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PubMed2000

Severe hyperkalemia in two renal transplant recipients treated with standard dose of trimethoprim-sulfamethoxazole.

Hyperkalemia is a serious electrolyte disorder and is a frequent finding in renal transplant recipients. Trimethoprim-induced hyperkalemia has been increasingly reported in recent years. We describe two renal transplant recipients who developed end-stage renal disease secondary to familial Mediterranean fever and presented with severe hyperkalemia secondary to the use of standard dose of trimethoprim. One of the patients had potential underlying adrenal insufficiency, which might be a contributing factor for the development of hyperkalemia. We concluded that renal transplant patients receiving even the standard dose of trimethoprim should be monitored closely for the development of hyperkalemia. They should be recognized as a group with increased risk in regard to their concurrent renal insufficiency, concomitant use of cyclosporine, and associated tubulointerstitial disease. Patients with secondary amyloidosis are at even greater risk, and subclinical adrenal insufficiency may be an underlying risk factor for the development of severe, life-threatening hyperkalemia among this group of patients.

Adult↗

PubMed1976

Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.

We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.

Acidosis↗

PubMed2004

The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model.

BACKGROUND: The administration of intravenous (IV) calcium to treat hyperkalemia resulting from digoxin poisoning is considered potentially dangerous, based on a body of older literature which, in sum, reported increased cardiac glycoside toxicity with calcium administration (increased arrhythmias, higher rate of death). OBJECTIVE: This pilot study sought to determine if the administration of calcium chloride when compared to normal saline would affect time to death when given to hyperkalemic, digoxin toxic swine. METHODS: Digoxin IV at 0.25 mg/kg was determined to be appropriately toxic for this study. When arrhythmias consistent with hyperkalemia developed, animals were given either IV calcium chloride (CaCl) bolus (10 mg/kg, Group 1, n=6) or normal saline volume equivalent (Group 2, n=6). Three intervals were observed: Interval 1: time interval from digoxin administration (T0) to when ECG changes consistent with hyperkalemia developed (at which point calcium chloride or normal saline was administered); Interval 2: time interval from the development of ECG changes consistent with hyperkalemia to asystole; Interval 3: time interval from digoxin administration to asystole. Both groups were monitored for changes in heart rhythms, serum potassium levels, and time to asystole. RESULTS: The intravenous digoxin dose of 0.25 mg/kg induced hyperkalemia, arrhythmias, and death approximately 1 h after administration in all animals studied. Group 1: Interval 1 averaged 18.75 (S.D. +/-7.96) min, Interval 2 averaged 16.75 (S.D. +/-17.17) min, and Interval 3 averaged 35.5 (S.D. +/-14.49) min range; Group 2: average Interval 1 24.8 (S.D. +/-4.71) min, Interval 2 averaged 19.5 (S.D.+/-15.92), Interval 3 averaged 44.3 (S.D. +/-13.80) minutes. There was no statistically significant difference between the groups at any time interval, Interval 1 (p=0.43), Interval 2 (p=0.65), Interval 3 (p=0.40). There was no difference in serum potassium throughout the study period. CONCLUSION: The administration of intravenous CaCl in the setting of hyperkalemia from acute digoxin toxicity did not affect mortality or time to death at the dose administered.

Animals↗

PubMed2005

Extreme hyperkalemia.

Hyperkalemia is a potentially fatal condition and is defined by a serum potassium level (K+) of greater than 5.5 mmol/L. The associated prevalence of cardiac arrhythmia increases directly with the degree of hyperkalemia. The danger in the majority of hyperkalemia cases is cardiac dysrhythmia, and often ventricular fibrillation or asystole is the terminating event. Although there are many previous reports addressing this threatening problem and associated therapeutic maneuvers, there have not been many previous reports citing the fatal concentration of hyperkalemia irrespective of the causes. However, it is uniformly accepted that a K+ concentration greater than 10.0 mmol/L is fatal unless urgent treatment is instituted. This report describes a case of nonfatal hyperkalemia of 14 mmol/L with intact survival and complete recovery. Potassium homeostasis is revisited, and some explanations are proffered regarding the protective mechanism against hyperkalemia, including transcellular flux, renal tubular function, and endocrine responses.

Cardiopulmonary Resuscitation↗

PubMed2003

Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases.

BACKGROUND: Nephrotoxicity is a well-known effect of cyclosporine (CsA) that causes a reduction in glomerular filtration rate through vasoconstriction of the afferent glomerular arterioles and may result in acute renal failure. Isolated CsA-induced hyperkalemia occurring through different mechanisms is also common. However, there are only a few "case reports" addressing this phenomenon in allogeneic bone marrow transplantation patients. In this report, we propose mechanisms and methods of managing CsA-associated hyperkalemia in allogeneic transplantation. METHODS: We report on four allogeneic blood stem- cell transplant cases and a review of the literature. RESULTS: Four adult leukemia patients underwent allogeneic peripheral blood stem cell transplantation and received CsA as a part of their graft-versus-host disease prophylaxis. The patients developed hyperkalemia, despite adequate kidney function. CsA seemed to be the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Renal tubule dysfunction and secondary hypoaldosteronism seemed to be the reasons for CsA-associated hyperkalemia. CONCLUSION: This report of four cases demonstrates that CsA should be considered among the possible causes of hyperkalemia in bone marrow transplantation. There may be a need for urgent intervention depending on the severity of hyperkalemia. Monitoring of blood CsA level and dose adjustment are important for the prevention of this complication.

Adult↗

PubMed1987

A rat model for hyperkalemia.

It is often necessary to have a small animal model for hyperkalemia for use in electrolyte and acid base experiments. In reviewing the literature, we found a paucity of such animal models, especially for acute hyperkalemia. We have had difficulty in inducing acute hyperkalemia in rats using potassium chloride alone either intravenously or intraperitoneally and felt the need for an easily reproducible small animal model for hyperkalemia. We gave experimental animals a combination of intraperitoneal amiloride 3 mg/kg and potassium chloride 2 meq/kg in two divided doses while control animals received only the potassium chloride. Initial serum potassiums were similar but at 2 hr, the experimental group had significantly higher serum potassium levels which were sustained throughout the 8 hr of the experiment. Arterial blood gas revealed no significant difference in blood pH values at all time points during the experiment. We conclude that the combination of amiloride and potassium chloride is useful to produce acute hyperkalemia in rats and that this hyperkalemia is sustained beyond 6 hr. This model is convenient for use in metabolic experiments requiring the use of acutely hyperkalemic rats.

Amiloride↗

PubMedDate not supplied

Glucose-insulin infusion for the early treatment of non-oliguric hyperkalemia in extremely-low-birth-weight infants.

In order to investigate the status of non-oliguric hyperkalemia and to evaluate glucose-insulin infusion treatment among extremely-low-birth-weight (ELBW) infants, 161 infants weighting less than 1000 gm at birth were enrolled for this study. They were divided into two groups: a hyperkalemic group and a non-hyperkalemic group. Hyperkalemia was defined here as a serum potassium level of greater than 6 mEq/L in a non-hemolyzed arterial blood sample. A glucose-insulin infusion was administered to the patients when hyperkalemia was detected in them during the first few days after birth. The infusion was discontinued when the serum potassium levels had been less than 6 mEq/L and stabilized for 6 hours. The incidence of non-oliguric hyperkalemia among ELBW infants in this study was 58% (93/161). The mean gestational age of neonates was 25.7 +/- 1.8 weeks (hyperkalemic) and 26.6 +/- 1.7 weeks (non-hyperkalemic). The mean rate of increases in serum potassium levels was 0.32 +/- 0.29 mEq/L/hr (hyperkalemic) and 0.13 +/- 0.12 mEq/L/hr (non-hyperkalemic). The incidence of severe intraventricular hemorrhage (IVH) was 19% (18/93) (hyperkalemic) and 4.4% (3/68) (non-hyperkalemic). The incidence of cardiac arrhythmia was 12% (11/93) (hyperkalemic) and 0% (non-hyperkalemic) respectively. Neonates with fewer weeks of gestation at birth and faster increases in serum potassium levels were associated with a more prominent tendency toward hyperkalemia. Hyperkalemia markedly increases the risk of severe IVH and arrhythmia for ELBW infants. A higher glucose infusion rate should be maintained to prevent hypoglycemia following insulin treatment.

Case-Control Studies↗

PubMed1991

Heparin-induced hyperkalemia: a prospective study.

Heparin is frequently used for the prophylaxis and treatment of deep venous thromboembolism and it induces hypoaldosteronism leading to hyperkalemia, an uncommon adverse effect. In an intensive prospective drug monitoring study, 154 inpatients at the Internal Medicine Unit of Hospital Sotero del Río, Santiago, Chile, received heparin in the period between March and November 1990. Mean age of the patients was 65.8 +/- 12.9 years and 56.5% were female. Twenty-one (13.6%) patients developed heparin-induced adverse reactions. Thirteen events were hyperkalemia, 7 ecchymoses and 1 hematuria. The monitoring team and attending physicians have agreed to classify 9 heparin-induced hyperkalemia cases as probable and the other 4 as possible. No adverse reaction was fatal but 8 of the patients had severe hyperkalemia. Almost all reactions were dose-related. Hyperkalemia was more frequent in patients with diabetes mellitus, metabolic acidosis and long-term heparin therapy. The frequency of hyperkalemia did not correlate with age, sex, renal impairment or with previous use of anti-inflammatory drugs, heparin or aspirin.

Adolescent↗

PubMed1988

Early onset hyperkalemia in extremely low birth weight infants.

The incidence of hyperkalemia and associated clinical features in extremely preterm infants were determined by reviewing medical records of 32 infants with birth weights of less than or equal to 800 g born during a 1-year period. Hyperkalemia, defined as serum potassium concentration of greater than 6.5 mEq/L, occurred in 12 infants on the first day of life and in four others on the second day. Six infants (38%) had electrocardiographic abnormalities associated with hyperkalemia. Infants with hyperkalemia were less mature than infants with normal potassium levels. All infants of less than 25 weeks' gestation developed hyperkalemia. Fluid intakes and urine flow rates were lower and body weight loss greater during the first 24 hours of hospitalization for hyperkalemic infants. Hyperkalemia frequently occurs within the first 48 hours of life in extremely immature infants. Serum potassium should be monitored closely to avoid life-threatening cardiac arrhythmias in these infants.

Humans↗

PubMed1996

Hyperkalemia alters endothelium-dependent relaxation through non-nitric oxide and noncyclooxygenase pathway: a mechanism for coronary dysfunction due to cardioplegia.

BACKGROUND: Reported results of hyperkalemia (cardioplegia or organ preservation solutions) on endothelial function are contradictory. The endothelium-dependent relaxation is related to three major mechanisms: cyclooxygenase, nitric oxide, and endothelium-derived hyperpolarizing factor (K+ channel related). The present study was designed to test the hypothesis that hyperkalemia may alter endothelial function through non-nitric oxide and noncyclooxygenase pathways. METHODS: Porcine coronary artery rings (5 to 10 in each group) were studied in organ chambers under physiologic pressure. After incubation with 20 or 50 mmol/L K+ for 1 hour, the response to substance P, an endothelium-dependent vasorelaxant peptide, in K+ (25 mmol/L)-induced contraction was studied in the presence of the cyclooxygenase inhibitor indomethacin (7 mumol/L), the nitric oxide biosynthesis inhibitor NG-nitro-L-arginine (L-NNA) (300 mumol/L), or the adenosine triphosphate-sensitive K(+)-channel blocker glybenclamide (3 mumol/L) in comparison with control arteries (69.8 +/- 4.6% of K+ contraction). RESULTS: Without exposure to hyperkalemia, indomethacin (with or without glybenclamide) did not alter but L-NNA significantly reduced the relaxation (39.7% +/- 3.7%, p < 0.001). After exposure to K+, the indomethacin- and L-NNA-resistant relaxation was further reduced (7.4% +/- 3.2% for 20 mmol/L K+, p < 0.0001; or 13.5% +/- 8.4% for 50 mmol/L K+, p < 0.05, compared with rings without exposure), whereas the indomethacin- and glybenclamide-resistant relaxation was not altered. Incubation with hyperkalemia (50 mmol/L) also significantly reduced the sensitivity (increased EC50) of the indomethacin- and L-NNA-resistant relaxation (-9.75 +/- 0.06 versus -9.33 +/- 0.04 log M, p < 0.01). CONCLUSIONS: Exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant, endothelium-dependent (endothelium-derived hyperpolarizing factor-related) relaxation. Our study may suggest a new mechanism of coronary dysfunction after exposure to hyperkalemia and open a new area for protection of coronary endothelium in cardiac surgery and for organ preservation in transplantation surgery.

Animals↗

PubMed2003

Factors predicting hyperkalemia in patients with cirrhosis receiving spironolactone.

OBJECTIVE: To evaluate the factors leading to hyperkalemia in patients with cirrhosis receiving spironolactone. DESIGN: An observational, analytical, case control study. PLACE AND DURATION OF STUDY: The Aga Khan University Hospital. Six months. SUBJECTS AND METHODS: One hundred and fifty consecutive patients (100 males, 50 females) with cirrhosis of liver, hospitalized for decompensated disease and receiving spironolactone for at least two weeks before admission, were included in this study. Patients with hyperkalemia (n=67) having potassium level >5 mmol/l were compared with patients who had normal potassium level 5 mmol/l (n=83). The parameters taken into account were age, gender of the patients, type and dose of diuretics along with concomitant medicines, diastolic blood pressure, edema, ascites, blood urea nitrogen, serum creatinine, electrolytes, bilirubin, albumin, prothrombin time, Child class, and Child Pugh score. RESULTS: Patients with hyperkalemia (K > 5 mmol/l) had higher blood urea nitrogen, serum creatinine and bilirubin levels (p= 0.004, 0.001 and 0.044 respectively). Their serum sodium and albumin levels were lower (p= 0.000 and 0.017 respectively). They had advanced cirrhosis with high Pugh score (p= 0.003). These patients were on higher dose of spironolactone (p =0.001). Multivariate analysis showed that dose of spironolactone >100 mg /day, serum creatinine >1.3 mg/dl, persistence of ascites and edema, and female gender were important predictors of development of hyperkalemia. CONCLUSION: Patients with cirrhosis receiving high dose of the diuretic, having edema, ascites and high serum creatinine are at the greater risk of developing hyperkalemia during spironolactone therapy.

Female↗

PubMed1981

Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia.

To establish the frequency and clinical and biochemical characteristics of hyporeninemic hypoaldosteronism (HH), we reviewed 100 consecutive cases of hyperkalemia (potassium content > 5.3 mEq/L). The most common cause was end-stage renal failure (34%). Other causes included overzealous potassium replacement, spironolactone therapy, hemolysis, acute renal failure, acidosis, thrombocytosis, and Addison's disease. Ten of 19 patients with unexplained hyperkalemia showed suppressed renin (0.12 to 1.3 ng/mL/hr) and aldosterone (5.4 to 21.6 ng/dL) responses to furosemide-posture challenge. Cortisol reserve was normal in HH. Fludrocortisone acetate therapy corrected the hyperkalemia. Other features of HH include low serum bicarbonate content, mild renal insufficiency, diabetes, and advanced age. The use of indomethacin and ibuprofen was associated with one case of HH each. Results suggest that HH is an overlooked cause of hyperkalemia, especially in patients whose hyperkalemia is unexplained.

Adult↗

PubMed1981

Hyperkalemia-induced bundle branch block and complete heart block.

Hyperkalemia was associated with complete heart block in one patient that resolved by first showing right anterior hemiblock). Then the right bundle branch block resolved, leaving the marked left axis deviation that was present before the hyperkalemic episode. Another patient with hyperkalemia had right bundle branch block with marked left axis deviation, both of which disappeared with correction of the hyperkalemia. These findings suggest that hyperkalemia can depress conduction in the His-Purkinje system and raise the possibility that hyperkalemia may induce complete heart block distal to the atrioventricular junction.

Aged↗

PubMed2006

Reports of hyperkalemia after publication of RALES--a pharmacovigilance study.

PURPOSE: A population-based study and anecdotal reports have indicated that the publication of the Randomized Aldactone Evaluation Study (RALES) was associated with not merely a broader use of spironolactone in the treatment of heart failure, but also with a coinciding sharp increase in hyperkalemia-associated morbidity/mortality in patients also being treated with ACE-inhibitors. Data mining algorithms (DMAs) are being applied to spontaneous reporting system (SRS) databases in hopes of obtaining early warnings/additional insights into post-licensure safety data. We applied two DMAs (i.e. multi-item gamma Poisson shrinker [MGPS] and proportional reporting ratios [PRRs]) to spontaneous reporting system (SRS) data to determine if these DMAs could have provided an earlier indication of a possible hyperkalemia safety issue. METHODS: MGPS and PRRs were retrospectively applied to US FDA-AERS, an SRS database. Year-by-year analysis and analysis of increasing cumulative time intervals were performed on cases in which both spironolactone and hyperkalemia and possibly related cardiac events had been reported. RESULTS: Neither of the DMAs initially provided a compelling signal of disproportionate reporting (SDR) for hyperkalemia after publication of RALES. However, using events consistent with clinical sequelae of hyperkalemia (e.g,. sudden death), SDRs were identified with PRRs. CONCLUSIONS: The quality and usefulness of data mining analysis is highly situation dependent and may vary with the knowledge and experience of the drug safety reviewer. Our analysis suggests that contemporary DMAs may have significant limitations in detecting increased frequency of labeled events in real-life prospective pharmacovigilance. There is a paucity of research in this area and we recommend further research for new approaches to detecting increased frequency of labeled events.

Adverse Drug Reaction Reporting Systems↗

PubMed1994

Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis.

OBJECTIVE: To investigate the efficacy of hemodialysis during cardiopulmonary resuscitation as an effective adjunct to the treatment of severe hyperkalemia. DESIGN: A prospective study. SETTING: In hospital dialysis units and intensive care units. PATIENTS: Renal failure patients who developed hyperkalemia induced cardiac arrest and failed to recover from conventional cardiopulmonary resuscitation (CPR) were included. Three patients entered into this study: 2 patients with chronic renal failure maintained on regular hemodialysis and one with acute renal failure who suffered from severe hyperkalemia. INTERVENTIONS: All three patients developed asystolic cardiac arrest with unrecordable blood pressure due to severe hyperkalemia. Aggressive CPR together with intravenous epinephrine, sodium bicarbonate and calcium chloride were instituted. External cardiac massage with cardiac defibrillation was unable to restore spontaneous heart action. After lack or response to intensive resuscitation, hemodialysis was performed concomitant with CPR to eliminate the potassium load. MEASUREMENTS AND RESULTS: Sinus rhythm and blood pressure were restored in all 3 patients but one of them eventually succumbed to her underlying disease. CONCLUSION: Hemodialysis during CPR is probably an effective adjunct to the treatment of severe hyperkalemia in patients with severe hemodynamic compromise and asystolic cardiac arrest.

Adult↗

PubMed1975

Disorders of impulse conduction and impulse formation caused by hyperkalemia in man.

In eight patients we have demonstrated manifold types of impairment of impulse conduction produced by hyperkalemia. These abnormalities of impulse conduction occurred either simultaneously or in sequence, and were located in the atria, in the A-V junction, in the fascicular distribution of the ventricular conduction system, or in the free ventricular walls. In association with the abnormalities of conduction, abnormal impulse formation was also frequently observed as manifested by acceleration of normal pacemakers or the emergence of ectopic pacemakers. In one patient hyperkalemia produced alteration in sinus and A-V junctional impulse formation which overshadowed conduction disorders. In all of the eight cases the hyperkalemia was considered to be noniatrogenic. Hyperkalemia appears to potentiate subclinical conduction abnormalities, especially in the His-Purkinje system. However, the presence of pre-existent intraventricular conduction defects such as a bifascicular block does not exclude the possibility that the site of an A-V conduction delay during hyperkalemia can be in the A-V node, as demonstrated by His bundle recording in one instance after development of second-degree (type I) A-V block.

Adolescent↗

PubMed1990

Ventilatory responses to hyperkalemia and exercise in normoxic and hypoxic goats.

The ventilatory response to moderate exercise is potentiated during hypoxia in goats, causing PaCO2 to decrease more from rest to exercise than in normoxia. We investigated the hypothesis that this response is due to the ventilatory stimulus provided by an interaction between exercise induced hyperkalemia and hypoxia. Plasma potassium concentration ([K+]), arterial blood gases and ventilation were measured in normoxia and hypoxia (PaO2 = 34-38 Torr) at rest and during steady-state exercise (5.6 kph; 5% grade) in seven goats. PaCO2 decreased during normoxic exercise (2.9 +/- 0.7 Tor; P less than 0.01), and decreased significantly more during hypoxic exercise (6.4 +/- 0.6 Torr; P less than 0.01). [K+] increased in both normoxic (1.0 +/- 0.1 mEq/L; P less than 0.01) and hypoxic (0.9 +/- 0.2 mEq/L; P less than 0.01) exercise, but these changes were not significantly different from each other. On a different day, resting goats were infused intravenously with 200 mM KCl for 5 min at a rate sufficient to obtain [K+] similar to exercise (8.6-12 ml/min) in normoxia and hypoxia. Hyperkalemia at rest caused similar PaCO2 decreases in normoxia (1.7 +/- 0.7 Torr; P less than 0.05) and hypoxia (1.7 +/- 0.5 Torr; P less than 0.01), but had no statistically significant effect on ventilation in either condition. These data indicate that hyperkalemia, at levels approximating those during moderate exercise, has a mild stimulatory effect on alveolar ventilation; however, hypoxia does not affect this response. We conclude that hyperkalemia does not provide sufficient ventilatory stimulation to account for exercise hyperpnea, nor does hypoxia potentiate the ventilatory stimulation from hyperkalemia at rest.

Animals↗

PubMed1993

Decreased erythrocyte Na+,K(+)-ATPase activity associated with cellular potassium loss in extremely low birth weight infants with nonoliguric hyperkalemia.

To determine whether a shift of potassium ions from the intracellular space to the extracellular space accounts, in part, for the hyperkalemia seen in extremely low birth weight infants, we examined potassium concentration in serum and erythrocytes from extremely low birth weight infants with hyperkalemia (n = 12) or with normokalemia (n = 27). In addition, to determine whether the shift of potassium was associated with low sodium-potassium-adenosinetriphosphatase (Na+,K(+)-ATPase) activity, we studied the activity of ATPase in the last 16 infants enrolled in the study. Fluid intake and output were measured during the first 3 days of life. Infants were considered to have hyperkalemia if the serum potassium concentration was 6.8 mmol/L or greater. Blood was obtained daily for intracellular sodium and potassium levels by means of lysis of erythrocytes. The remaining erythrocyte membranes were frozen and analyzed for Na+,K(+)-ATPase activity. There were significantly lower intracellular potassium/serum potassium ratios in the infants with hyperkalemia for each day of the 3-day study (p < 0.001). In the hyperkalemic group, there was lower Na+,K(+)-ATPase activity than in the infants with normokalemia (p = 0.006). Low Na+,K(+)-ATPase activity was associated with lower intracellular potassium/serum potassium ratios (p = 0.006), higher serum potassium values (p = 0.02), and lower intracellular potassium concentration (p = 0.009). The urinary data demonstrated that there was no difference in glomerulotubular balance between the two groups. We conclude that nonoliguric hyperkalemia in extremely low birth weight infants may be due, in part, to a shift of potassium from the intracellular space to the extracellular space associated with a decrease in Na+,K(+)-ATPase activity.

Bilirubin↗