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At least 19 recordsLinked to original sources
PubMed2004

Hypercalciuria in familial hyperkalemia and hypertension accompanies hyperkalemia and precedes hypertension: description of a large family with the Q565E WNK4 mutation.

Familial hyperkalemia and hypertension (FHH; pseudohypoaldosteronism type II) is an autosomal dominant disorder characterized by hyperkalemia, hypertension, and low renin. WNK1 kinase overexpression and WNK4 kinase inactivating missense mutations cause FHH. When expressed in frog oocyte, WNK4 inhibits Na-Cl cotransporter surface expression, and WNK1 relieves this inhibition. We have reported hypercalciuria in subjects with the WNK4 Q565E mutation. In contrast, in subjects with WNK1 overexpression, normocalciuria was found. Here we report a major extension of our previously described kindred that contains 34 subjects, 18 of them affected by the mutation. Hypertension was diagnosed in 13 affected subjects at the age of 31 +/- 12 yr. Five of the affected or obligatory affected subjects had stroke, in four at the age of 50-62 yr. Seven subjects with FHH were diagnosed 27 yr previously. All four subjects who were normotensive at diagnosis became hypertensive during follow-up. The mean time between detection of hyperkalemia and appearance of hypertension was 13 yr. In the extended kindred, compared with the unaffected subjects, affected subjects had hyperkalemia, low transtubular potassium gradient, hyperchloremia, low bicarbonate, higher aldosterone, and marked suppression of renin. Urinary calcium levels in affected and unaffected subjects were 0.85 +/- 0.27 and 0.28 +/- 0.12 mmol/mmol creatinine, respectively (P < 0.0001). Hypercalciuria was accompanied by lower serum calcium levels [9.44 +/- 0.15 vs. 9.81 +/- 0.31 mg/dl (2.36 +/- 0.04 vs. 2.45 +/- 0.08 mmol/liter); P = 0.01], supporting a mechanism of renal calcium leak. The six affected, currently normotensive subjects had the same degree of hyperkalemia, hypercalciuria, and low renin as the affected hypertensive subjects. We conclude that in FHH with WNK4 mutations, with time all affected subjects will apparently develop hypertension. Hypercalciuria accompanies hyperkalemia, and both precede hypertension. Based on the recent findings that WNK4 regulates the renal outer medullary potassium channel as well as epithelial Cl(-)/base exchanger and the Na(+)-K(+)-2Cl(-) cotransporter, we suggest that WNK4 interacts with a calcium channel or transporter.

Adult↗
PubMed1976

Electrocardiogram in Hyperkalemia: electrocardiographic pattern of anteroseptal myocardial infarction mimicked by hyperkalemia-induced disturbance of impulse conduction.

In a patient with renal failure and shortness of breath, Q waves transiently appeared in the right precordial leads of the electrocardiogram (ECG) during episodes of hyperkalemia, without a substantial change in mean electrical axis. With restoration of the plasma potassium level to normal, R waves reappeared in these leads. It is concluded that the transient development of Q waves in the right precordial leads during hyperkalemia resulted from a hyperkalemia-induced conduction disturbance. Hyperkalemia, by affecting conduction in Purkinje fibers of ventricular muscle, or both, disturbed the normal sequence of septal and anterior wall depolarization and resulted in an ECG pattern that mimicked that of anteroseptal myocardial infarction. Clinically, hyperkalemia-induced conduction disturbances of this type must be included in the differential diagnosis of the ECG that suggests an anteroseptal myocardial infarction.

Adult↗
PubMed2006

Hyperkalemia of the blood-primed ECLS circuit does not result in post-initiation hyperkalemia in infants < 10 kg.

OBJECTIVE: To assess the risk of hyperkalemia with blood-primed extracorporeal life support (ECLS) circuits in infants < 10 kg. DESIGN: Retrospective cohort study of all neonatal and pediatric patients < 10 kg placed on ECLS from May 1998 to April 2001. MEASUREMENTS AND MAIN RESULTS: Data collection including patient weight, patient potassium levels pre- and post-initiation of ECLS, potassium level of the primed ECLS circuit, age of the packed red blood cell (PRBC) unit, type of preservative, and preservative reduction status. Seventy-six circuits were available for the analysis. The age of the PRBC unit and preservative reduction status significantly affected the potassium level of the primed ECLS circuit. Multivariate linear regression analysis showed no significant effect on the post-ECLS initiation patient potassium level with respect to the PRBC age, the preservative reduction status, the patient potassium level prior to ECLS initiation, and the potassium level of the primed ECLS circuit. CONCLUSIONS: Initiation of ECLS in infants < 10 kg should not be delayed unnecessarily to perform preservative reduction or to utilize PRBC units of a specific age, as hyperkalemia of the primed ECLS circuit is not associated with systemic hyperkalemia in the patient post-initiation of ECLS.

Blood Preservation↗
PubMed1997

Alkalinization is ineffective for severe hyperkalemia in nonnephrectomized dogs. Hyperkalemia Research Group.

OBJECTIVE: To determine whether alkalinization with sodium bicarbonate (NaHCO3) in near-lethal hyperkalemia either lowers potassium (K) rapidly or shortens duration of cardiac conduction disturbances. METHODS: A controlled canine laboratory investigation of 3 treatments for severe hyperkalemia. Conditioned dogs (n = 8; 17-30 kg) received, in random order, 2 mmol/kg of each of 3 treatments (matched in sodium and water) in separate experiments > or = 1 week apart: 1.05% NaHCO3 over 60 minutes (infusion therapy); 8.4% NaHCO3 over 5 minutes, then 14 mL/kg sterile water over 55 minutes (bolus therapy); 8.4% NaCl over 5 minutes, then 14 mL/kg sterile water over 55 minutes (saline therapy). Prior to administering one of the above therapies, the animals were anesthetized with 0.5-2.5% isoflurane and ventilated to maintain a normal PCO2. After 30 minutes of equilibration, 2 mmol/kg/hr (loading dose) of a 2-mmol/mL KCl solution was given until idioventricular or relative junctional bradycardic dysrhythmias were sustained for 15 minutes. Then KCl was decreased to 1 mmol/kg/hr (maintenance dose) for 2 hours and 45 minutes. Treatment was begun after 45 minutes of maintenance KCl infusion. RESULTS: The pretreatment K level (all studies) was 9.06 +/- 0.82 mmol/L (mean +/- SD). Although the mean K level decreased more after saline therapy than after bolus therapy at every time, differences were neither statistically significant nor clinically important during the first 30 minutes. The means of the differences in decreases (saline minus bolus) were small, 0.26 (95% CI, -0.48 to 1.00) at 15 minutes, 0.16 (95% CI, -0.67 to 0.98) at 30 minutes. Dysrhythmia duration was shorter with bolus therapy than for saline therapy in only 1 of 5 dogs (p = 0.38). CONCLUSIONS: Hypertonic saline bolus lowered plasma K as effectively as NaHCO3 bolus in this animal model within the first 30 minutes. Clinically meaningful decreases due to alkalinization alone within 30 minutes are unlikely.

Animals↗
PubMedDate not supplied

Predictors of the development of hyperkalemia in patients using angiotensin-converting enzyme inhibitors.

BACKGROUND/AIMS: Angiotensin-converting enzyme inhibitors (ACEI) are the antihypertensives of choice in patients with chronic renal failure (CRF). ACEI by decreasing the synthesis of aldosterone, the main regulator of serum potassium, predispose to the development of hyperkalemia. Although hyperkalemia with administration of ACEI is uncommon in patients with a normal renal function, a preexisting abnormality in potassium hemostasis, as seen in patients with chronic renal failure, may increase the risk of hyperkalemia. METHOD: To determine the predictors of development of hyperkalemia (K >5.1 mEq/l) in patients on ACEI, we retrospectively reviewed medical records of 119 patients followed in our renal clinic. RESULTS: The mean age of the patients was 56 +/- (SD) 13 (range 20-84) years. Sixty-three percent were males, and 37% were females. Sixty-seven percent had a history of diabetes. Eighty five percent of the patients had CRF [creatinine clearance (CrCl) <80 ml/min]. The baseline serum Cr was 2.3 +/- 1.2 (range 0.6-6.9) mg/dl, and the CrCl was 50 +/- 27.5 ml/min. Of the 119 patients 46 (38.6%) developed hyperkalemia (mean K 5.68 +/- 0.3, range 5.2-6.7 mEq/l). Ninety-six percent of the patients who developed hyperkalemia had CRF, and 84% were diabetics. Pearson product-moment correlation revealed a significant positive correlation of hyperkalemia with Cr and a negative correlation of hyperkalemia with CrCl and HCO(3) (Cr: r = 0.42, p < 0.0001; CrCl: r = -0.34, p < 0.0001; HCO(3): r = -0.41, p < 0.0001). Multivariate logistic regression analysis revealed diabetes and serum creatinine to be the main predictors of hyperkalemia. In 31 patients hyperkalemia resolved either with a low-potassium (2 g/day) diet or with diet and a decrease in the dose of ACEI. In 15 patients ACEI had to be discontinued due to persistent hyperkalemia. CONCLUSIONS: We conclude that hyperkalemia is common in patients with CRF on ACEI. The majority of the patients who develop hyperkalemia on ACEI have CRF and diabetes. A large number of patients with CRF require discontinuation of ACEI due to hyperkalemia and are deprived of their renoprotective effects.

Adult↗
PubMed2000

Indications for hospitalization of patients with hyperkalemia.

BACKGROUND: Although the methods for the appropriate management of patients with hyperkalemia are well established, no criteria for hospital admission of patients with this common electrolyte disorder have been promulgated. OBJECTIVES: To examine the current practices regarding hospitalization of patients with hyperkalemia and to consider appropriate criteria for admission. PATIENTS AND METHODS: We evaluated a consecutive series of patients hospitalized for hyperkalemia and excluded patients who developed hyperkalemia after admission. For comparison, we selected a series of patients with a similar degree of hyperkalemia who were treated as outpatients. Hyperkalemia was classified as minimal, moderate, or severe. The causes of hyperkalemia were identified, and the therapeutic maneuvers used were ascertained. Although the study did not have the power to determine the relative safety of the 2 therapeutic approaches, we compared the outcomes of the 2 groups of patients. RESULTS: The inpatient group consisted of 11 patients who were admitted for the treatment of hyperkalemia, and we identified 12 patients who received outpatient therapy for hyperkalemia. The patients in the 2 treatment groups were similar with respect to age and the values of serum urea nitrogen, creatinine, and potassium prior to the identification of hyperkalemia. The mean +/-SD potassium concentrations at baseline were 5.4+/-0.7 mmol/L in the inpatients and 5.5+/-0.5 mmol/L in the outpatients. The mean +/-SD potassium concentration in the inpatients was 6.7+/-0.8 mmol/L at the time of hospital admission, compared with 6.7+/-0.5 mmol/L in the outpatients at the time that hyperkalemia occurred. Similar proportions of both groups (6 of 11 inpatients and 7 of 12 outpatients) had moderate or severe hyperkalemia. CONCLUSIONS: Patients admitted to the hospital were clinically indistinguishable from patients treated as outpatients. The justification for the decision to admit patients to the hospital or to treat them as outpatients was often not evident. We suggest criteria for hospitalization, which include severe hyperkalemia (> or =8.0 mmol/L, with changes other than peaked T waves on the electrocardiogram), acute worsening of renal function, and supervening medical problems.

Aged↗
PubMed1991

The ability of physicians to predict hyperkalemia from the ECG.

STUDY OBJECTIVE: To determine whether physicians blinded to the serum potassium level can predict hyperkalemia (potassium concentration of more than 5.0 mmol/L) from the ECG. DESIGN: ECGs of patients at high risk for hyperkalemia were interpreted retrospectively by two physicians blinded not only to the specific clinical diagnosis of the patient and to their serum potassium measurement but also to each other's interpretation. The physicians predicted the presence or absence of hyperkalemia as well as the severity of hyperkalemia on a nominal scale (mild, moderate, or severe). SETTING: The emergency department of a university-affiliated urban county hospital. PATIENTS: Two hundred twenty consecutive patients admitted to the hospital from the ED with a diagnosis of renal failure or hyperkalemia. Eighty-seven patients had hyperkalemia, and 133 did not. RESULTS: The sensitivities of the readers for predicting hyperkalemia were .43 and .34, respectively (best positive predictive value, .65). The respective specificities for detecting hyperkalemia were .85 and .86 (best negative predictive value, .69). When only patients with moderate-to-severe hyperkalemia (potassium of more than 6.5 mmol/L) were analyzed, sensitivities were .62 and .55. The readers' ability to predict the severity of hyperkalemia was equally poor. CONCLUSION: The ECG is not a sensitive method of detecting hyperkalemia, even in high-risk patients. The specificity of the ECG is better for hyperkalemia, but empiric treatment of hyperkalemia based on the ECG alone will lead to mistreatment of at least 15% of patients.

Adult↗
PubMed1998

Hyperkalemia in outpatients using angiotensin-converting enzyme inhibitors. How much should we worry?

BACKGROUND: Hyperkalemia is a potentially life-threatening complication resulting from the use of angiotensin-converting enzyme (ACE) inhibitors; data to guide the intensity of monitoring for or responding to hyperkalemia in outpatients are limited. METHODS: Case-control methodological procedures were used to identify risk factors for hyperkalemia. Outpatients prescribed ACE inhibitors during 1992 and 1993 at a Veterans Affairs medical center general medicine clinic were identified. Case patients had a potassium level higher than 5.1 mmol/L on the day of clinic visit while using an ACE inhibitor; controls had a potassium level lower than 5.0 mmol/L on the day of clinic visit while using an ACE inhibitor and had no elevated potassium level during the study period. Predictor variables measured included type and dosage of ACE inhibitor; serum chemistries; comorbidities; concurrent drug use; and age. Case patients were followed up for 1 year after the index episode of hyperkalemia. Follow-up variables included changes in therapy with ACE inhibitor, maximum potassium for each change, and mortality. RESULTS: Of 1818 patients using ACE inhibitors, 194 (11%) developed hyperkalemia. Results of laboratory studies indicating a serum urea nitrogen level higher than 6.4 mmol/L (18 mg/dL), creatinine level higher than 136 mumol/L (1.5 mg/dL), congestive heart failure, and long-acting ACE inhibitors were independently associated with hyperkalemia; concurrent use of loop or thiazide diuretic agent was associated with reduced risk. After 1 year of follow-up, 15 (10%) of 146 case patients remaining on a regimen of an ACE inhibitor developed severe hyperkalemia (potassium level > 6.0 mmol/L). A serum urea nitrogen level higher than 8.9 mmol/L (25 mg/dL) and age more than 70 years were independently associated with subsequent severe hyperkalemia. CONCLUSIONS: Mild hyperkalemia is common in medical outpatients using ACE inhibitors, especially in those with renal insufficiency or congestive heart failure. However, once hyperkalemia is identified during the use of ACE inhibitors, subsequent severe hyperkalemia is uncommon in patients younger than 70 years with normal renal function.

Ambulatory Care↗
PubMed2002

Purine metabolism and release during cardioprotection with hyperkalemia and hypothermia.

This work investigates whether purine metabolism and release is related to cardioprotection with hyperkalemia and hypothermia. Langendorff guinea-pig hearts were used to either monitor metabolism during ischemia or to measure functional recovery, myocardial injury and release of purine during reperfusion. Hearts underwent 30 min ischemia using one of the following protocols: control (normothermic buffer), hyperkalaemia (high-potassium buffer), hypothermia (20 degrees C) and hyperkalemia + hypothermia. At the end of 30 min ischemia, hyperkalemia was associated with similar metabolic changes (rise in purine and lactate and fall in adenine nucleotides) to control group. Accumulation of purine was due to a rise in inosine, xanthine and hypoxanthine and was largely prevented by hypothermia and hyperkalemia + hypothermia. Upon reperfusion, there was a time-dependent release of all purine, lactate and AMP. A fast (peak in less than 20 sec) release of inosine, xanthine, hypoxanthine and lactate was highest in control followed by hyperkalemia then hypothermia and little release in hyperkalemia + hypothermia. Adenosine and AMP release was slow (peak at 3 min), only significant in control and was likely to be due to sarcolemmal disruption as the profile followed lactate dehydrogenase release. Recovery (left ventricular developed pressure) was 63% control, 82% hyperkalemia, 77% hypothermia and 98% for hyperkalemia + hypothermia. The loss of purine during reperfusion but not their production during ischemia is related to cardioprotection with hyperkalemia. The possibility that the consequences of hyperkalemia modulate a sodium-dependent purine efflux, is discussed. The reduced loss of purine in hypothermia or in hyperkalemia + hypothermia is likely to be due to a lower metabolic activity during ischemia.

Adenine↗
PubMed1997

Hyperkalemia in the elderly: drugs exacerbate impaired potassium homeostasis.

OBJECTIVE: To review the pathophysiology underlying the predisposition to hyperkalemia in the elderly; the medications that disrupt potassium balance and promote the development of hyperkalemia in the elderly; the prevention of hyperkalemia in elderly patients treated with potassium-altering medications; and the appropriate management of hyperkalemia when it develops. METHODS AND MAIN RESULTS: A MEDLINE search of the literature (1966-1996) using the terms hyperkalemia, drugs, elderly, and treatment was conducted and pertinent review articles, textbooks, and personal files were consulted. Elderly subjects appear to be predisposed to the development of hyperkalemia on the basis of both innate disturbances in potassium homeostasis and comorbid disease processes that impair potassium handling. Hyperkalemia in the elderly is most often precipitated by medications that impair cellular uptake or renal disposal of potassium. This electrolyte disorder is best prevented by recognition of at-risk physiology in the aged, avoidance of therapy with certain high-risk medications, and monitoring of plasma potassium concentration and renal function at intervals appropriate for the medication prescribed. Management of hyperkalemia entails identification of the clinical manifestations of severe hyperkalemia, stabilization of cardiac tissue, promotion of cellular potassium uptake, and ultimately removal of potassium from the body. CONCLUSIONS: Geriatric patients should be considered at risk of developing hyperkalemia, especially when they are prescribed certain medications. Potassium levels should be monitored at appropriate intervals when these patients are treated with potassium-altering medications. Appropriate management of hyperkalemia in the elderly can avoid life-threatening neuromuscular and cardiac complications.

Aged↗
PubMed2006

Quantification of the risk and predictors of hyperkalemia in patients with left ventricular dysfunction: a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) trials.

BACKGROUND: Limited data are available to predict the occurrence of hyperkalemia. Risk assessment is complicated by the lack of consistency of definition between trials. METHODS: We conducted a retrospective analysis of the SOLVD to evaluate the incidence of hyperkalemia and the value of several baseline characteristics as predictors of hyperkalemia in patients with left ventricular dysfunction. RESULTS: The incidence of hyperkalemia was 6.0% and 1.1% using a definition of > or = 5.5 and > or = 6.0 mmol/L, respectively. Independent predictors of hyperkalemia (> or = 5.5 mmol/L) were randomization to enalapril, baseline serum creatinine, serum potassium, New York Heart Association functional class III or IV, a history of diabetes, and atrial fibrillation (all P < .05). The use of loop diuretics was also associated with an increased risk of hyperkalemia but only in patients included in the SOLVD prevention trial. Similar results were obtained when renal function was evaluated using the estimated creatinine clearance. CONCLUSIONS: The definition of hyperkalemia is important when evaluating its incidence in clinical trials. Renal dysfunction, baseline serum potassium, diabetes, atrial fibrillation, New York Heart Association functional class, and treatment with an angiotensin-converting enzyme inhibitor are factors associated with the development of hyperkalemia in patients with left ventricular dysfunction. More specifically, our results suggests that before initiating drugs that can cause hyperkalemia in patients with heart failure, a strong consideration should be given to calculate creatinine clearance and that patients with a creatinine clearance < 60 mL/min should undergo a close monitoring of their serum potassium to prevent the development of hyperkalemia.

Aged↗
PubMed2005

Resolution of hypertension during pregnancy in familial hyperkalemia and hypertension with the WNK4 Q565E mutation.

OBJECTIVE: Secondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. The purpose of the study was to examine the course of pregnancy in hypertensive women with familial hyperkalemia and hypertension. STUDY DESIGN: We prospectively studied 2 pregnancies of a woman with familial hyperkalemia and hypertension and the Q565E WNK4 mutation (pregnancies 1 and 2) and retrospectively studied the course of 2 pregnancies in another woman who was an affected member of this largest family described in the literature. RESULTS: Both women had hypertension (170-190/105-110 mm Hg), hyperkalemia (5.3-6.0 mmol/L), and hypercalciuria, all of which were well controlled by thiazides. During pregnancies, thiazides were discontinued; throughout the pregnancy, the blood pressure remained normal at 120 to 130/75 to 85 mm Hg; however, hyperkalemia and hypercalciuria, which were documented in pregnancies 1 and 2, persisted. Renin and aldosterone levels (which were measured in pregnancies 1 and 2) rose towards their end. Four normal infants were born. A woman with familial hyperkalemia and hypertension of unknown molecular defect who had 2 pregnancies with hypertension exacerbation and premature deliveries was described previously. CONCLUSION: In familial hyperkalemia and hypertension with the WNK4 mutation, pregnancy ameliorates hypertension; however, hyperkalemia and hypercalciuria persist. This dissociation may shed light on the pathogenesis of familial hyperkalemia and hypertension, on pregnancy-related hypertension, and on the mechanism of action of WNK4 kinase, a major regulator of cellular ion transport.

Adult↗
PubMed1992

Hyperkalemia in very low birth weight infants.

PURPOSE: To assess the frequency and pathogenesis of hyperkalemia in the very low birth weight infant. METHODS: Infants who weighed less than 1000 gm at birth were prospectively entered into the study within 12 hours of birth. Potential risk factors for hyperkalemia were assessed. Body weight, fluid and electrolyte balance, serum levels of sodium and potassium, creatinine clearance, fractional sodium excretion, and urine sodium/potassium ratio were measured every 8 hours for 72 hours. Measurements of plasma renin, serum aldosterone, and plasma atrial natriuretic factor were made at study entry and repeated when hyperkalemia (serum potassium greater than 6.5 mmol/L) occurred or at 72 hours. Infants in whom hyperkalemia developed were compared with those in whom it did not. RESULTS: Thirty-one infants completed the study; hyperkalemia developed in 16 (51.6%). The only difference in the occurrence of perinatal complications was the more frequent occurrence of pH less than 7.20 in infants with subsequent development of hyperkalemia. Creatinine clearance, urine output, and potassium excretion were significantly lower in the hyperkalemia group during the first 24 hours. Serum potassium concentration at 24 hours was inversely related to urine output in the prior 24 hours. Fractional sodium excretion, urine sodium/potassium ratio, and levels of renin, aldosterone, and atrial natriuretic factor did not differ between groups. CONCLUSIONS: Hyperkalemia is a frequent complication in very low birth weight infants. Infants with low urinary flow rates during the first few hours after birth are at greatest risk for the development of hyperkalemia.

Aldosterone↗
PubMed1998

Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines.

BACKGROUND: Hyperkalemia is a common, potentially life-threatening disorder. Electrocardiograms are considered to be sensitive indicators of the presence of hyperkalemia. Since the treatment of hyperkalemia involves relatively few maneuvers and because its success can be objectively scored, we investigated how physicians manage this disorder and how successful their prescribed therapy is. We also sought to determine whether treatment could be improved by providing the treating physicians with therapy guidelines on a real-time basis. METHODS: Consecutive patients with hyperkalemia were identified by review of laboratory records. During the observation-only phase of the study, demographic data, contributing causes, electrocardiogram findings, treatments used, compliance with prescribing guidelines, and patient outcome were recorded. During the subsequent notification phase of the study, treatment recommendations were sent to the patient's ward when the elevated potassium value was noted. The same outcome data were collected. RESULTS: There were 127 episodes of hyperkalemia during the observation-only phase and 115 during the notification phase. No patients died or had life-threatening cardiac arrhythmias. Electrocardiographic abnormalities consistent with hyperkalemia were observed in only 14% of episodes. Renal failure (77%), drugs (63%), and hyperglycemia (49%) contributed to most episodes. Treatments used were exchange resin (51%), insulin (46%), calcium (36%), bicarbonate (34%), and albuterol (4%). The agents were equally efficacious. The time to first treatment was shorter in patients with potassium levels of 6.5 mmol/L or more than in patients with lower values (2.1 +/- 2.2 vs 2.8 +/- 2.4 hours; P<.05). Treatment was better in the intensive care unit than on regular wards. Only 39% of episodes during the observation-only period met the predetermined criteria for monitoring and diagnosis, initial treatment, and follow-up. During the notification period, physician performance was no better; only 42% of episodes met all criteria. The laboratory transmitted a copy of the guidelines to the patient's ward only 38% of the time. In a separate analysis of these episodes, there was no improvement in treatment. Physicians who did not receive the notification fulfilled all treatment criteria more often than physicians who did (50% vs 30%; P<.05). CONCLUSIONS: Although treatment of hyperkalemia was frequently suboptimal, no serious arrhythmias and no deaths complicated management of 242 episodes of severe hyperkalemia. A narrowly targeted effort to improve physician management of a disorder with discrete treatment options did not improve therapy.

Adolescent↗
PubMed2000

Hyperkalemia in hospitalized patients.

OBJECTIVE: Evaluate the prevalence of hyperkalemia (potassium > 5.5 mmol/l) in hospitalized patients not on dialysis, as well as the association of medications, impaired renal function and comorbid conditions with hyperkalemia. DESIGN: A retrospective case-control method. SETTING: A tertiary care teaching hospital. PATIENTS: Hyperkalemic adults not on dialysis with age and sex matched controls. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The use of medications associated with hyperkalemia and renal function using a calculated creatinine clearance were compared in the hyperkalemic and control groups. RESULTS: 35 adult patients with hyperkalemia who were not receiving dialysis were identified, with a prevalence in the hospitalized population of 3.3%. The hyperkalemic patients were older than the general hospital population (p < 0.05). Compared with controls, hyperkalemic patients: had a lower creatinine clearance (p < 0.05), were more likely to be taking angiotensin-converting enzyme inhibitors (p < 0.05), and had an increased frequency of diabetes mellitus (p < 0.001). All of the control patients survived their hospitalization, but the mortality rate in the hyperkalemic group was 17% (p < 0.0001). None of the deaths were directly attributable to hyperkalemia. CONCLUSIONS: Hyperkalemia is more frequent in older patients and is usually mild. Hyperkalemia is associated with diabetes mellitus, diminished renal function and the use of angiotensin-converting enzyme inhibitors. An elevated serum potassium level in a hospitalized patient may be a marker for a significantly increased risk of death, which is due to underlying medical problems and is not a consequence of the hyperkalemia.

Adult↗
PubMed1996

Frequency of hyperkalemia in recipients of simultaneous pancreas and kidney transplants with bladder drainage.

Hyperkalemia is the most frequent electrolyte abnormality found in whole organ transplant recipients receiving either cyclosporine (CsA) or tacrolimus (FK506). Recipients of a simultaneous pancreas kidney (SPK) transplant with bladder drainage may be particularly susceptible to hyperkalemia secondary to sodium loss from the bladder-drained pancreas, leading to decreased sodium delivery to potassium secretory sites of the kidney. We looked at the incidence of hyperkalemia in 34 type I diabetic SPK recipients transplanted at our center over the period from 1993 to 1995 and compared this with a cohort of 25 type I diabetic recipients of a kidney alone (K(Tx)) transplant. The incidence of hyperkalemia was 73.5% in recipients of an SPK, while it was 44% in K(Tx) recipients (P<0.05). CsA levels were higher, on average, in the SPK group (339 ng/ml+/-62 versus 272 ng/ml+/-58 in the K(Tx) group, P<0.05). However, CsA levels were not different between groups at the time of hyperkalemia, 320+/-74 versus 298+/-49 for SPK and K(Tx), respectively. CsA levels at the time of hyperkalemia were not different from those at the time of normokalemia. Other medications, serum bicarbonate, and renal function were not different in the groups. SPK recipients appear to have a greater incidence of hyperkalemia than kidney alone transplant recipients. This difference cannot be explained by higher acute CsA levels, other medications, or worse renal function. The increased incidence of hyperkalemia may, in part, be secondary to decreased sodium delivery to the transplanted kidney.

Adult↗