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PubMed1991

Extrarenal potassium tolerance in chronic renal failure: implications for the treatment of acute hyperkalemia.

The role of extrarenal potassium homeostasis is well recognized as a major mechanism for the acute defense against the development of hyperkalemia. The purpose of this report is to examine whether or not the various mechanisms of extrarenal potassium regulation are intact in patients with end-stage renal disease (ESRD). The available data suggest that with the development of ESRD and the uremic syndrome there is impaired extrarenal potassium metabolism that is related to a defect in the Na,K-adenosine triphosphatase (ATPase). The responsiveness of uremic patients to the various effector systems that regulate extrarenal potassium handling is discussed. Insulin is well positioned to play an important role in the regulation of plasma potassium concentration in patients with impaired renal function. The role of basal insulin may be even more important than previously appreciated, since somatostatin infusion causes a much greater increase in the fasting plasma potassium in rats with renal failure than in controls. Furthermore, stimulation of endogenous insulin by oral glucose results in a greater intracellular translocation of potassium in uremic rats than in controls. Under at least two common physiologic circumstances, feeding and vigorous exercise, endogenous catecholamines might also act to defend against acute increments in extracellular potassium concentration. However, it is important to appreciate that the response to beta 2-adrenoreceptor-mediated internal potassium disposal is heterogeneous as judged by the variable responses to epinephrine infusion. Based on the evidence presented in this report, a regimen for the treatment of life-threatening hyperkalemia is outlined. Interpretation of the available data demonstrate that bicarbonate should not be relied on as the sole initial treatment for severe hyperkalemia, since the magnitude of the effect of bicarbonate on potassium is variable and may be delayed. The initial treatment for life-threatening hyperkalemia should always include insulin plus glucose, as the hypokalemic response to insulin is both prompt and predictable. Combined treatment with beta 2-agonists and insulin is also effective and may help prevent insulin-induced hypoglycemia.

Acute Disease↗
PubMed1985

Lethal hyperkalemia associated with severe hyperglycemia in diabetic patients with renal failure.

Two patients with diabetic nephropathy on maintenance hemodialysis developed extreme hyperkalemia (7.9 and 9.3 mmol/L, respectively) in association with severe episodes of hyperglycemia (1,152 and 1,185 mg/dL, respectively). The increase in serum potassium was out of proportion to the degree of metabolic acidosis that both patients had, and no exogenous source of hyperkalemia could be identified. Despite treatment efforts both patients died shortly after arrival as a consequence of cardiac arrest. It is proposed that the hyperosmolality of extracellular fluid produced by severe hyperglycemia drives potassium passively out of the cells, therefore favoring the rapid development of hyperkalemia. Insulin deficiency could also play a role. This situation is particularly dangerous in individuals with impaired renal function. Adequate blood glucose control in diabetic patients on dialysis is important to avoid life-threatening hyperkalemia.

Aged↗
PubMed1985

Hyperkalemia complicating digoxin toxicity in a patient with renal failure.

We describe the occurrence of hyperkalemia in a stable hemodialysis patient who developed digoxin toxicity. The patient had been receiving digoxin for 2 years. His maintenance digoxin dose was increased from 0.125 to 0.25 mg three times a week, which resulted in a toxic serum level of 4.9 ng/mL (therapeutic range is 0.8 to 2.0 ng/mL). As a consequence of the digoxin toxicity, he became hyperkalemic (7.8 mEq/L), and this value returned to normal only after the digoxin level was lowered by a combination of oral charcoal and dialysis. This study shows how readily hyperkalemia can occur in an anephric patient manifesting digoxin toxicity. Thus, potentially lethal hyperkalemia can occur in hemodialysis patients who ingest therapeutic quantities of digoxin. Digoxin toxicity should be added to the differential diagnosis of hyperkalemia in patients with renal failure. This can occur despite the absence of a history of massive ingestion of a cardiac glycoside.

Aged↗
PubMed1986

Profound hyperkalemia without electrocardiographic manifestations.

Although the electrocardiogram (ECG) is not considered a reliable indicator of mild to moderate hyperkalemia, profound elevations of serum potassium concentration generally produce classic ECG manifestations. We report two cases of severe hyperkalemia (greater than 9.0 mEq/L) in which the ECGs did not reveal the expected manifestations of hyperkalemia. Thus, even with profound serum potassium elevations, the ECG cannot reliably be used to exclude the presence of hyperkalemia or to monitor therapy designed to lower the serum potassium concentration.

Aged↗
PubMed1999

Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy.

Epsilon-aminocaproic acid (Amicar) is used to treat severe hemorrhage refractory to usual medical management. This antifibrinolytic drug has been associated with a number of renal complications. However, there are no descriptions of this medication causing hyperkalemia. This report describes the development of hyperkalemia in a patient with underlying chronic renal insufficiency treated with intravenous epsilon-aminocaproic acid. The patient, who underwent coronary artery bypass grafting, had no other obvious cause for the acute increase in serum potassium concentration. Based on data in animals and humans, the cationic amino acids lysine and arginine have been shown to enter muscle cells in exchange for potassium and lead to hyperkalemia through a shift of potassium from the intracellular to the extracellular space. Epsilon-aminocaproic acid, a synthetic amino acid structurally similar to lysine and arginine, also has been noted to cause an acute increase in serum potassium in anephric dogs infused with this medication. It is probable that the mechanism underlying the increase in serum potassium with epsilon-aminocaproic acid is also based on the shift of potassium from the intracellular to the extracellular space. Hence, it appears that intravenous epsilon-aminocaproic acid can also cause hyperkalemia in humans.

Acute Disease↗
PubMed2002

Involvement of K(Ca2+) channels in the local abnormalities and hyperkalemia following the ischemia-reperfusion injury of rat skeletal muscle.

Patch-clamp technique was used to investigate the properties of the muscular Ca2+-activated K+ channel (K(Ca2+)) in the ischemic and ischemic-reperfused rat muscle fibers and the possible involvement of this ion channel in the reperfusion-dependent hyperkalemic state. The properties of the muscular K(Ca2+) channel were unaltered following 4 h of ischemia of the lower limbs and that the serum K+ level did not change following ischemia. In contrast, after 3 h of reperfusion an over-activation of K(Ca2+) channel was observed which was related to the increase in the number of functional channels per patch area. Currents from cation aselective channels were also routinely detected in these muscles and ion channel abnormalities similar to those observed in the ischemic-reperfused muscles were also found in the contralateral muscles. Significant hyperkalemia was observed following 3 h of reperfusion. Administration of L-NAME (10 mg.kg(-1)), a nitric-oxide synthase (NOS) inhibitor, during reperfusion prevented the increase of K(Ca2+) channel activity and the activation of the cation aselective channel. The L-NAME treatment also partially antagonised the characteristic hyperkalemia observed following reperfusion. In contrast, D-NAME (20 mg.kg(-1)), the inactive antipode on NOS enzyme administered to the rats during reperfusion failed to prevent the overactivation of the K(Ca2+) channel or the hyperkalemia. Our results indicate that overactivation of K(Ca2+) channel found in the muscles following reperfusion is either directly or indirectly related to NOS activation, and contributes to the hyperkalemia. Moreover, the discovery of abnormalities similar to those of the ischemic-reperfused muscles in the contralaterals suggests that proinflammatory molecules were released from the ischemic area, accentuating the pathological state.

Animals↗
PubMed1990

Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure.

These studies were performed in patients with chronic renal failure to understand the mechanism(s) of hyperkalemia secondary to hypertonic NaCl infusion. In 10 patients, after intravenous infusion of either 5% or 2.5% NaCl (6 mEq per kg body wt for 120 minutes in both solutions), the maximum increase in plasma potassium averaged 0.6 (range 0.3 to 1.3) mmol/liter (P less than 0.01) or 0.3 (range 0.2 to 0.6) mmol/liter (P less than 0.01), respectively. The rise of both plasma potassium and osmolality was significantly higher during 5% NaCl than during 2.5% NaCl infusion (P less than 0.01). A significant linear correlation (P less than 0.01) between plasma potassium and osmolality was observed. Urinary potassium excretion was increased to a similar extent by 5% NaCl and 2.5% NaCl infusion. The observed hyperkalemia, secondary to NaCl infusion, was independent of venous pH, plasma bicarbonate, anion gap, insulin levels, and urinary norepinephrine and epinephrine excretion, and was associated with a fall in plasma aldosterone concentration. In separate studies, nine patients were treated with desoxycorticosterone acetate (DOCA; 20 mg i.m. for three days) before receiving saline (5%) infusion. DOCA did not prevent the level increase in plasma potassium that remained significantly correlated with plasma osmolality (P less than 0.01). In conclusion, hypertonic NaCl infusion in patients with renal failure causes a clinically relevant hyperkalemia despite increased renal excretion of potassium. This hyperkalemia is independent of acid-base or hormonal mechanisms known to regulate extrarenal homeostasis of potassium, and is strictly correlated with a rise in plasma osmolality.

Acid-Base Equilibrium↗
PubMed1997

Hyperkalemia associated with cyclosporine (CsA) use in bone marrow transplantation.

Two adult leukemia patients underwent allogeneic bone marrow transplantation and received cyclosporine (CsA) as part of their immunosuppressive therapy. Despite adequate kidney function, both patients developed hyperkalemia. Cyclosporine was the only pharmaceutical agent to which this electrolyte abnormality could be attributed. Although the mechanism of the hyperkalemia is unclear, it seems to be related to an aldosterone-resistant state. Cyclosporine-induced hyperkalemia is a relatively common occurrence; however, there is only a single 'case report' addressing this phenomenon in bone marrow transplantation patients. We propose both mechanisms and methods of managing CsA-associated hyperkalemia in allogeneic transplantation patients.

Adult↗
PubMedDate not supplied

Hyperkalemia in dialysis patients.

Serious hyperkalemia is common in patients with end-stage renal disease (ESRD) and accounts for considerable morbidity and death. Mechanisms of extrarenal disposal of potassium (gastrointestinal excretion and cellular uptake) play a crucial role in the defense against hyperkalemia in this population. In this article we review extrarenal potassium homeostasis and its alteration in patients with ESRD. We pay particular attention to the factors that influence the movement of potassium across cell membranes. With that background we discuss the emergency treatment of hyperkalemia in patients with ESRD. We conclude with a review of strategies to reduce the risk of hyperkalemia in this population of patients.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Results of a National Survey in Germany on incidence and therapy of the nonoliguric hyperkalemia of the premature infant].

BACKGROUND: Although nonoliguric hyperkalemia of the premature infant is a common problem, in many hospitals it is not observed. It is characterized by an excessive increase in serum potassium concentration (serum-[K (+)]) at 24 hours after birth. Recently, salbutamol has been recommended to treat hyperkalemia. There are no controlled trials in premature infants. During the first minutes of salbutamol infusions paradoxical increases in serum-[K (+)] may occur. We asked for possible reasons for the variable incidence of the disorder. We wanted to know if salbutamol is currently applied and if initial increases in serum-[K (+)] during salbutamol infusions have been observed. MATERIALS AND METHODS: National survey in Germany. RESULTS: Questionnaires of 132 hospitals caring for premature infants < 30 gestational weeks. The incidence of hyperkalemia was 0 - 40 %. At least 25 % of all hospitals measured serum-[K (+)] not before the second day after birth. 52 hospitals had applied salbutamol. Nine hospitals reported increases in serum-[K (+)] associated with salbutamol therapy. However, it was common practice to measure serum-[K (+)] 1 hour (median, range 0.25 - 12 hours) after the start of the infusion. Two cases of cardiac arrhythmias during salbutamol infusion were reported. DISCUSSION AND CONCLUSIONS: The variable incidence of hyperkalemia may result from the fact that many hospitals do not measure serum-[K (+)] on the first day after birth. Common practice made it potentially impossible to determine the frequency of initial increases in serum-[K (+)] during salbutamol infusion. However, these data should be available, before controlled trials on salbutamol treatment in premature infants can be initiated.

Albuterol↗
PubMed2000

Lidocaine-induced conduction disturbance in patients with systemic hyperkalemia.

We report 2 cases in which lidocaine, given for wide-complex tachycardia in the presence of hyperkalemia, precipitated profound conduction disturbance and asystole. The electrophysiologic effects of hyperkalemia and its interaction with lidocaine are reviewed. In patients with known hyperkalemia and wide-complex tachycardia, treatment should be directed at hyperkalemia, rather than following treatment algorithms for wide-complex tachycardia.

Adult↗
PubMed1990

Hyperkalemia in diabetic ketoacidosis.

Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients.

Adult↗
PubMed1996

Case report: severe hyperkalemia in a geriatric patient receiving standard doses of trimethoprim-sulfamethoxazole.

A case is reported of a 96-year-old woman with congestive heart failure, hypertension, and chronic obstructive pulmonary disease who presented with altered mental status and severe hyperkalemia, a serum potassium 9.3 meq/L, and electrocardiograph changes. The patient was discharged 1 week prior, with a normal serum potassium, receiving trimethoprim-sulfamethoxazole for urinary tract infection and pneumonia. Serum potassium measurements returned to normal after discontinuation of the drug. Other causes of hyperkalemia were ruled out. Mild hyperkalemia due to trimethoprim-sulfamethoxazole was first reported in 1983 in a 69-year-old woman in whom leukemia with leukopenia developed. In literature to date, mild hyperkalemia in younger geriatric patients has been described. Trimethoprim is thought to act by inhibiting amiloride sensitive sodium channels in the distal nephron and impairing renal potassium secretion in a dose dependent manner. The authors report the case, review the literature, and discuss age-related reduction in renal function as a possible etiology.

Aged↗
PubMed2000

Pathophysiological mechanisms of postrevascularization hyperkalemia in orthotopic liver transplantation.

The underlying mechanisms of hyperkalemia occurring immediately after revascularization in orthotopic liver transplantation (OLT) are unknown. We investigated the possible pathophysiological mechanisms of hyperkalemia in relation to the donor and recipient. The study included 64 consecutive patients undergoing OLT. Recipients were divided into two groups: Group 1 consisted of 47 patients with serum K(+) concentration <5.5 mmol/L at 1-min postrevascularization, and Group 2 consisted of 17 patients with serum K(+) exceeding 5.5 mmol/L. Increased serum K(+) concentration, more progressive metabolic acidosis, and decreased mean arterial blood pressure and cardiac index during the anhepatic phase were recognized in Group 2. Multiple regression analysis showed that cardiac index, serum lactate, and serum K(+) concentration during the anhepatic phase were independent and significant factors that could predict serum K(+) concentration 1-min postrevascularization. Hyperkalemia at 1-min postrevascularization did not correlate with the extent of preservation injury of the graft liver (represented by the peak value of aspartate aminotransferase measured within the first 72 h after OLT) or the duration of cold ischemia. We conclude that hyperkalemia occurring immediately after revascularization in OLT is mainly caused by metabolic acidosis as a result of insufficient cardiac output during the anhepatic phase.

Adult↗
PubMed1981

Effects of bupivacaine and lidocaine on AV conduction in the isolated rat heart: modification by hyperkalemia.

The intrinsic cardiotoxicities of bupivacaine and lidocaine were examined in the isolated, perfused rat heart. The perfusates contained no protein and were equilibrated with a gas mixture of 95 per cent O2 and 5 per cent CO2. Autonomic activity, competitive binding, and postseizure hypoxia and acidosis were absent in this experimental model. The effects of the two local anesthetics were evaluated at normokalemia (5.9 mEq/l) and hyperkalemia (9.0 mEq/l). For normokalemia, the ratio of the potency of bupivacaine to that of lidocaine was 14 for slowing ventricular rate to 50 per cent of control, 6 for slowing atrial rate to 50 per cent of control, and 17 for doubling of the PR interval. The action of bupivacaine to slow ventricular rate was due to an inhibitory effect on both AV conduction and atrial rate. For lidocaine, ventricular slowing was mediated mainly by an inhibition of atrial rate with decreased AV conduction playing a minor role. Hyperkalemia of 9.0 mEq/l had little effect on heart rate or AV conduction in the absence of bupivacaine or lidocaine. It did, however, greatly potentiate the effect of both local anesthetics to slow ventricular rate. For bupivacaine, ventricular slowing to 50 per cent of control during hyperkalemia was accomplished almost entirely via an inhibition of AV conduction, while for lidocaine it occurred because of inhibition of both AV conduction and atrial rate. Regardless of the mechanism, hyperkalemia of this degree increased the ventricular slowing effect of both bupivacaine and lidocaine.

Animals↗
PubMed1993

Life-threatening hyperkalemia associated with captopril administration.

Angiotensin converting enzyme (ACE) inhibitors have become commonly used medications for hypertension and congestive heart failure. These agents are noted for their low incidence of adverse effects; but in certain cases, these effects can be life-threatening. Severe hyperkalemia is one of the potentially dangerous effects of the ACE inhibitors. While cases of life-threatening hyperkalemia associated with the use of ACE inhibitors have been described previously, in no instance was dialysis required. Herein, we report a case of acute hyperkalemia in a patient with congestive heart failure and renal insufficiency, the resolution of which required hemodialysis. The hyperkalemia in this case occurred without an increase in the patient's azotemia. In addition, the patient did not respond to attempts to effect the intracellular shift of potassium. This suggested that there may have been a defect in internal potassium homeostasis.

Aged↗
PubMed2003

Antenatal steroid treatment prevents severe hyperkalemia in very low-birthweight infants.

BACKGROUND: Hyperkalemia is seen quite often in very low-birthweight (VLBW) infants and concentrations sometimes become high enough to cause cardiac arrhythmia. The purpose of the present study was to identify factors that increase serum concentrations of potassium in VLBW infants. METHODS: Retrospective comparative analysis was performed on 140 VLBW infants who had been admitted to the Toho University Perinatal Center between January 1993 and December 1999 and needed mechanical ventilation for respiratory distress. Serum concentrations of potassium at 24 and 48 h of age were compared in two groups of infants, those whose mothers did and did not receive antenatal steroid treatment. Risk factors for severe hyperkalemia were analyzed by multiple linear regression models and Pearson's partial correlation analysis. RESULTS: Antenatal steroid treatment reduced serum potassium concentrations significantly at 24 and 48 h, as well as the incidence of cardiac arrhythmia and necessity for glucose insulin treatment for severe hyperkalemia. Multiple linear regression showed the serum potassium concentration at 24 h of age was associated with antenatal steroid hormone treatment, 24 h fluid intake volume, serum sodium concentrations at 24 h, gestational weeks and sampling site. Serum concentration of potassium at 48 h of age was associated with blood urea nitrogen, gestational week, serum sodium concentration at 48 h of age and fluid intake between 24 and 48 h of age. Urine output volume and serum creatinine concentrations were not correlated with potassium concentrations at either age. CONCLUSION: Antenatal steroid hormone treatment can reduce early hyperkalemia in VLBW infants and also the incidence of cardiac arrhythmia and the use of glucose insulin treatment.

Female↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: aldosterone receptor antagonism: interface with hyperkalemia in heart failure.

Aldosterone receptor antagonism (ARA) is an increasingly well-accepted element of heart failure therapy. The experimental underpinnings for the use of ARA in heart failure are strong being linked to a variety of tissue-based cardiac effects characteristic of drugs in this class. However, the benefits of ARA therapy do not come without some risk since drugs in this class are potent inhibitors of renal potassium (K+) elimination. Thus, some increment in serum K+, up to and including the development of overt hyperkalemia (typically defined as a serum K+ value in excess of 6.0 mEq/L), is to be expected whenever they are used. Hyperkalemia attributable to ARA relates to several factors including ARA dose, patient predisposition to hyperkalemia, as in the case of renal failure, and dietary intake of K+. The risk of some change in serum K+ with ARA should not be a deterrent to use of drugs in this class but, rather should prompt careful surveillance for the onset of this potentially life-threatening electrolyte disturbance. The frequency of such scrutiny should be patient-specific and based on the constellation of risk factors for hyperkalemia.

Adrenergic beta-Antagonists↗