with age by 1 ml/min/year after 40 years of age, although serum creatinine remains constant because of reduction of muscle mass. Reduction of water intake may occur in the elderly because of a reduced sensation of thirst; this is associated with a tendency to lose water with urine. The capacity to respond to sodium load is impaired in aged kidneys, thereby leading to ECV expansion and hypertension. But there is also, in the elderly, a reduced capacity for retaining sodium (FENa is higher than in young subjects), making old subjects sensitive to salt depletion and ECV contraction. Hypernatraemia (Nas > 150 mmol/l) is not infrequent in the elderly (1%) and is usually due to water deficiency (old subjects should be forced to drink), and rarely to iatrogenic excess of sodium. It is the abrupt occurrence of severe hypernatraemia that causes neurological symptoms due to dehydration and brain shrinking, which may lead to cerebral haemorrhage and death. Hyponatraemia (Nas < 130 mmol/l) is frequent among the elderly (7-11%) and is mainly due to water overload, which is usually iatrogenic. Hypovolaemic hyponatraemia occurs when salt depletion causes ECV contraction > 10%, and is due to water retention in an attempt to normalize ECV. Hypervolaemic hyponatraemia is due to ADH hypersecretion because of a decrease in 'effective' circulating blood volume. 'Pseudohyponatraemia' may occur because of hyperlipidaemia or hyperproteinaemia. It is the abrupt occurrence of severe hyponatraemia that causes neurological symptoms (water intoxication), secondary to the oedomatous swelling of the brain within the skull. While rapidly occurring hyponatraemia may be lethal, slowly occurring hyponatraemia is usually asymptomatic. Rapid correction of hyponatraemia may cause cerebral dehydration and 'osmotic demyelination syndrome' ('central pontine myelinosis'). Decrease (e.g. by diuretics) or increase (e.g. by ACE-inhibitors, non-steroidal anti-inflammatory drugs, beta-blockers) or serum potassium may occur in the elderly. Diuretics should be used with caution in elderly subjects to avoid salt depletion, hypotension and renal function impairment.

Acute decreases in serum potassium augment blood pressure

Potassium depletion is a risk factor for cardiovascular diseases, including hypertension, and frequently is encountered in patients with end-stage renal disease. Since the treatment of end-stage renal disease might result in K + depletion and postdialysis hypokalemia, we investigated the relationship between acute K + removal by hemodialysis and changes in blood pressure at the completion of treatment compared with predialysis and 1-hour postdialysis blood pressure. The effects of three different dialysate potassium concentrations ([K −] d; 1.0, 2.0, and 3.0 mmol/L) were investigated in 11 patients. Hemodialysis-induced K + removal, serum [K +], total body K +, and blood pressure were measured. The use of 1.0, 2.0, or 3.0 mmol/L [K +] d resulted in the removal of 77.0 ± 6.5, 54.5 ± 7.9, and 42.5 ± 9.9 mmol of K + per treatment, respectively ( P < 0.05, [K +] d 1.0 v [K +] d 3.0). Predialysis and postdialysis serum [K +] were 4.9 ± 0.2 and 3.6 ± 0.1 mEq/L for 1.0 mmol/L [K +] d, 5.1 ± 0.3 and 3.9 ± 0.1 mEq/L for 2.0 mmol/L [K +] d, and 5.3 ± 0.3 and 4.2 ± 0.2 mEq/L for 3.0 mmol/L [K +] d, respectively ( P < 0.001 for each [K +] d). The baseline total body K + corrected for gender, age, and race was 92% of predicted normal level and did not change significantly with the use of different [K +] d. Blood pressure decreased during hemodialysis as excess fluid was removed, regardless of [K +] d. Significant increases in blood pressure did occur 1 hour postdialysis compared with levels measured at the completion of treatment (“rebound hypertension”) when hemodialysis was performed with 1.0 and 2.0 mmol/L, but not with 3.0 mmol/L [K +] d. Mean blood pressure increased from 93.4 ± 4.6 mm Hg and 92.3 ± 3.1 mm Hg for 1.0 and 2.0 mmol/L [K +] d to 106.9 ± 5.7 mm Hg ( P < 0.05) and 102.1 ± 4.6 mm Hg ( P < 0.05), respectively. In contrast, mean blood pressure was 94.6 ± 5.0 mm Hg and 94.3 ± 7.4 mm Hg at completion and 1 hour postdialysis with 3.0 mmol/L [K +] d. The results of this study demonstrate that an acute decrease in serum potassium due to hemodialysis produces “rebound hypertension” that is likely mediated, at least in part, by constriction of arterioles in the systemic circulation.

Effects of Losartan on a Background of Hydrochlorothiazide in Patients With Hypertension

The purpose of this multicenter trial was to compare the antihypertensive efficacy and safety of losartan potassium (losartan), a selective angiotensin II receptor antagonist, when added to hydrochlorothiazide in hypertensive patients whose blood pressure was not adequately controlled by 25 mg hydrochlorothiazide monotherapy. After a 4-week monotherapy period of 25 mg hydrochlorothiazide, 304 patients with trough (22 to 26 hours postdose) sitting diastolic pressure between 93 and 120 mm Hg were maintained on 25 mg hydrochlorothiazide and randomized double-blind into treatment arms consisting of either 25, 50, or 100 mg losartan or placebo once daily for 12 weeks. The reductions in sitting diastolic pressure for patients treated with 25, 50, or 100 mg losartan concomitantly administered with 25 mg hydrochlorothiazide were significantly greater (P < or = .05) than the reductions observed in the 25 mg hydrochlorothiazide plus placebo group beginning 1 week after randomization. The antihypertensive response in all groups was greater at week 3 than week 1, with some additional decrease in blood pressure in some groups at later times. Sitting systolic pressures were also significantly reduced in each group over time. Standing blood pressures at week 12 were similar to sitting blood pressures. A dose-response relationship to losartan was observed in this patient population. The percentages of the total drug-related clinical adverse experiences as assessed by the investigator were generally similar in the 25, 50, and 100 mg losartan plus 25 mg hydrochlorothiazide groups (10.3%, 24.4%, and 20.0%, respectively) compared with the placebo plus 25 mg hydrochlorothiazide group (24.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Excessive hypokalemia and hyperkalemia following head injury

A sudden decrease of serum potassium below 2.5 mmol/l carries the risk of dangerous arrhythmias and requires immediate replacement therapy [6]. We refer to a patient with a brain stem compression after head injury, who developed a profound hypokalemia (K+ = 1.2 mmol/l) with life-threatening arrhythmias, probably due to a catecholamine induced intracellular potassium shift (beta-2-stimulation). Only by aggressive potassium replacement up to 80 mmol/h (610 mmol/16 h) could potassium levels be increased and cardiac arrhythmias terminated. Although replacement therapy was stopped when the serum K(+)-level increased to 2.4 mmol/l, 3.5 h later the patient became hyperkalemic (8.1 mmol/l). This was probably due to a secondary shift of potassium from intra- to extracellular space. In patients with severe head trauma and the potential risk of excessive catecholamine release special attention must be paid to changes in potassium balance.

Beta-adrenoceptor agonists do not stimulate daytime melatonin secretion in healthy subjects a double blind placebo controlled study

Noradrenergic stimulation of pineal β-adrenoceptors results in melatonin secretion.To investigate β-adrenoceptor mediated plasma melatonin responses in humans, ritodrine, salbutamol (β2-adrenoceptor agonists) and dobutamine (β1-adrenoceptor agonist) were infused from 0900 to 1200 h to 8 healthy subjects (four men and four women) in a double blind, crossover, placebo controlled study. Ritodrine and salbutamol significantly increased plasma cyclic AMP and decreased serum potassium concentrations indicating the presence of β2-adrenoceptor stimulation. Dobutamine substantially increased systolic blood pressure corresponding to its β1-adrenoceptor agonist propriety. However, neither β2- nor β1-adrenoceptor stimulation modified plasma melatonin concentration. These results show that β-adrenoceptor agonists do not increase daytime plasma melatonin concentration

Enalapril versus bendroflumethiazide in type 2 diabetes complicated by hypertension

In a double-blind, double-dummy, randomized, multi-centre study, the effects of bendroflumethiazide vs. enalapril on blood pressure, glycaemic control, lipoprotein concentrations and albuminuria were compared in non-proteinuric, hypertensive type 2 diabetic patients; they were treated for 20 weeks with either bendroflumethiazide 2.5-5.0 mg (n = 59) or enalapril 10-20 mg (n = 55). Age, fasting plasma glucose, HbA1c and BMI were similar in the groups. Systolic and diastolic blood pressure were reduced in both groups. Bendroflumethiazide was accompanied by minor but significant elevations in fasting plasma glucose and serum C-peptide. HbA1c was increased during both treatments. Lipoproteins and urinary albumin/creatinine ratio were stable. Bendroflumethiazide caused a decrease in serum potassium and an increase in serum urate. No significant correlations were observed between the decline in blood pressure and changes in the metabolic risk factors. Baseline levels of age, sex, BMI, blood pressure or urinary albumin/creatinine ratio were not related to changes in blood pressure, metabolic parameters or urinary albumin/creatinine ratio.

Influence of Postexercise Glucose Ingestion upon Serum Potassium Levels and ECG Function

Thirteen trained runners were studied to determine whether postexercise glucose ingestion contributes to electrocardiogram (ECG) alterations by enhancing decreases in serum potassium (K+) concentrations. For the two randomly ordered trials, subjects ingested a 100 g (25% w/v glucose polymer) drink, either alone or with the addition of 3 g of potassium chloride (KCl), within 15 min following a 90-min run. ECG parameters, serum K+, and glucose concentrations were measured preexercise (Time 0), 2-3 min post-exercise (Time 1), and 25 (Time 2) and 60 (Time 3) min postexercise. The data suggest that postexercise glucose ingestion may cause ECG changes that are not directly related to the return of K+ to muscle, and that these changes, although characteristic of hypokalemia, may be related to serum glucose excursions rather than to absolute levels of serum K+. The addition of KCl may have prevented these changes by delaying gastric emptying of glucose.

Effects of corticosteroids on urinary ammonium excretion in humans.

This study was designed to examine the selective effects of glucocorticoid and mineralocorticoid classes of steroid hormones on urinary ammonium excretion in humans. In 22 10-day studies, normal male volunteers received either 9 alpha-fludrohydrocortisone or hydrocortisone, alone or with the receptor antagonist spironolactone or mifepristone. The small but significant increase in ammonium excretion noted with the administration of 9 alpha-fludrohydrocortisone was associated with a significant decrease in serum potassium. In contrast, a significantly larger increase in ammonium excretion was noted with hydrocortisone, without concomitant electrolyte changes. Spironolactone did not alter the effect on ammonium excretion by either corticosteroid, whereas mifepristone markedly blunted the hydrocortisone-induced increase in urinary ammonium excretion. It was concluded that glucocorticoids increase urinary ammonium excretion in humans and that this effect occurs through binding to the Type II (glucocorticoid) receptor rather than by cross-occupancy of the Type I (mineralocorticoid) receptor.

Suspected Albuterol Intoxication In A Dog

SummaryA suspected case of intoxication of a dog by the beta2‐adrenergic agonist albuterol is discussed. Clinical abnormalities observed included hypokalemia, weakness, tachycardia, tachypnea, hyperthermia, and delirium. Treatment with high‐dose potassium supplementation helped to resolve these abnormalities.Adrenergic control of potassium homeostasis is beta2‐mediated and causes the intracellular uptake of potassium, primarily in liver and muscle. The mechanism of action of albuterol in decreasing serum potassium, its clinical applications in humans, and possible application in dogs are discussed.

Water Intoxication in a Schizophrenic Patient with Rhabdomyolysis

We report a case of water intoxication in a 54-year-old female schizophrenic patient with rhabdomyolysis. She had been admitted to a mental hospital, and treated with spiperone 6 mg daily. On August 3, 1992, the coma following a convulsion occurred. Laboratory data initially showed marked hyponatremia and hypochloremia with decreased serum potassium, and a gradual increase in serum creatine phosphokinase (CPK). The elevation in serum CPK with marked hyponatremia observed in the present patient was probably caused by excessive drinking of water. In this patient, the CPK elevation revealed the rhabdomyolysis.

Renal Papillary Cytoplasmic Granularity and Potassium Depletion Induced by Carbonic Anhydrase Inhibitors in Rats

Renal papillary cytoplasmic granularity (RPCG) induced by carbonic anhydrase inhibitors (CAIs) in rats is characterized by the accumulation of dense secondary lysosomes in epithelial, endothelial, and interstitial cells and may be related to drug-induced potassium depletion. Female Sprague-Dawley rats were given the CAI, acetazolamide, by gavage. Half were supplemented with 1% potassium chloride in the drinking water. Two treated groups were allowed to recover for 1 or 2 mo. Potassium supplementation inhibited RPCG by 80% but produced little amelioration of the mild 13% decrease in serum potassium induced by 200 mg/kg/day acetazolamide for 28 days. Acetazolamide-induced RPCG is reversible because 1- and 2-mo recovery periods decreased the incidence by 75% and 80%, respectively. The results support the hypothesis that RPCG is related to potassium depletion secondary to carbonic anhydrase inhibition. Because supplementation of potassium chloride had little effect on serum potassium, these data suggest that depletion of renal medullary potassium content is important in the pathogenesis of RPCG as previously suggested by others. Other types of diuretics that produce hypokalemia as a side effect may not deplete medullary potassium since RPCG has not been reported in humans or animals given these drugs.

Serum electrolytes and catecholamines after cardioversion from ventricular tachycardia and atrial fibrillation.

We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed stimulation, but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine, then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells.

Effects of terbutaline on basal thermogenesis of human skeletal muscle and Na‐K pump after 1 week of oral use—a placebo controlled comparison with propranolol.

1. A double-blind placebo-controlled study was conducted on the effects of oral terbutaline (beta 2-adrenoceptor agonist) and propranolol (beta 1 beta 2-adrenoceptor antagonist) on basal heat production of skeletal muscle, measured ex vivo by direct microcalorimetry. Terbutaline slow-release 7.5 mg, propranolol 80 mg, and matching placebo were randomly administered twice daily for 1 week to 15 healthy males, using a cross-over design. 2. Resting heat production in biopsied vastus lateralis was lowered by median 27% (P < 0.01) after terbutaline medication as compared with placebo. The cause of this hypometabolism at the cellular level is obscure but may possibly be explained by desensitization of beta 2-receptors. 3. Propranolol decreased the metabolic rate by 17% (P > 0.3); this might imply that the sympathetic nervous system is playing only a minor role in the regulation of basal metabolic rate in muscle, or that up-regulation of beta-receptors had influenced the decline. 4. The muscle utilized about 6% of its total energy for the Na-K pump as assessed after inhibition by ouabain. 5. Serum potassium was significantly lowered by terbutaline and slightly increased by propranolol with no relationship between changes in extracellular levels and muscle content of potassium under resting conditions. Energy values for the Na-K pump in muscle after 1 week of terbutaline or propranolol medication were similar to placebo. The results are not consistent with the hypothesis that decreased serum potassium during continuous beta 2-adrenoceptor agonist treatment is due to a chronically activated Na-K pump, at least not in resting muscle.

Pharmacodynamics of Atracurium in Clinical Practice

To determine which factors influenced the pharmacodynamics of atracurium in clinical practice, the steady-state plasma concentration of atracurium for 90% paralysis (Cpss90) was measured in 100 adult patients. Neuromuscular block was maintained at 88%-92% of the control response by adjusting the target concentration being delivered by preprogrammed intravenous atracurium infusion. The Cpss90 was measured empirically from plasma samples taken when the block had been stable for 15 min with no adjustment in the infusion rate for 20 min. To describe how factors influenced the Cpss90 of atracurium, a model was developed by multiple stepwise linear regression analysis. Influencing variables retained in the final model were plasma potassium concentration, intraoperative administration of gentamicin, and premedication with papaveretum and hyoscine. The model predicted that the Cpss90 of atracurium would decrease with decreasing serum potassium according to the relationship log10(Cpss90) = 2.380 + 0.171 x [K mmol/L] (n = 100; ANOVA, P < 0.001). Intraoperative administration of gentamicin modified this relationship resulting in a 25.1% decrease in the predicted Cpss90 (n = 15; ANOVA, P < 0.001). Premedication with papaveretum and hyoscine also modified this relationship resulting in a 21.2% decrease in predicted Cpss90 (n = 30; ANOVA, P < 0.001). The model predicted that administration of both would decrease the Cpss90 by 41.0%. Patients aged > or = 70 yr had a slight, but statistically insignificant, increase in the Cpss90 compared to younger adult patients. No other factor was found to influence the Cpss90, including patient sex, body fluid, and other drugs administered in the perioperative period, including calcium channel antagonists and ranitidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin Decreases the Serum Potassium Concentration during the Anhepatic Stage of Liver Transplantation

Severe hyperkalemia is a serious problem during orthotopic liver transplantation. The effectiveness of insulin in decreasing serum potassium concentration during the anhepatic stage of orthotopic liver transplantation was investigated. Forty patients with serum potassium concentrations greater than 4.0 mM/L at the onset of the anhepatic stage were randomized into two groups. Control group patients (n = 20) received no treatment, and treatment group patients (n = 20) received an intravenous bolus of regular insulin (20 u) 10 min into the anhepatic stage, followed by a glucose infusion (500 ml 5% dextrose in water) over 15 min. In the control group, the potassium concentration did not change, whereas in the treatment group, it decreased from 4.70 +/- 0.54 to 4.18 +/- 0.63 mM/L (mean +/- SD) within 15 min and to 3.57 +/- 0.55 mM/L 60 min after therapy. The potassium concentration was less in the treatment group than in the control group within 30 min of treatment (3.97 +/- 0.52 vs. 4.49 +/- 0.43 mM/L, respectively; P < 0.05). The potassium concentration increased similarly 30 s after graft reperfusion in both groups of patients, but was less in the treatment group (5.91 +/- 1.63 vs. 7.37 +/- 1.67 mM/L, respectively; P < 0.05). The potassium concentration returned to prereperfusion levels within 5 min after graft reperfusion. In patients undergoing orthotopic liver transplantation, the administration of insulin rapidly decreases serum potassium concentration, even in the absence of the liver, suggesting an important contribution by extrahepatic tissues in the insulin-stimulated uptake of potassium.

Mineralocorticoid therapy lowers serum potassium in patients with end-stage renal disease.

Hyperkalemia is a commonly encountered problem in dialysis patients with end-stage renal disease. In this study we evaluated the effect of mineralocorticoid therapy (MCT; fludrocortisone 0.1-0.3 mg per os daily) on serum potassium of hyperkalemic end-stage renal disease patients. Consecutive monthly clinical and biochemical profiles 3-6 months before and after MCT were compared. Twenty-one patients with a mean age (+/- SE) of 54 +/- 4 years (11 male and 10 female) were studied. Two patients were dropped from this study because they required a change in prescription of dialysis after starting MCT. Mean serum potassium levels significantly fell (p < 0.001) during the post-MCT period (4.9 +/- 0.1 mEq/l) compared with potassium levels during the pre-MCT (5.6 +/- 0.1 mEq/l) period. All patients except 1 showed a reduction in serum potassium levels after MCT. Pre- and post-MCT values were not different for body weight, mean blood pressure, blood urea nitrogen, serum glutamic-oxaloacetic transaminase, lactate dehydrogenase, sodium, chloride, bicarbonate, creatinine and albumin. Since the majority of the patients were anuric (n = 15), a decrease in serum potassium values in the post-MCT period was not due to loss of potassium in the urine. MCT appears to decrease serum potassium values in patients with end-stage renal disease by extrarenal mechanisms. We conclude that MCT can be used safely to lower serum potassium in patients with end-stage renal disease.