Acquired hyperkalaemia leading to periodic paralysis: an emergency department perspective.

Hyperkalaemia is one of the common electrolyte imbalances dealt with in the emergency department and is caused by extracellular accumulation of potassium ions above normal limits usually greater than 5.0-5.5 mmol/L. It is found in a total of 1-10% of hospitalised patients usually associated with chronic kidney disease and heart failure. The presentation can range from being asymptomatic to deadly arrhythmias. The appearance of symptoms depends on the rate of change rather than just the numerical values. The rare presentation includes periodic paralysis characterised by the sudden onset of short-term muscle weakness, stiffness or paralysis. Management goals are directed towards reducing potassium levels in emergency settings and later on avoiding the triggers for future attacks. In this case, we present a man in his 50s with the generalised weakness later on diagnosed as hyperkalaemic periodic paralysis secondary to tumour lysis syndrome. Emergency physicians dealing with common electrolyte imbalances should keep a sharp eye on their rare presentation and their precipitating factors and should act accordingly.

Calcineurin inhibitor-related hyperkalemia is caused by hyporeninemic hypoaldosteronism and fludrocortisone is an effective treatment: Report of a case series and review of the literature.

INTRODUCTION: Calcineurin inhibitors (CNIs) are widely used in transplantation. Although CNI-related hyperkalemia is common (10%-60.6%), the underlying pathogenetic mechanism is not well-elucidated and may lead to dose adjustment or treatment withdrawal. OBJECTIVE: The aim of this study is to describe CNI-related hyperkalemia due to hyporeninemic hypoaldosteronism in pediatric transplant recipients who were successfully treated with fludrocortisone. METHOD: In a total of 55 hematopoietic stem cell (HSCT) and 35 kidney transplant recipients followed according to institutional immunosuppression protocols, recipients diagnosed with CNI-related hyperkalemia were reviewed. Recipients who were receiving intravenous fluid, potassium, or were diagnosed with hemolysis, acute graft rejection, or had an eGFR < 30 mL/min/1.73m2, were excluded. A detailed analysis of clinical history as well as biochemical studies was carried out to reveal possible pathophysiology. RESULTS: Three pediatric transplant recipients (one HSCT, two kidney transplantation) with findings of hyperkalemia, hyponatremia, and a mild elevation in blood urea nitrogen while on CNIs were recruited. Urinary potassium excretion was diminished while sodium excretion was increased. Plasma aldosterone levels were low, and renin was not increased in response. Primary adrenal insufficiency was ruled out, and hyporeninemic hypoaldosteronism was diagnosed. CNI-related hyperkalemia was detected earlier in case 1, who had HSCT (22 days), than in the second and third cases, who had kidney transplantation (24 and 30 months post-transplantation, respectively). The discrepancy was hypothesized to be explained by higher overall CNI dose due to higher serum target CNI used in HSCT than kidney transplantation. Electrolyte imbalance was reversed upon administration of physiologic dose fludrocortisone (0.05 mg, daily), while fludrocortisone was ceased after CNI withdrawal in case 1, which is additional evidence for the etiological association of CNIs and hyporeninemic hypoaldosteronism. CONCLUSION: Our three cases strengthen the premise that CNI-related hyperkalemia may be due to hyporeninemic hypoaldosteronism, and the timing and severity may be related to CNI dose. Fludrocortisone is a safe and effective treatment in CNI-related hyperkalemia, providing maintenance of CNIs, which are one of the essential therapeutic agents for pediatric transplantation.

A rare case of essential thrombocythemia with pseudo-hyperkalemia.

Essential thrombocythemia (ET) is a rare clonal stem cell disorder that affects the production of platelets in the bone marrow. This condition causes an overproduction of platelets, which can lead to blood clots and other complications. Potassium, on the other hand, is an essential mineral that plays a vital role in various bodily functions, including nerve impulses and muscle contractions. Here, in this case report, we investigated a case of pseudo-hyperkalemia caused by essential thrombocythemia in a 77-year-old woman with very high platelet counts. Moreover, this case report, which has no similar examples in the literature review, is important for clinicians.

Prolonged postoperative hypoaldosteronism related to hyperkalemia in patients with aldosterone-producing adenoma.

Hyperkalemia is developed in a part of patients with aldosterone-producing adenoma (APA) after adrenalectomy, suspected to be due to the insufficiency of aldosterone secretion. The purpose of this study is to determine the frequency and characteristics of prolonged postoperative hypoaldosteronism (PPHA) using chemiluminescent enzyme immunoassay (CLEIA). We studied 58 patients with APA with long time after adrenalectomy and whose PAC was measured using a CLEIA kit. The PAC value measured using CLEIA was significantly lower than that of using RIA between two consecutive visits before and after the shift of measuring method of PAC (median [interquantile range], 123.0 [99.8-164.0] vs. 39.5 [15.8-64.2] pg/mL, p < 0.01). PAC was below the minimum limit of quantification (4.0 pg/mL) of the CLEIA kit at least once in nine patients (15.5%) who had PPHA. The PPHA group were older (mean ± standard deviation, 61.3 ± 8.5 vs. 50.5 ± 10.1 years, p < 0.01) and had lower eGFR (60.3 ± 14.0 vs. 82.3 ± 22.8 mL/min/1.73 m2, p < 0.01) than the non-PPHA group. The frequency of postoperative hyperkalemia (maximum serum potassium >5.5 mEq/L) was higher in the PPHA group than in the non-PPHA group (55.6% vs. 8.2%, p < 0.01). In conclusion, a few patients with APA long time after adrenalectomy had unmeasurable PAC using CLEIA. PPHA is likely to develop in patients with APA after adrenalectomy who are older and have impaired renal function. Additionally, PPHA is related to the occurrence of postoperative hyperkalemia.

Pseudohyperkalemia in chronic lymphocytic leukemia: Prevalence, impact, and management challenges.

The term pseudohyperkalemia refers to a false elevation in serum potassium levels due to potassium release from cells in vitro. Falsely elevated potassium levels have been reported in patients with thrombocytosis, leukocytosis, and hematologic malignancies. This phenomenon has been particularly described in chronic lymphocytic leukemia (CLL). Leukocyte fragility, extremely high leukocyte counts, mechanical stress, higher cell membrane permeability related to an interaction with lithium heparin in plasma blood samples, and metabolite depletion due to a high leukocyte burden have been reported to contribute to pseudohyperkalemia in CLL. The prevalence of pseudohyperkalemia is up to 40%, particularly in the presence of a high leukocyte count (>50 × 109/L). The diagnosis of pseudohyperkalemia is often overlooked, which may result in unnecessary and potentially harmful treatment. The use of whole blood testing and point-of-care blood gas analysis, along with thorough clinical evaluation, may help differentiate between true and pseudohyperkalemic episodes.

Usefulness of Alternative Therapy with Hydrocortisone in the Postoperative Management of Severe Primary Aldosteronism.

Mineralocorticoid deficiency (MD) with hyperkalemia is an important complication of adrenalectomy in patients with primary aldosteronism (PA). We herein report a 52-year-old man with refractory hypertension, hypokalemia, and severe renal dysfunction due to PA caused by a right adrenal adenoma. His estimated glomerular filtration rate (eGFR) transiently increased immediately after adrenalectomy but then gradually declined, and he developed hyperkalemia. A postoperative endocrine examination revealed MD. Considering the patient's hypertension and severe renal dysfunction, we administered hydrocortisone instead of fludrocortisone, which improved the hyperkalemia and stopped the decline in the eGFR. Alternative therapy with hydrocortisone may be useful in such patients with MD.

Prognostic value of contralateral suppression on kidney function after surgery in patients with primary aldosteronism.

BACKGROUND AND OBJECTIVE: Adrenalectomy for primary aldosteronism (PA) has been associated with decreased kidney function after surgery. It has been proposed that elimination of excess aldosterone unmasks an underlying failure of the kidney function. Contralateral suppression (CLS) is considered a marker of aldosterone excess and disease severity, and the purpose of this study was to assess the hypothesis that CLS would predict change in kidney function after adrenalectomy in patients with PA. DESIGN AND PATIENTS: Patients with PA referred for adrenal venous sampling (AVS) between May 2011 and August 2021 and who were subsequently offered surgical or medical treatment were eligible for the current study. RESULTS: A total of 138 patients were included and after AVS 85/138 (61.6%) underwent adrenalectomy while 53/138 (38.4%) were treated with MR-antagonists. In surgically treated patients the estimated glomerular filtration rate (eGFR) was reduced by 11.5 (SD: 18.5) compared to a reduction of 5.9 (SD: 11.5) in medically treated patients (p = .04). Among surgically treated patients, 59/85 (69.4%) were classified as having CLS. After adrenalectomy, patients with CLS had a mean reduction in eGFR of 17.5 (SD: 17.6) compared to an increase of 1.8 (SD: 12.8) in patients without CLS (p < .001). The association between CLS and change in kidney function remained unchanged in multivariate analysis. Post-surgery, 16/59 (27.1%) patients with CLS developed hyperkalemia compared to 2/26 (7.7%) in patients without CLS (p = .04). CONCLUSION: This retrospective study found that CLS was a strong and independent predictor of a marked reduction of eGFR and an increased risk of hyperkalemia after adrenalectomy in patients with PA.

Brugada Phenocopy In Hyperkalaemia - A Rare Ecg Finding.

Hyperkalaemia is a potentially fatal clinical problem frequently seen in the emergency department (ED). It causes a spectrum of electrocardiogram (ECG) changes such as peaked T-waves, prolonged PR interval, widened QRS complexes, intraventricular/fascicular/bundle branch blocks, etc. Brugada Phenocopy (BrP) is a rare ECG finding seen in severe hyperkalaemia associated with the prevalence of malignant cardiac arrhythmias and all-cause mortality. Unlike Brugada Syndrome (BrS) it is a transient phenomenon and completely resolves with the normalization of hyperkalaemia. Here we report a Brugada Phenocopy (BrP) case observed in a middle-aged male with severe hyperkalaemia.

Dyskalemia in people at increased risk for heart failure: findings from the heart 'OMics' in AGEing (HOMAGE) trial.

AIMS: In people at risk of heart failure (HF) enrolled in the Heart 'OMics' in AGEing (HOMAGE) trial, spironolactone reduced circulating markers of collagen synthesis, natriuretic peptides, and blood pressure and improved cardiac structure and function. In the present report, we explored factors associated with dyskalaemia. METHODS AND RESULTS: The HOMAGE trial was an open-label study comparing spironolactone (up to 50 mg/day) versus standard care in people at risk for HF. After randomization, serum potassium was assessed at 1 and 9 months and was defined as low when ≤3.5 mmol/L (hypokalaemia) and high when ≥5.5 mmol/L (hyperkalaemia). Multivariable logistic regression models were constructed to identify clinical predictors of dyskalaemia. A total of 513 participants (median age 74 years, 75% men, median estimated glomerular filtration rate 71 mL/min/1.73 m2 ) had serum potassium available and were included in this analysis. At randomization, 88 had potassium < 4.0 mmol/L, 367 had potassium 4.0-5.0 mmol/L, and 58 had potassium > 5.0 mmol/L. During follow-up, on at least one occasion, a serum potassium < 3.5 mmol/L was observed in 6 (1.2%) and <4.0 mmol/L in 46 (9%) participants, while a potassium > 5.0 mmol/L was observed in 38 (8%) and >5.5 mmol/L in 5 (1.0%) participants. The median (percentile25-75 ) increase in serum potassium with spironolactone during the study was 0.23 (0.16; 0.29) mmol/L. Because of the low incidence of dyskalaemia, for regression analysis, hypokalaemia and hyperkalaemia thresholds were set at <4.0 and >5.0 mmol/L, respectively. The occurrence of a serum potassium > 5.0 mmol/L during follow-up was positively associated with the presence of diabetes mellitus {odds ratio [OR]: 1.21 [95% confidence interval (CI) 2.14; 3.79]} and randomization to spironolactone (OR: 2.83 [95% CI 1.49; 5.37]). Conversely, the occurrence of a potassium concentration < 4.0 mmol/L was positively associated with the use of thiazides (OR: 2.39 [95% CI 1.32; 4.34]), blood urea concentration (OR: 2.15 [95% CI 1.34; 3.39] per 10 mg/dL), and history of hypertension (OR: 2.32 [95% CI 1.02; 5.29]) and negatively associated with randomization to spironolactone (OR: 0.30 [95% CI 0.18; 0.52]). CONCLUSIONS: In people at risk for developing HF and with relatively normal renal function, spironolactone reduced the risk of hypokalaemia and, at the doses used, was not associated with the occurrence of clinically meaningful hyperkalaemia.

Moderate Hypothermic Circulatory Arrest Model in Rats: A New Model with Hyperkalemia-Induced Cardioplegia.

BACKGROUND: Moderate hypothermic circulatory arrest (MHCA) is a safe and effective method of cardiopulmonary bypass (CPB). However, most present rat models involve a deep hypothermic circulatory arrest, which cannot exactly reflect the clinical situation. The aim of this study was to establish a novel and safe rat model of MHCA with hyperkalemia-induced cardioplegia to study the pathophysiology of potential complications. METHODS: Ten adult male Sprague-Dawley rats (age, 16-18 weeks; weight, 450-550 g) were used. The entire CPB circuit consisted of a reservoir, peristaltic pump, membrane oxygenator, heat exchanger, and hemoconcentrator, all of which were connected via silicon tubing. The prime solution was approximately 19 mL. The right jugular vein, right femoral artery, and left femoral artery were cannulated. Blood was drained from the right atrium through the right jugular vein and perfused to the rats via the left femoral artery. CPB was commenced at a full flow rate. The rats were cooled to a rectal temperature of 25°C, and cardioplegia was induced by systemic hyperkalemia. After that, MHCA was carried out for 30 min. At the same time, system self-ultrafiltration was carried out to decrease the concentration of potassium by a hemoconcentrator. The circulatory arrest was followed by reperfusion and over 30 min of rewarming. CPB carefully was terminated. Blood in the circuit slowly was centrifuged for autotransfusion. Blood gas and hemodynamic parameters were recorded at each time point before CPB, before MHCA, at 10 min after the initiation of rewarming, and after CPB. RESULTS: All CPB and MHCA procedures successfully were achieved. One rat died of respiratory failure. Cardioplegia with systemic hyperkalemia was induced by 1 mL of 10% potassium chloride injected into the reservoir, and the concentration of potassium was maintained at 17 ± 3 mmol/L. Cardiac function and blood pressure were stable after the operation. CONCLUSIONS: A novel and safe rat model of MHCA with hyperkalemia-induced cardioplegia successfully was established.

Initial and terminal T wave angle as hyperkalemia indicator in chronic kidney disease.

BACKGROUND: Hyperkalemia is one prevalent complication in chronic kidney disease and is considered fatal since it potentially causes malignant arrhythmias and mortality. It is associated with electrocardiography (ECG) changes, such as peaked T wave in all ECG leads. However, the universal definition of the peaked T wave is still unclear, with low sensitivity and specificity. AIM: This study aims to determine the predictive value of initial and terminal T wave angle in detecting hyperkalemia among CKD patients. METHODS: A cross-sectional study was conducted at Dr. Soetomo General Hospital, including all adult hospitalized CKD patients. A caliper was used to measure T wave morphology. The initial deflection angle (Tia) and terminal deflection angle (Tta) were calculated from an arctan of T peak amplitude and the respective initial or terminal length. The receiver operating characteristics (ROC) curve was analyzed to determine the area under the curve (AUC) and optimal cutoff. RESULTS: A total of 220 CKD patients were enrolled in this study, with 98 patients with hyperkalemia (potassium >5.0). The majority of the patients were male, with a mean age of 51.12 ± 12.58 years. Ti-Tp duration, Tp-Tt duration, Tia, Tta, and Tp amplitude were significantly higher in the hyperkalemia group (all p < 0.05). A Spearman correlation analysis demonstrated a significant positive correlation of Tia (r = 0.346 and p < 0.001) and Tta (r = 0.445 and p < 0.001) with potassium levels in the participants. The optimal cutoff angle for Tta was 66.20° (sensitivity = 67.3% and specificity = 73.8%) and Tia was 61.07° (sensitivity = 66.3% and specificity = 69.7%). CONCLUSION: The terminal T wave angle outperformed the initial angle in predicting hyperkalemia in CKD patients.

Sodium and Potassium Dysregulation in the Patient With Cancer.

Sodium and potassium disorders are pervasive in patients with cancer. The causes of these abnormalities are wide-ranging, are often primary or second-order consequences of the underlying cancer, and have prognostic implications. The approach to hyponatremia should focus on cancer-related etiologies, such as syndrome of inappropriate antidiuretic hormone, to the exclusion of other causes. Hypernatremia in non-iatrogenic forms is generally due to water loss rather than excessive sodium intake. Debilitated or dependent patients with cancer are particularly vulnerable to hypernatremia. Hypokalemia can occur in patients with cancer due to gastrointestinal disturbances, resulting from decreased intake or increased losses. Renal losses can occur as a result of excessive mineralocorticoid secretion or therapy-related nephrotoxicity. The approach to hyperkalemia should be informed by historical and laboratory clues, and pseudohyperkalemia is particularly common in patients with hematological cancers. Hyperkalemia can be seen in primary or metastatic disease that interrupts the adrenal axis. It can also develop as a consequence of immunotherapy, which can cause adrenalitis or hypophysitis. Tumor lysis syndrome (TLS) is defined by the development of hyperkalemia and is a medical emergency. Awareness of the electrolyte abnormalities that can befall patients with cancer is vital for its prompt recognition and management.

Electrolytes disturbances in cancer patients.

PURPOSE OF REVIEW: Hypernatremia, hyperphosphatemia, hypocalcaemia, hyperkalaemia and hypermagnesemia are electrolytes disturbances that can arise in cancer patients in relation to unique causes that are related to the cancer itself or its treatment and can lead to delay or interruption of cancer therapy. This article summarizes these main causes, the proposed pathophysiology and the recommended management for these disturbances. RECENT FINDINGS: There have been many cancer drugs approved in the field of oncology over the past several years and a subset of these drugs have been associated with electrolytes disturbances. This includes, for example, immune checkpoint inhibitor related hyperkalemia, fibroblast growth factor 23 inhibitor associated hyperphosphatemia and epidermal growth factor receptor inhibitor associated hypomagnesemia and hypocalcaemia. SUMMARY: This article provides an updated review of certain electrolytes disturbance in cancer patients and allows clinicians to have a greater awareness and knowledge of these electrolyte abnormalities in efforts to early recognition and timely management.

[Pseudohyperkalemia: clinical chemistry for the clinician]. / Pseudohyperkaliëmie: klinische chemie voor clinici.

BACKGROUND: Hyperkalemia is an electrolyte disorder requiring medical attention because it can cause cardiac arrhythmias. Pseudohyperkalemia is the phenomenon of an elevated potassium concentration that is present in the blood sample but not in the patient. Pseudohyperkalemia can be caused by hemolysis, leukocytosis, thrombocytosis, seasonal pseudohyperkalemia, potassium release from muscle cells due to fist clenching during venipuncture, and contamination due to blood withdrawal from an intravenous line over which potassium was administered. Rarer causes include EDTA contamination and familial pseudohyperkalemia. CASE DESCRIPTION: A 23-year old woman was admitted with ascites due to polycythemia vera and essential thrombocytosis for which hydroxycarbamide was started. The reported serum potassium concentrations were 6.1 and 6.8 mmol/l. The use of spironolactone was discontinued and she was treated with sodium polystyrene sulfonate and insulin-glucose infusion. The serum potassium concentration only decreased on the ninth day of admission, when the thrombocyte count was normalizing. A diagnosis of pseudohyperkalemia due to thrombocytosis was established. CONCLUSION: Knowledge of the causes of pseudohyperkalemia and interaction between the clinician and clinical chemist aids in the differentiation between true hyperkalemia and pseudohyperkalemia and may prevent unnecessary diagnostics and harmful treatment.

Experience with the potassium binder patiromer in hyperkalaemia management in heart failure patients in real life.

AIMS: Hyperkalaemia (HK) is common in heart failure (HF) patients, related to renal dysfunction and medical treatment. It limits medical therapy optimization, which impacts prognosis. New potassium (K) binders help control HK, allowing better medical management of HF. METHODS AND RESULTS: A retrospective multicentre register included all outpatients with HF and HK (K ≥ 5.1 mEq/L) treated with patiromer according to current recommendations. We evaluated analytic and clinical parameters before starting the treatment and at 7, 30 and 90 days, as well as adverse events related to patiromer and treatment optimization. We included 74 patients (71.6% male) with a mean age of 70.8 years (SD 9.2). Sixty-seven patients (90.5%) presented HK in the previous year. Forty patients (54.1%) underwent down-titration of a renin-angiotensin-aldosterone inhibitor (RAASi) or a mineralocorticoid receptor antagonist (MRA), and 27 (36.5%) stopped any of them due to HK. Initial K was 5.5 mEq/L (SD 0.6), with a significantly reduction at 7 days (4.9 mEq/L (SD 0.8); P < 0.001), maintained at 90 days (4.9 mEq/L (SD 0.8); P < 0.001). There were no other electrolyte disturbances, with a slight improvement in renal function [glomerular filtration rate 39.6 mL/min (SD 20.4) to 42.7 mL/min (SD 23.2); P = 0.005]. Adverse events were reported in 33.9% of patients, the most common being hypomagnesaemia (16.3%), gastrointestinal disturbances (14.9%) and HK (2.8%). Withdrawal of patiromer was uncommon (12.2%) due to gastrointestinal disturbances in 66.7% of cases. Nine patients (12.2%) started on a RAASi, and 15 patients (20.3%) on an MRA during the follow-up. Forty-five patients (60.8%) increased the dose of RAASi or MRA, increasing to target doses in 5.4 and 10.8% of patients, respectively. At 90 days, NTproBNP values were reduced from 2509.5 pg/mL [IQR 1311-4,249] to 1396.0 pg/mL [IQR 804-4263]; P = 0.003, but the reduction was only observed in those who optimized HF medical treatment [NTproBNP from 1950.5 pg/mL (IQR 1208-3403) to 1349.0 pg/mL (IQR 804-2609); P < 0.01]. NYHA functional class only improved in 7.5% of patients, corresponding with those who optimized HF medical treatment. Compared with the previous 3 months before patiromer treatment, the rate of hospitalization was reduced from 28.4 to 10.9% (P < 0.01), and the emergency room visits from 18.9 to 5.4% (P < 0.01). CONCLUSIONS: In a real-life cohort of patients with HF, patiromer reduced and maintained K levels during 3 months of follow-up. The most common adverse events were hypomagnesaemia and gastrointestinal disturbances. Patiromer helps optimize medical treatment, increasing the percentage of patients treated with RAASi and MRA at target doses. At the end of follow-up, natriuretic peptides values and hospital visits were reduced, suggesting the benefit of optimizing HF medical treatment.