Maintain Serum Potassium Levels Research Articles

Abstract P538: Abnormal Serum Potassium is Associated With Risk of Chronic Kidney Disease Progression and All-Cause Mortality in Patients With Chronic Kidney Disease

Introduction: Chronic Kidney Disease (CKD) is a major risk factor for end-stage renal disease (ESRD) and premature death. It remains unclear if abnormal serum potassium is associated with CKD progression. We assessed the prospective relationship between serum potassium with both CKD progression and all-cause mortality among participants with CKD in the Chronic Renal Insufficiency Cohort (CRIC) Study. Methods: The CRIC study is a prospective cohort study of 3,939 participants with CKD from seven locations in the United States. Serum potassium was calculated as the cumulative mean from serum samples collected at baseline and annual follow-up visits prior to developing an event. Clinical cut points were used to group serum potassium: hypokalemia (<3.5 mmol/L), normokalemia (≥3.5 and ≤5.0 mmol/L), and hyperkalemia (>5.0 mmol/L). Kidney disease progression was defined as either incident end-stage renal disease or a 50% decline in estimated glomerular filtration rate (eGFR) from baseline. Cox proportional hazards models were used to examine the associations between serum potassium and CKD progression and all-cause mortality adjusting for baseline age, sex, race/ethnicity, education, clinic site, body mass index, cigarette smoking, alcohol drinking, physical activity, history of diabetes, hypercholesterolemia, and cardiovascular disease, use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, use of diuretics, use of other antihypertensive medications, and eGFR. Results: CRIC patients had a mean age of 57.7 years, were 45.1% female, and 41.9% Non-Hispanic Black. The prevalence of hypokalemia and hyperkalemia was 2.5% and 7.3%, respectively. Over an average 6.5 and 11.0 years of follow-up for CKD progression and all-cause mortality, respectively, 1,784 CKD progression events and 1,621 deaths occurred. Hypokalemia had a hazard ratio (HR) of 1.65 [95% confidence interval (CI): 1.25-2.10; p=.0004] for CKD progression compared with normokalemia. Similarly, hyperkalemia had a HR of 1.76 (95% CI, 1.50-2.06, p<.0001) for CKD progression compared to normokalemia. The HR for all-cause mortality were 1.57 (95% CI, 1.13-2.18; p=.0066) for hypokalemia compared with normokalemia, and 1.43 (95% CI, 1.19-1.72, p=.0001) for hyperkalemia compared with normokalemia, after multivariable adjustment. Conclusions: Our study found that abnormally high and low serum potassium is associated with increased risk of CKD progression and all-cause mortality. These findings suggest that interventions that maintain serum potassium levels in the normal range may reduce the risk of CKD progression and premature death among patients with CKD.

Combined Lung-Liver Transplantation Can Be Safely Performed in Patients with Hypokalemic Periodic Paralysis

<h3>Introduction</h3> Combined lung-liver transplantation (CLLT) is rare and accounts for <0.01% of multiorgan transplants performed. Due to its infrequency, the criteria for CLLT candidacy have not been clearly elucidated. However, since post-transplant rehabilitation is critical for a successful outcome, any condition that may compromise a patient's postoperative mobility is considered a potential contraindication to transplantation. We report our experience with CLLT in a patient who had hypokalemic periodic paralysis (HPP), a rare genetic disorder that affects muscle ion channels and manifests as hypokalemia with episodes of severe weakness or paralysis. To our knowledge, we present the first reported case of transplantation in a HPP patient. <h3>Case Report</h3> The patient was a 63-year-old male with 7-year history of idiopathic pulmonary fibrosis and cryptogenic cirrhosis. Other comorbidities included HPP since childhood. His HPP exacerbations, which manifested as weakness without respiratory symptoms, were precipitated by various medications and were treated with correction of hypokalemia. He was previously declined for CLLT by 9 other programs due to his age and HPP, but our multidisciplinary team determined that the patient's HPP could be adequately managed and should not preclude him from CLLT. While hospitalized for progressive respiratory failure, donor organs became available. Bilateral lungs and a liver were recovered from a brain-dead donor. Bilateral lung transplantation was performed followed by orthotopic liver transplantation. There were no intraoperative complications. Standard post-transplant care was initiated after surgery. He was transferred out of the ICU on postoperative day (POD) #5, and was discharged to home on POD #22. The patient's postoperative hospitalization was complicated by antibody-mediated rejection (AMR) from <i>de novo</i> donor-specific antibodies. His AMR was adequately managed with methylprednisone, plasmapheresis, and intravenous immunoglobulins. Meticulously maintaining serum potassium levels above 4 mEq/L and avoiding precipitating medications sufficiently prevented any HPP exacerbations. The patient has been home for 8 months and has been doing well. <h3>Summary</h3> The limits on candidacy for CLLT have not been clearly defined, but we demonstrated for the first time that CLLT can be safely performed in patients with HPP.

Nutritional management in patients with chronic kidney disease.

The global prevalence of chronic kidney disease (CKD) is increasing with the aging of populations worldwide. As kidney function declines, the accumulation of metabolic waste products and excessive electrolytes can significantly impair the health of patients with CKD. As nutritional management of patients with CKD is thought to control uremic symptoms and provide beneficial effects on the progression of kidney dysfunction, the diet of patients with CKD should be an important consideration in their care. Many guidelines recommend limiting protein intake in these patients, as high-protein diets aggravate kidney dysfunction. Excess sodium may be associated with CKD progression and all-cause mortality and, therefore, limiting salt intake is generally recommended. Low potassium is associated with muscle weakness and hypertension, whereas high potassium is associated with cardiac arrhythmia. Therefore, recent guidelines recommend adjusting dietary potassium intake on an individual basis to maintain serum potassium levels within the normal range. Appropriate dietary calcium intake is recommended to maintain calcium balance in patients with CKD G3, G4. Given the many dietary considerations for patients with CKD, effective nutritional management is challenging. Individualized strategies are needed to ensure the best outcome for patients with CKD.

Is it time to rethink about protocols for managing intraoperative serum potassium and blood glucose levels during off-pump coronary artery bypass surgery?

Background A low perioperative serum potassium level ( 200 mg/dl) during cardiac surgery is a preventable cause of high morbidity and mortality. In this study, we measured the changes in intraoperative levels of serum potassium and blood glucose in adult patients undergoing elective off-pump coronary artery bypass (OPCAB) surgery, while administering insulin intraoperatively as per the present guidelines. Patients and methods Thirty-six adults, aged 18–65 years, undergoing elective OPCAB surgery were enrolled in this study. Arterial blood gas analysis was performed at predetermined intraoperative time points to measure serum potassium and blood glucose levels as primary variables. Base excess, pH, and HCO3− were recorded as secondary variables. Insulin infusion was started according to the sliding scale, whenever blood glucose was more than 180 mg/dl. Intravenous potassium was supplemented, when serum potassium was less than 4 mEq/l. Quantitative variables were compared with baseline using paired t test and repeated measure analysis of variance was used for comparison across follow up. Results Potassium chloride had to be continuously administered intravenous to maintain serum potassium levels more than 4 mEq/l throughout OPCAB surgery. There was a highly significant (P Conclusion Patients are prone to hypokalemia and hyperglycemia during OPCAB surgery, despite following the current guidelines. More studies are needed to formulate a better insulin infusion protocol for maintaining normoglycemia and guidelines need to be formulated for continuous intraoperative potassium infusion during OPCAB surgery.

Dialysate Potassium, Dialysate Magnesium, and Hemodialysis Risk.

One of the fundamental goals of the hemodialysis prescription is to maintain serum potassium levels within a narrow normal range during both the intradialytic and interdialytic intervals. Considering the extraordinarily high rate of cardiovascular mortality in the hemodialysis population, clinicians are obligated to explore whether factors related to dialytic potassium removal can be modified to improve clinical outcomes. Observational studies and circumstantial evidence suggest that extreme concentrations of serum and dialysate potassium can trigger cardiac arrest. In this review, we provide an overview of factors affecting overall potassium balance and factors modulating potassium dialysate fluxes in dialysis, and we review data linking serum and dialysate potassium concentrations with arrhythmias, cardiovascular events, and mortality. We explore potential interactions between serum and dialysate magnesium levels and risks associated with dialysate potassium levels. Finally, we conclude with proposed dialytic and novel nondialytic approaches to optimize outcomes related to potassium homeostasis in patients on hemodialysis. Dialysis clinicians need to consider changes in the overall clinical scenario when choosing dialysate potassium concentrations, and an effective change in practice will require more frequent serum potassium monitoring and responsive dialysis care teams.

Decreasing IV Potassium in Pediatric Cardiac Intensive Care: Quality Improvement Project.

IV potassium supplementation is commonly used in the pediatric cardiovascular ICU. However, concentrated IV potassium chloride doses can lead to life-threatening complications. We report results of a quality improvement project aimed at decreasing concentrated IV potassium chloride exposure. Retrospective evaluation of a quality improvement project aimed at reducing IV potassium chloride exposure. Pediatric cardiac ICU. All patients admitted to pediatric cardiac ICUs in April 2013 to September 2013 (preprotocol) and October 2013 to April 2014 (postprotocol). A quality improvement team developed a potassium protocol aimed at maintaining serum potassium levels 3.0-5.5 mEq/L, via algorithm focused on early enteral supplementation. All patients receiving IV diuretics who had a serum potassium level less than 4.5 mEq/L and urine output more than 0.5 mL/kg/hr had protocol initiated with potassium chloride-containing IV fluids or enteral potassium chloride. Concentrated IV potassium chloride infusions were limited to asymptomatic patients with serum potassium less than 2.0 mEq/L and high-risk patients at less than 3.0 mEq/L. Serum potassium levels were measured once daily, and protocolized adjustments were made based on this level and concurrent diuretic therapy. Serum potassium, potassium chloride supplementation, patient cost, fluid administration, and arrhythmia incidence were compared pre and post protocol. Four hundred forty-three admissions were included (234 pre protocol and 209 post protocol). No significant differences were found in demographics. There was no difference in mean morning serum potassium after protocol implementation (3.85 [0.77] mEq/L before protocol and 3.89 [0.75] mEq/L after protocol; p = 0.90). Concentrated IV potassium chloride administration was decreased by 86% (331 vs 47 doses). With protocol, there was decreased incidence in days with one measured episode of hyperkalemia (11 vs 4/1,000 patient-days; p = 0.02) and a trend toward decreased hypokalemia (433 vs 400/1,000 patient-days; p = 0.05). Arrhythmia incidence was similar (p = 0.59). Protocolized potassium management in pediatric cardiac intensive care patients decreased concentrated IV potassium chloride exposure and incidence of hyperkalemia. Lower potassium treatment threshold for IV potassium chloride was not associated with increased arrhythmias.

Serum Potassium Levels and Short-Term Outcomes in Patients With ST-Segment Elevation Myocardial Infarction.

Current guidelines recommend maintaining serum potassium levels between 4.0 and 5.0 mEq/L (1 mEq/L = mmol/L) in patients with acute myocardial infarction. However, these guidelines are based on studies conducted before the β blocker and reperfusion era. We retrospectively analyzed 6613 patients diagnosed with ST-segment elevation myocardial infarction (STEMI) who presented without renal insufficiency. Patients were categorized into 5 groups according to mean serum potassium levels: <3.5, 3.5 to <4.0, 4.0 to <4.5, 4.5 to <5.0, and ≥5.0 mEq/L. Patients with potassium levels of 4.0 to <4.5 mEq/L had the lowest predefined event rates, which were 6.4% for 7-day malignant arrhythmia, 3.7% for 7-day mortality, and 5.3% for 30-day mortality. Compared with the reference group (4.0 to <4.5 mEq/L), multivariate regression analysis revealed significantly higher 30-day mortality risk in patients with potassium level of 4.5 to <5.0 (hazard ratio [HR]: 1.52, 95% confidence interval [CI]: 1.17-1.98; P = .002) and even higher risk in patients with potassium level of ≥5.0 mEq/L (HR: 1.80, 95% CI: 1.22-2.66; P = .002). The lowest 30-day mortality was observed in patients with STEMI having potassium levels between 4.0 and 4.5 mEq/L, and a level >4.5 mEq/L significantly increased mortality risk.

Serum Potassium Levels and Mortality in Acute Myocardial Infarction

Clinical practice guidelines recommend maintaining serum potassium levels between 4.0 and 5.0 mEq/L in patients with acute myocardial infarction (AMI). These guidelines are based on small studies that associated low potassium levels with ventricular arrhythmias in the pre-β-blocker and prereperfusion era. Current studies examining the relationship between potassium levels and mortality in AMI patients are lacking. To determine the relationship between serum potassium levels and in-hospital mortality in AMI patients in the era of β-blocker and reperfusion therapy. Retrospective cohort study using the Cerner Health Facts database, which included 38,689 patients with biomarker-confirmed AMI, admitted to 67 US hospitals between January 1, 2000, and December 31, 2008. All patients had in-hospital serum potassium measurements and were categorized by mean postadmission serum potassium level (<3.0, 3.0-<3.5, 3.5-<4.0, 4.0-<4.5, 4.5-<5.0, 5.0-<5.5, and ≥5.5 mEq/L). Hierarchical logistic regression was used to determine the association between potassium levels and outcomes after adjusting for patient- and hospital-level factors. All-cause in-hospital mortality and the composite of ventricular fibrillation or cardiac arrest. There was a U-shaped relationship between mean postadmission serum potassium level and in-hospital mortality that persisted after multivariable adjustment. Compared with the reference group of 3.5 to less than 4.0 mEq/L (mortality rate, 4.8%; 95% CI, 4.4%-5.2%), mortality was comparable for mean postadmission potassium of 4.0 to less than 4.5 mEq/L (5.0%; 95% CI, 4.7%-5.3%), multivariable-adjusted odds ratio (OR), 1.19 (95% CI, 1.04-1.36). Mortality was twice as great for potassium of 4.5 to less than 5.0 mEq/L (10.0%; 95% CI, 9.1%-10.9%; multivariable-adjusted OR, 1.99; 95% CI, 1.68-2.36), and even greater for higher potassium strata. Similarly, mortality rates were higher for potassium levels of less than 3.5 mEq/L. In contrast, rates of ventricular fibrillation or cardiac arrest were higher only among patients with potassium levels of less than 3.0 mEq/L and at levels of 5.0 mEq/L or greater. Among inpatients with AMI, the lowest mortality was observed in those with postadmission serum potassium levels between 3.5 and <4.5 mEq/L compared with those who had higher or lower potassium levels.

Lack of Correlation Between Thiazide‐Induced Hyperglycemia and Hypokalemia: Subgroup Analysis of Results from the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) Study

To determine whether changes in serum glucose, serum potassium, and plasma insulin levels are correlated in a cohort of hypertensive patients. Prespecified subgroup analysis of results from a prospective, multicenter, randomized, open-label, parallel-group study. Setting. Primary care clinics at three tertiary care medical centers. Community-based ambulatory population of 202 patients (age range 17-65 yrs) with a new diagnosis of hypertension, untreated hypertension, or known hypertension, who were previously treated with fewer than three antihypertensive drugs and had no evidence of cardiovascular disease or diabetes mellitus. Intervention. Monotherapy with oral hydrochlorothiazide 12.5 or 25 mg/day for 9 weeks. Fasting serum glucose, serum potassium, and plasma insulin levels were obtained at baseline (before hydrochlorothiazide therapy was started) and after 9 weeks of therapy. Significant elevations were noted in fasting serum glucose (mean +/- SD 3.42 +/- 10.38 mg/dl, p<0.0001) and plasma insulin (2.35 +/- 9.47 microU/ml, p<0.0001) levels, and a significant reduction in serum potassium level (0.30 +/- 0.44 mEq/L, p<0.0001) was noted. No significant correlation was observed between changes in fasting serum glucose and potassium levels (r = 0.022, 95% confidence interval (CI) -0.120-0.164, p=0.757) or between changes in serum potassium and plasma insulin levels (r = -0.112, 95% CI -0.256-0.037, p=0.140). Changes in serum glucose levels did not differ significantly between patients maintaining serum potassium levels of 4.0 mEq/L or greater and those with levels below 4.0 mEq/L. Changes in serum potassium and serum glucose levels were not correlated in individuals receiving hydrochlorothiazide monotherapy; thus maintenance of normal potassium levels may not attenuate the risk of thiazide diuretic-induced hyperglycemia.

Vasopressin-receptor antagonists in heart failure

The role of arginine vasopressin in heart failure and the use of vasopressin receptor antagonists in the treatment of heart failure are reviewed. Arginine vasopressin (AVP) functions in the regulation of plasma osmolarity and blood pressure. In heart failure, AVP worsens heart failure by causing vasoconstriction of arteries and veins, potentially contributing to remodeling of the left ventricle and causing fluid retention and worsening of hyponatremia. Two V(2)-receptor antagonists, tolvaptan and lixivaptan, and one combined V(1a)- and V(2)-receptor antagonist, conivaptan, have shown promise for use in patients with heart failure. All three agents have been shown to increase free water excretion and increase serum sodium levels while maintaining serum potassium levels. They have not been shown to decrease renal function or the glomerular filtration rate and are well tolerated, with thirst being the major adverse effect during clinical trials. Because of their effects on sodium, vasopressin antagonists need to be carefully monitored to ensure that serum sodium levels do not increase too quickly and put the patient at risk for overcorrection or osmotic demyelination syndrome. In addition, patients need to be monitored for signs of dehydration secondary to increased urine excretion. To date, studies have not consistently shown improvements in patient symptoms or weight reduction. However, early data suggest that at least one agent, tolvaptan, does not alter mortality. Based on data from available clinical trials, vasopressin antagonists may offer a new treatment option for patients with congestive heart failure. However, these agents do not currently appear to delay the progression of heart failure or decrease mortality.

Potassium Supplementation, Diet vs Pills: A Randomized Trial in Postoperative Cardiac Surgery Patients

Cardiac surgery patients are commonly treated with diuretics, which can result in hypokalemia requiring potassium supplementation. Our objective was to determine whether cardiac surgery patients receiving therapy with potassium-wasting diuretics can safely and beneficially maintain serum potassium levels by eating potassium-rich foods. A prospectively randomized trial of diet vs medication supplementation of potassium was undertaken. Patients who were to undergo cardiac surgery and who would be receiving therapy with oral furosemide postoperatively were eligible for the study. Forty-eight patients were enrolled in the trial, and 38 patients completed the study. Patients received either potassium-rich foods (diet) or potassium chloride pills (medication). There was no significant difference in mean (+/- SD) serum potassium concentrations between groups preoperatively (4.25 +/- 0.30 vs 4.29 +/- 0.33 mEq/L, respectively), on postoperative day 3 (4.23 +/- 0.40 vs 4.27 +/- 0.40 mEq/L, respectively), or postoperative day 4 (4.23 +/- 0.48 vs 4.24 +/- 0.33 mEq/L, respectively) for the diet and medication groups. Length of stay was significantly lower in the diet group (5.0 +/- 0.9 vs 6.3 +/- 2.2 days, respectively). When asked their preferences for method of supplementation, 79% of patients preferred the diet method. Cardiac surgery patients receiving therapy with diuretics can maintain serum potassium levels at clinically adequate concentrations by eating potassium-rich foods. Length of stay was significantly reduced. This method of potassium supplementation demonstrates the potential for reduced costs and increased patient satisfaction.

Interaction of the sympathetic nervous system and electrolytes in congestive heart failure

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neurohormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane β 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na +K +-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of the sympathetic nervous system in heart failure is facilitated by concomitant activation of the reninangiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a β 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/ liter.