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At least 127 records · Page 7Linked to original sources
PubMed2003

Amiodarone attenuates fluoride-induced hyperkalemia in vitro.

UNLABELLED: Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals.

Amiodarone↗
PubMed1996

Hyperkalemia alters EDHF-mediated hyperpolarization and relaxation in coronary arteries.

Hyperkalemic solutions are widely used to preserve organs for transplantation and for cardiac surgery. The present study was designed to test the hypothesis that hyperkalemia may alter endothelial function through a non-nitric oxide (NO) pathway, since preliminary studies have shown that the NO pathway may not be affected. Porcine coronary artery rings were studied in organ chambers. After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced. Incubation with hyperkalemia also significantly increased the concentration eliciting 50% of the maximal response to A23187 and bradykinin. A23187-induced hyperpolarization of the membrane potential was significantly reduced by hyperkalemic incubation. However, 1-h incubation with hyperkalemia does not affect the endothelial Ca2+ concentration. We conclude that exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant endothelium-dependent relaxation and endothelium-dependent hyperpolarization. This reduction in the relaxation and hyperpolarization is related to the endothelium-derived hyperpolarizing factor by affecting its effect on the smooth muscle cell, probably through partially depolarizing the membrane, and the Ca2(+)- activated K+ channels rather than by affecting its biosynthesis and/or release in the endothelial cell. Our study may suggest a new mechanism for coronary dysfunction after exposure to hyperkalemic cardioplegia and organ preservation solutions.

Animals↗
PubMed1997

Mechanism of the exercise hyperkalemia: an alternate hypothesis.

A progressive hyperkalemia is observed as exercise intensity increases. The current most popular hypothesis for the hyperkalemia is that the Na+-K+ pump cannot keep pace with the K+ efflux from muscle during the depolarization-repolarization process of the sarcolemmal membrane during muscle contraction. In this report, we present data that suggest an alternate hypothesis to those previously described. Because phosphocreatine (PCr) is a highly dissociated acid and creatine is neutral at cell pH, the concentration of nondiffusible anions decreases, and an alkaline reaction takes place when PCr hydrolyzes. This creates a state of cation (K+) excess and H+ depletion in the cell. To examine the balance of K+ and H+ for exercising muscle during the early period of exercise when PCr changes most rapidly, catheters were inserted into the brachial artery and femoral vein (FV) in five healthy subjects who performed two 6-min cycle ergometer exercise tests at 40 and 85% of peak oxygen uptake. FV blood was sampled every 5 s during the first 2 min, then every 30 s for the remaining 4 min of exercise and the first 3 min of recovery, and then less frequently for the next 12 min. Arterial sampling was every 30 s during exercise and simultaneous with FV sampling during recovery. Arterial K+ concentration ([K+]) increase lagged FV [K+] increase. The hyperkalemia observed during early exercise results from K+ release from skeletal muscle. FV [K+] increased by 5 s of the start of exercise and followed the rate of H+ loss from the FV blood for the first 30 s of exercise. FV lactate and Na+ kinetics differed from K+ kinetics during exercise and recovery. As predicted from the PCr hydrolysis reaction, the exercising limb took up H+ and released K+ at the start of exercise (first 30 s) at both exercise intensities, resulting in a FV metabolic alkalosis. K+ release was essentially complete by 3 min, the time at which oxygen uptake (and, presumably, PCr) reached its asymptote. These findings lead us to hypothesize that the early K+ release by the cell takes place with H+ exchange and that the major mechanism for the exercise hyperkalemia is the reduction in nondiffusible intracellular anions in the myocyte as PCr hydrolyzes.

Adult↗
PubMed1980

Pseudomyocardial infarction associated with acute bifascicular block due to hyperkalemia.

A case with lymphocytic lymphoma showing unusual ECG findings consisting of pseudoacute anteroseptal myocardial infarction associated with acute bifascicular block (a combination of right bundle branch block and left anterior hemiblock) secondary to hyperkalemia is presented. To our knowledge, this is the first reported case showing such unusual hyperkalemia-induced ECG abnormalities. No evidence of myocardial infarction (acute or old) was found in this case on the post-mortem examination. The importance of recognizing pseudomyocardial infarction in hyperkalemia is emphasized to distinguish from true myocardial infarction. In addition, it has been stressed that hyperkalemia is one of the important causes of acute bifascicular block.

Acute Disease↗
PubMedDate not supplied

Hyperkalemia secondary to concurrent pharmacotherapy in a patient receiving home parenteral nutrition.

We report a case of probable combined octreotide- and heparin-induced hyperkalemia. The patient had been receiving home parenteral nutrition, enoxaparin, and octreotide for 10 months. She required very little potassium in her PN solution to maintain serum potassium concentrations in the normal range. The patient reportedly did not receive other medications or have clinical conditions that, to our knowledge, cause hyperkalemia. She maintained normal renal function throughout the hospitalization and did not appear to have any significant acid-base disorders. Practitioners should be aware of the potential for octreotide and heparin to cause hyperkalemia. Regular monitoring of serum potassium concentrations should be done for patients receiving octreotide and heparin to avoid hyperkalemia.

Anticoagulants↗
PubMed1991

Pentamidine-associated nephrotoxicity and hyperkalemia in patients with AIDS.

The incidences of pentamidine-associated nephrotoxicity and hyperkalemia were determined from a retrospective review of records in AIDS patients using standard definitions for both toxicities. There were 37 patients, mean age 35.6 +/- 7.7 years and mean initial creatinine clearance (Clcr) 96 mL/min (1.6 mL/s). The mean pentamidine dose was 255 +/- 60 mg/d (3.87 +/- 0.33 mg/kg/d). The mean total dose was 2900 +/- 1600 mg given over 11.6 +/- 5.9 days (range 3-21 d). In 28 patients who were nephrotoxic (8 mild, 6 moderate, 14 severe), 27 episodes were possibly or probably pentamidine-associated. Total dose and days to nephrotoxicity onset were 1570 +/- 710 mg and 6.4 +/- 2.8 days (range 2-15 d), respectively. Nine patients became hyperkalemic (one required countermeasures) and all cases were pentamidine-associated. Total dose and days to hyperkalemia onset were 2510 +/- 1460 mg and 9.2 +/- 4.9 days (range 3-16 d), respectively. Mean baseline potassium increased and Clcr decreased significantly during therapy (from 4.2 to 4.9 mEq/L and from 96 to 70 mL/min, respectively). No correlation between nephrotoxicity or hyperkalemia and initial renal function was found, but significant correlations were found between the total pentamidine dose or duration and the percent of renal function remaining. AIDS patients have a high incidence of pentamidine-associated nephrotoxicity (up to 73 percent) and hyperkalemia (24 percent) with a trend to earlier onset of the former.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Studies to determine the basis for hyperkalemia in recipients of a renal transplant who are treated with cyclosporine.

Hyperkalemia is commonly encountered in patients who receive a renal transplant and the immunosuppressive drug, cyclosporine. There is also a high incidence of hypertension (which is thought to be due to expansion of the extracellular fluid volume) and hyperchloremic metabolic acidosis in this group of patients. This constellation of findings led to the suspicion of the possibility that their basis might be type II hypoaldosteronism. To test this hypothesis, 12 patients with hyperkalemia (plasma K+, 5.1 +/- 0.2 mmol/L at the time of study) while receiving cyclosporine were studied. Patients who had diabetes mellitus, those receiving drugs known to cause hyperkalemia (e.g., beta blockers, angiotensin-converting enzyme inhibitors, K(+)-sparing diuretics), or those with a serum creatinine greater than 200 mumol/L were excluded. The renal response to hyperkalemia was inappropriate because the transtubular K+ concentration gradient (TTKG) was only 4.3 +/- 0.4 compared with a TTKG of 13 +/- 1, 2 h after 50 mmol of KCl was given to normal subjects. The TTKG, after administration of 200 micrograms of fludrocortisone, was still very low (5.6 +/- 0.6) in the patients compared with that of controls (12 +/- 1). After administration of 250 to 500 mg of acetazolamide to increase the delivery of bicarbonate to the distal nephron, the TTKG rose significantly to 11 +/- 1 in patients on cyclosporine, compared with 17 +/- 1 in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed2002

Effects of thyroxine on hyperkalemia and renal cortical Na+, K+ - ATPase activity induced by cyclosporin A.

Cyclosporin A (CsA)-induced hyperkalemia is caused by alterations in transepithelial K+ secretion resulting from the inhibition of renal tubular Na+, K+ -ATPase activity. Thyroxine enhances renal cortical Na+, K+ -ATPase activity. This study investigated the effect of thyroxine on CsA-induced hyperkalemia. Sprague-Dawley rats were treated with either CsA, thyroxine, CsA and thyroxine, or olive-oil vehicle. CsA resulted in an increase in BUN and serum K+, along with a decrease in creatinine clearance, fractional excretion of potassium, and renal cortical Na+, K+ -ATPase activity, as compared with oil vehicle administration. Histochemical study showed reduced Na+, K+ -ATPase activity in the proximal tubular epithelial cells of the CsA-treated compared with the oil-treated rats. Histologically, isometric intracytoplasmic vacuolation, disruption of the arrangement and swelling of the mitochondria, and a large number of lysosomes in the tubular epithelium were characteristic of the CsA-treated rats. Co-administration of thyroxine prevented CsA-induced hyperkalemia and reduced creatinine clearance, Na+, K+ -ATPase activity, and severity of the histologic changes in the renal tubular cells when compared with the CsA-treated rats. Thyroxine increased the fractional excretion of potassium via the preservation of Na+, K+ -ATPase activity in the renal tubular cells. Thus, the beneficial effects of thyroxine may be suited to treatment modalities for CsA-induced hyperkalemia.

Animals↗
PubMedDate not supplied

Heparin-induced life-threatening hyperkalemia.

Hyperkalemia may occur in many clinical settings and lead to serious events. Heparin-induced hyperkalemia is presumably less well recognized than other untoward effects of heparin treatment and more frequent than commonly perceived. To draw attention to this clinically relevant occurrence, we report 2 cases of life-threatening bradyarrhythmia associated with heparin prescription. Heparin-induced hyperkalemia is mediated by an enzymatic block in the synthesis of aldosterone; however, in most cases severe hyperkalemia occurs in the presence of additional factors influencing potassium homeostasis. Patients treated with heparin should be stratified and adequately monitored according to the outlined risk profile.

Aged↗
PubMed1992

[Hyperkalemia during prolonged use of angiotensin II-converting enzyme inhibitors in end-stage renal insufficiency].

Hyperkalemia is a severe complication of end-stage renal failure. To evaluate whether ACE inhibitors may even worsen the propensity to develop hyperkalemia in this condition, we have analyzed retrospectively pre-dialytic blood pressure and serum potassium in 15 patients on chronic hemodialysis before and during long-term ACE inhibition. This treatment induced a significant drop in blood pressure (from 173 +/- 3/90 +/- 2 to 159 +/- 5/85 +/- 2 mm Hg [p < 0.05]), whereas serum potassium increased from 4.9 +/- 0.2 to 5.5 +/- 0.2 mM (p < 0.05), irrespective of the dosage of ACE inhibitor and of the residual diuresis. Hyperkalemia was well tolerated and was corrected in all patients by dialysis; treatment was discontinued in only one case. In conclusion, ACE inhibitors represent effective antihypertensive treatment in end-stage renal failure. However, long-term ACE inhibition may be accompanied by a worsening of hyperkalemia, which could be accounted for by a reduced effect of aldosterone on extrarenal potassium homeostasis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Hyperkalemia: mechanisms, etiology, and treatment.

Hyperkalemia may follow failure of glomerular filtration or tubular secretion of potassium. Tubular secretory failure may be secondary to deficient aldosterone or tubular insensitivity to this hormone. In either case glomerular insufficiency magnifies the problem. Increased potassium intake alone is a rare cause of increased serum potassium. The well recognized sequential treatment of hyperkalemia is reviewed. Most important is the establishment of the cause of hyperkalemia as these emergency measures are being taken. A history of drug intake, establishment of the acid-base status of the patient and the presence of underlying disease must be ascertained. The management of hyperkalemia remains an intriguing challenge in the office and hospital practice of medicine.

Humans↗
PubMed1992

Persistent hyperkalemia in a patient with diabetes mellitus: a reversible defect in kaliuresis during bicarbonaturia.

The purpose of this report is to apply recent advances in the understanding of the physiology of the excretion of potassium to a patient who had hyperkalemia due to a low rate of excretion of potassium. The defect was first suspected during therapy for diabetic ketoacidosis, when the concentration of potassium in plasma was unusually high (7.3 mmol/l) on admission and the deficit of potassium, as judged from the quantity of potassium infused to maintain normokalemia (40 mmol/24 h), was much less than expected. After recovery from diabetic ketoacidosis, hyperkalemia persisted despite near-normal values for creatinine and glucose in plasma. Excretion of potassium was low, considering the stimulus of hyperkalemia, and did not rise appreciably after the acute or chronic administration of a mineralocorticoid. The transtubular potassium concentration gradient (TTKG) did not exceed 6 after a large dose of fludrocortisone (200 micrograms) was administered. Notwithstanding, the TTKG rose to 14.4 following the intake of acetazolamide. We speculate that the basis for the hyperkalemia was type II hypoaldosteronism.

Bicarbonates↗
PubMed2005

Life-threatening hyperkalemia during a combined therapy with the angiotensin receptor blocker candesartan and spironolactone.

We describe a hypertensive nephrosclerosis patient presenting with severe hyperkalemia due to a combination therapy of the angiotensin receptor blocker (ARB) candesartan and spironolactone despite mildly decreased renal function. Recently, ARBs are replacing the ACE inhibitors. The combined therapy with ARB and spironolactone will eventually become the standard regimen. The strict attention and close monitoring of serum potassium should be mandatory in combination therapy to prevent hyperkalemia. Assessment of trans-tubular potassium gradient (TTKG) and fractional excretion of potassium (FEK) before starting the therapy would help in identifying the patients at higher risk of developing hyperkalemia. Co-administration of thiazide or loop diuretics is recommended to reduce the risk of hyperkalemia.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

[Anesthetic management of exploratory laparotomy for a patient with panperitonitis with hyperkalemia: a case report of spontaneous rupture of the urinary bladder].

A 71-year-old woman was admitted with panperitonitis, hyperkalemia and acute renal failure. Immediately after a large amount of ascites had been drained by laparotomy, hyperkalemia and acidosis were remarkably improved. During the operation, rupture of the urinary bladder was detected and repaired. The level of potassium and renal function became normal the next morning, and it seemed that peritoneal-self-dialysis had been related to hyperkalemia and acute renal failure. Rupture of the urinary bladder is very rare but should be considered in any cases of acute abdomen with hyperkalemia and acute renal failure.

Acidosis↗
PubMedDate not supplied

[Treatment of extreme hyperkalemia caused by diabetic ketoacidosis, potassium-sparing diuretics and potassium substitutes].

Grave hyperkalemic is a serious metabolic disorder. Its treatment fell into the fields of urgent medicine because of the risk of malignant cardiac arrhythmias that can be fatal for the patient. The article deals with the treatment of a 49-year-old female patient with decompensated liver cirrhosis and diabetes mellitus in whom grave hyperkalemia (9 mmol/1) with typical electrocardiographic changes was provoked by potassium saving diuretics combined with furosemide and the additional potassium substituted drugs, as well as development of diabetic ketoacidosis. Thanks to intensive medicinal treatment and constant follow-up of the patient rapid disappearance of hyperkalemia and ketoacidosis was observed. The success of medicinal therapy can be expected in cases of extreme hyperkalemia and relative hypokaliaemia. Intracellular hyperkaliaemia must be treated, without delay, with dialysis. Potassium saving diuretics and furosemide do not require additional potassium drugs, especially in risk patients in whom hyperkalemia may develop because of other existing diseases.

Acute Disease↗
PubMed1990

[Hyperkalemia with potassium-sparing and potassium-losing diuretics. Results from the Comprehensive Hospital Drug Monitoring Bern (CHDM)].

Of 5047 in-patients in the Division of Internal Medicine, Zieglerspital Bern (regional/teaching hospital), admitted from 1982 to 1985, 2412 were treated with at least one diuretic. The hospital records of these patients were reviewed with regard in particular to serum potassium and creatinine values as well as potassium supplementation. On the basis of this evaluation the patients were assigned to 6 different treatment groups and the relative occurrence rate of hyperkalemia probably related to drug treatment was determined. Of the 590 patients treated with only potassium losing diuretics, none was found to show a hyperkalemia event; of the 742 patients on potassium losing diuretics and potassium supplementation, 27 (3.6%) developed hyperkalemia. In the 439 patients under combined diuretics (potassium sparing with potassium losing) without potassium substitution, 76 (17.3%), and in the 381 under combined diuretics with potassium substitution 24 (6.3%), developed hyperkalemia. The further groups of patients are also described. Renal function was estimated by the formula of Cockcroft and Gault. Reduced renal function is a significant risk-factor for hyperkalemic events under combined diuretics. All hyperkalemic events were within a serum potassium range of 5.1-7.0 mmol/l.

Creatinine↗
PubMed1989

Thrombocytosis and hyperkalemia revisited.

A major concern of physicians caring for patients is the development of hyperkalemia, a potentially life-threatening event requiring accurate determination of its etiology. After metabolic and iatrogenic causes have been excluded, factitious hyperkalemia must be considered, one cause of which may be the method of laboratory determination. Hyperkalemia associated with thrombocytosis has been previously described but is a fact commonly overlooked in the evaluation of a patient with hyperkalemia. We compared the potassium levels in simultaneous serum and plasma samples from patients with normal and elevated platelet counts, since platelet activation during clot formation is associated with release of potassium. We found consistently higher potassium levels in serum (containing products of activated platelets) than in plasma (containing nonactivated platelets). The greatest discrepancy in potassium levels was in patients with thrombocytosis. This preliminary study suggests that if there is no obvious explanation for an elevated serum potassium the plasma potassium level should be measured, particularly in patients with elevated platelet counts.

False Positive Reactions↗
PubMed1988

Mechanisms of hyperkalemia in systemic lupus erythematosus.

We found that nearly 10% of 142 patients with systemic lupus erythematosus (SLE) had persistent, unexplained hyperkalemia. Renal mineralocorticoid resistance has been suggested to account for the hyperkalemia in SLE. We studied the renin-aldosterone response to intravenous furosemide (60 mg) and upright posture and the renin response to converting enzyme inhibition (captopril, 50 mg) and upright posture in five patients with SLE and hyperkalemia (group 1) and five normokalemic patients with SLE (group 2). Renal function was comparable. Plasma chloride level was higher and bicarbonate level slightly lower in group 1 than in group 2. Plasma cortisol level was normal in all patients. None of the patients was receiving nonsteroidal anti-inflammatory drugs or corticosteroids at the time of study. Basal plasma renin concentration and plasma aldosterone level were not significantly different between the two groups, although both tended to be higher in group 2. However, four of the five patients in group 1 had significantly blunted renin response to captopril compared with group 2. The same four patients also had blunted renin and aldosterone responses to furosemide. Thus, the majority of hyperkalemic patients with SLE had an impaired renin and aldosterone response to stimulation. We conclude that hyporeninemic hypoaldosteronism plays a key role in the pathogenesis of hyperkalemia in SLE.

Adult↗