Potassium Homeostasis Research Articles

Effects of sodium glucose cotransporter 2 inhibitors on the risk of hyperkalemia in patients on mineralocorticoid receptor antagonist: a systematic review and meta-analysis

Abstract Background Occurrence of hyperkalemia has been a great limitation in the full implementation of a guideline-directed medical therapy especially in patients with heart failure. Recent developments have exhibited the positive role of SGLT2 inhibitors, not only on the cardiovascular outcomes but also conferred renal protection. Purpose We explored the effects of SGLT2i and MRA combination on the risk of developing hyperkalemia. Methods Randomized controlled trials on SGLT2i versus placebo in patients already on MRA regardless of heart failure status reporting outcomes of potassium homeostasis were searched using Pubmed, CENTRAL, and ScienceDirect. Outcome of interest was the effects on the risk of hyperkalemia. Pooled hazard ratios with 95% confidence intervals were used as effect estimates using fixed-effects model. Results Four studies were included with a total of 8,996 patients. There was a significant reduction on the risk of hyperkalemia in the MRA with SGLT2i group (HR 0.53, 95% CI 0.39–0.73, p<0.0001) compared to MRA without SGLT2i group. Conclusion SGLT2i provides significant risk reduction on the development of hyperkalemia in patients already on a mineralocorticoid receptor antagonist. Funding Acknowledgement Type of funding sources: None.

A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls

A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls

Assessing potassium levels in critically ill patients with heart failure: application of a group-based trajectory model.

Abnormalities in potassium homeostasis are frequently seen in hospitalized patients. A poor outcome in heart failure (HF) has been linked to both hypokalaemia and hyperkalaemia. The studies on the connection between variations in potassium levels and all-cause mortality remain scarce. We delineated trajectories of potassium levels and investigated the association of these trajectories with all-cause mortality of critically ill patients with HF. A retrospective analysis of blood potassium levels (9 times) in patients with HF after being admitted to the intensive care unit (ICU). Potassium levels were divided into three groups according to the first serum potassium level in ICU and thereafter categorized as follows: hypokalaemia group (n=336) (<3.5mmol/L), normal blood potassium-level group (n=3322) (3.5-5.0mmol/L), and hyperkalaemia group (n=395) (>5.0mmol/L). According to the group-based trajectory modelling (GBTM), the hyperkalaemia group and the normal blood potassium-level group can be divided into three trajectory groups: the low-level stable group, the medium-level stable group, and the high-level decline group. The hypokalaemia group can be divided into two trajectory groups: the low-level rise group and the high-level rise group. A total of 4053 HF patients were included (mean age 71.81±13.12years, 54.90% males, 45.10% females). After adjusting for possible confounding variables, in the hyperkalaemia group, the low-level stable group had lower 28day [high-level decline group vs. low-level stable group hazard ratio (HR), 95% confidence interval (CI): 2.917, 1.555-5.473; P<0.05] and 365day (high-level decline group vs. low-level stable group HR, 95% CI: 2.854, 1.820-4.475; P<0.05) all-cause mortality. In the normal blood potassium-level group, the medium-level stable group had lower 28day (medium-level stable group vs. low-level stable group HR, 95% CI: 0.776, 0.657-0.918; P<0.05) and 365day (medium-level stable group vs. low-level stable group HR, 95% CI: 0.827, 0.733-0.934; P<0.05) all-cause mortality. In the hypokalaemia group, the cumulative survival of the high-level rise group and the low-level rise group did not differ significantly. Critically ill patients with HF have blood potassium trajectories. And the trajectories are associated with all-cause mortality for hyperkalaemia and normal blood potassium-level patients. GBTM is a granular method to describe the evolution of blood potassium, which may increase the current knowledge of blood potassium-level adjustment.

The Role of Urinary Potassium Examination on the Progressivity of Chronic Kidney Disease: A Narrative Literature Review

Kidneys play an important role in potassium homeostasis. The important role of the kidneys in maintaining potassium balance is reflected in the high level of potassium disturbances in patients with decreased kidney function, especially patients with severely decreased renal function and patients who have comorbidities, such as diabetes, hypertension, or heart failure. Chronic kidney disease is characterized by abnormalities of kidney structure or function that persist for more than 3 months, have many complex causes, and have a major impact on global health status. There are several methods to measure the amount of potassium intake consumed, including a food frequency questionnaire, dietary recall, temporary urine potassium examination, and 24-hour urine potassium examination. The standard gold measurement for evaluating urinary potassium excretion is through 24-hour urine collection. This literature review aims to describe the role of urinary potassium excretion in assessing the progression of chronic kidney disease.

Aldosterone as a Mediator of Cardiovascular Damage.

Besides the physiological regulation of water, sodium, and potassium homeostasis, aldosterone modulates several physiological and pathological processes in the cardiovascular system. At the vascular level, aldosterone excess stimulates endothelial dysfunction and infiltration of inflammatory cells, enhances the development of the atherosclerotic plaque, and favors plaque instability, arterial stiffness, and calcification. At the cardiac level, aldosterone increases cardiac inflammation, fibrosis, and myocardial hypertrophy. As a clinical consequence, high aldosterone levels are associated with enhanced risk of cardiovascular events and mortality, especially when aldosterone secretion is inappropriate for renin levels and sodium intake, as in primary aldosteronism. Several clinical trials showed that mineralocorticoid receptor antagonists reduce cardiovascular mortality in patients with heart failure and reduced ejection fraction, but inconclusive results were reported for other cardiovascular conditions, such as heart failure with preserved ejection fraction, myocardial infarction, and atrial fibrillation. In patients with primary aldosteronism, adrenalectomy or treatment with mineralocorticoid receptor antagonists significantly mitigate adverse aldosterone effects, reducing the risk of cardiovascular events, mortality, and incident atrial fibrillation. In this review, we will summarize the major preclinical and clinical studies investigating the cardiovascular damage mediated by aldosterone and the protective effect of mineralocorticoid receptor antagonists for the reduction of cardiovascular risk in patients with cardiovascular diseases and primary aldosteronism.

Transcriptome-Wide Analysis Revealed the Potential of the High-Affinity Potassium Transporter (HKT) Gene Family in Rice Salinity Tolerance via Ion Homeostasis.

The high-affinity potassium transporter (HKT) genes are key ions transporters, regulating the plant response to salt stress via sodium (Na+) and potassium (K+) homeostasis. The main goal of this research was to find and understand the HKT genes in rice and their potential biological activities in response to brassinosteroids (BRs), jasmonic acid (JA), seawater, and NaCl stress. The in silico analyses of seven OsHKT genes involved their evolutionary tree, gene structures, conserved motifs, and chemical properties, highlighting the key aspects of OsHKT genes. The Gene Ontology (GO) analysis of HKT genes revealed their roles in growth and stress responses. Promoter analysis showed that the majority of the HKT genes participate in abiotic stress responses. Tissue-specific expression analysis showed higher transcriptional activity of OsHKT genes in roots and leaves. Under NaCl, BR, and JA application, OsHKT1 was expressed differentially in roots and shoots. Similarly, the induced expression pattern of OsHKT1 was recorded in the seawater resistant (SWR) cultivar. Additionally, the Na+ to K+ ratio under different concentrations of NaCl stress has been evaluated. Our data highlighted the important role of the OsHKT gene family in regulating the JA and BR mediated rice salinity tolerance and could be useful for rice future breeding programs.

Hyperkalemia in Chronic Kidney Disease: Links, Risks and Management.

Hyperkalemia is a common clinical problem with potentially fatal consequences. The prevalence of hyperkalemia is increasing, partially due to wide-scale utilization of prognostically beneficial medications that inhibit the renin-angiotensin-aldosterone-system (RAASi). Chronic kidney disease (CKD) is one of the multitude of risk factors for and associations with hyperkalemia. Reductions in urinary potassium excretion that occur in CKD can lead to an inability to maintain potassium homeostasis. In CKD patients, there are a variety of strategies to tackle acute and chronic hyperkalemia, including protecting myocardium from arrhythmias, shifting potassium into cells, increasing potassium excretion from the body, addressing dietary intake and treating associated conditions, which may exacerbate problems such as metabolic acidosis. The evidence base is variable but has recently been supplemented with the discovery of novel oral potassium binders, which have shown promise and efficacy in studies. Their use is likely to become widespread and offers another tool to the clinician treating hyperkalemia. Our review article provides an overview of hyperkalemia in CKD patients, including an exploration of relevant guidelines and nuances around management.

Kir5.1 channels: potential role in epilepsy and seizure disorders.

Inwardly rectifying potassium (Kir) channels are broadly expressed in many mammalian organ systems, where they contribute to critical physiological functions. However, the importance and function of the Kir5.1 channel (encoded by the KCNJ16 gene) have not been fully recognized. This review focuses on the recent advances in understanding the expression patterns and functional roles of Kir5.1 channels in fundamental physiological systems vital to potassium homeostasis and neurological disorders. Recent studies have described the role of Kir5.1-forming Kir channels in mouse and rat lines with mutations in the Kcnj16 gene. The animal research reveals distinct renal and neurological phenotypes, including pH and electrolyte imbalances, blunted ventilatory responses to hypercapnia/hypoxia, and seizure disorders. Furthermore, it was confirmed that these phenotypes are reminiscent of those in patient cohorts in which mutations in the KCNJ16 gene have also been identified, further suggesting a critical role for Kir5.1 channels in homeostatic/neural systems health and disease. Future studies that focus on the many functional roles of these channels, expanded genetic screening in human patients, and the development of selective small-molecule inhibitors for Kir5.1 channels, will continue to increase our understanding of this unique Kir channel family member.

Hydrogen Sulfide Modulates Salinity Stress in Common Bean Plants by Maintaining Osmolytes and Regulating Nitric Oxide Levels and Antioxidant Enzyme Expression

The purpose of the present study is to investigate the role of hydrogen sulfide (H2S), in improving resistance to common bean salt stress. Method shows that common bean seeds were soaked in water and in two concentrations of sodium hydrosulfide (50 and 100 µM) for 8 h. After 25 days from sowing, the pots were irrigated with water and with two concentrations of NaCl (75 and 150 mM) until the end of the experiment. Results revealed that H2S relieved salt stress by decreasing growth inhibition and photosynthetic characteristics, and increasing osmolyte contents (proline and glycine betaine). Furthermore, H2S reduced oxidative damage by lowering lipid peroxidation, electrolyte leakage, and reactive oxygen species production such as hydrogen peroxide, hydroxyl radicals, and superoxide anion by increasing non-enzymatic antioxidants such as ascorbic acid and glutathione, as well as enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX), glutathione reductase (GR), and nitrate reductase (NR). Meanwhile, salt stress and H2S application increased the endogenous level of H2S, which was accompanied by an increase in nitric oxide concentration. H2S, in particular, maintained sodium (Na+) and potassium (K+) homeostasis in the presence of excess NaCl. In general, H2S effectively reduced oxidative stress in common bean plants by increasing relative expression levels of copper-zinc superoxide dismutase (Cu-ZnSOD), CAT, and glutathione S-transferase (GST). Applying H2S to common bean plants could protect them from salinity stress by maintaining the Na+/K+ balance, boosting endogenous H2S and nitric oxide levels, and preventing oxidative damage by increasing antioxidant activity.

A quantitative systems pharmacology model of plasma potassium regulation by the kidney and aldosterone.

Plasma potassium regulation within a narrow range is vital for life. The risk for hyperkalemia increases when kidney function is impaired and with therapeutic interventions such as mineralocorticoid receptor antagonists (MRAs). The kidney maintains potassium homeostasis by matching potassium intake and excretion, in part through the action of aldosterone. A mechanistic mathematical model was developed and used to investigate the effect of renal impairment and MRAs on plasma potassium levels. The model describes renal potassium filtration, reabsorption, and secretion along the nephron; potassium-aldosterone regulatory feedbacks; whole body potassium balance; and the pharmacologic effects of MRAs. The model was calibrated by fitting (1) the plasma potassium and aldosterone response to potassium infusion in humans on high/low potassium diets, and (2) the acute potassium excretion response to spironolactone. The model was validated by predicting steady-state plasma potassium with sustained spironolactone treatment in hyperaldosteronism patients. The model was then used to demonstrate that (1) declining renal function alone has a small effect on plasma potassium for GFR > 30ml/min, but an increasing effect as GFR approaches end stage renal disease (GFR ~ 15ml/min) (2) the effect of increasing potassium intake has minimal effect at normal GFRs but increasing effect on plasma potassium as GFR declines, and 3) MRAs have a minor effect on plasma potassium when GFR is normal, but cause larger increases as GFR falls below 60ml/min. This model provides a quantitative framework for investigating integrated impacts of diseases and therapies in this complex system.

Ion-Selective Electrodes for Measuring Potassium in Erythrocytes: a Model for Clinical Interpretation of the Results (a Pilot Study).

Potassium content in erythrocytes was measured using a blood gas analyzer with ion-selective electrodes in parallel with the laboratory procedure. Patients from intensive care units were randomly selected for the study. No correlations of potassium with other plasma parameters have been found, however its buffer dependence on chlorine in plasma has been established. Minimal value of potassium concentration in erythrocytes (for 356 measurements) was 68.2 mmol/L, maximal - 210.2 mmol/L.Following the logic of the acid-base status, a nomogram for clinical interpretation of intracellular potassium homeostasis has been developed. The low values are mainly connected with the deficit of potassium which is impossible to determine in blood plasma (e.g. in severe metabolic alkalosis or diuretic therapy). The elevated concentration of potassium in erythrocytes is caused by eryptosis: released potassium is absorbed by normal erythrocytes (protection from hyperkalaemia). So, the increased concentration of potassium indicates directly the presence of eryptosis triggers, i.e. inflammatory mediators, oxidative stress, and others, for example in sepsis. The results of the study have shown that measurement of potassium concentration in erythrocytes with the help of ion-selective electrodes is an effective method of monitoring its intracellular homeostasis. Potassium in erythrocytes is an independent biological marker which can provide clinically relevant information.

Approach to Hyperkalemia

Hyperkalemia is one of the most common electrolytic disorders encountered in clinical practice. Serum potassium concentration is tightly regulated by cellular transfer via insulin, catecholamines, and acid-base equilibrium and secondarily by the kidney via aldosterone and renal flow. Severe hyperkalemia can result in dangerous and potentially life-threatening manifestations, mainly cardiac in nature. It is therefore crucial for physicians to be able to identify the causes of hyperkalemia and provide appropriate treatment. This approach article provides an overview of potassium homeostasis, diagnostic strategies, and treatment guidelines for patients with mild, moderate, and severe hyperkalemia.

Potassium homeostasis: sensors, mediators, and targets.

Transmembrane potassium (K) gradients are key determinants of membrane potential that can modulate action potentials, control muscle contractility, and influence ion channel and transporter activity.Daily K intake is normally equal to the amount of K in the entire extracellular fluid (ECF) creating a critical challenge - how to maintain ECF [K] and membrane potential in a narrow range during feast and famine.Adaptations to maintain ECF [K] include sensing the K intake, sensing ECF [K] vs. desired set-point and activating mediators that regulate K distribution between ECF and ICF, and regulate renal K excretion. In this focused review, we discuss the basis of these adaptions, including (1) potential mechanisms for rapid feedforward signaling to kidney and muscle after a meal (before a rise in ECF [K]), (2) how skeletal muscles sense and respond to changes in ECF [K], (3) effects of K on aldosterone biosynthesis, and (4) how the kidney responds to changes in ECF [K] to modify K excretion. The concepts of sexual dimorphisms in renal K handling adaptation are introduced, and the molecular mechanisms that can account for the benefits of a K-rich diet to maintain cardiovascular health are discussed. Although the big picture of K homeostasis is becoming more clear, we also highlight significant pieces of the puzzle that remain to be solved, including knowledge gaps in our understanding of initiating signals, sensors and their connection to homeostatic adjustments of ECF [K].

Structural basis for c-di-AMP–dependent regulation of the bacterial stringent response by receptor protein DarB

The bacterial second messenger c-di-AMP controls essential cellular processes, including potassium and osmolyte homeostasis. This makes synthesizing enzymes and components involved in c-di-AMP signal transduction intriguing as potential targets for drug development. The c-di-AMP receptor protein DarB of Bacillus subtilis binds the Rel protein and triggers the Rel-dependent stringent response to stress conditions; however, the structural basis for this trigger is unclear. Here, we report crystal structures of DarB in the ligand-free state and of DarB complexed with c-di-AMP, 3′3′-cGAMP, and AMP. We show that DarB forms a homodimer with a parallel, head-to-head assembly of the monomers. We also confirm the DarB dimer binds two cyclic dinucleotide molecules or two AMP molecules; only one adenine of bound c-di-AMP is specifically recognized by DarB, while the second protrudes out of the donut-shaped protein. This enables DarB to bind also 3′3′-cGAMP, as only the adenine fits in the active site. In absence of c-di-AMP, DarB binds to Rel and stimulates (p)ppGpp synthesis, whereas the presence of c-di-AMP abolishes this interaction. Furthermore, the DarB crystal structures reveal no conformational changes upon c-di-AMP binding, leading us to conclude the regulatory function of DarB on Rel must be controlled directly by the bound c-di-AMP. We thus derived a structural model of the DarB–Rel complex via in silico docking, which was validated with mass spectrometric analysis of the chemically crosslinked DarB–Rel complex and mutagenesis studies. We suggest, based on the predicted complex structure, a mechanism of stringent response regulation by c-di-AMP.

The transcription factor OsMYBc and an E3 ligase regulate expression of a K+ transporter during salt stress.

Sodium (Na+) and potassium (K+) homeostasis is essential for plant survival in saline soils. A member of the High-Affinity K+ Transporter (HKT) family in rice (Oryza sativa), OsHKT1;1, is a vital regulator of Na+ exclusion from shoots and is bound by a MYB transcription factor (OsMYBc). Here, we generated transgenic rice lines in the oshkt1;1 mutant background for genetic complementation using genomic OsHKT1;1 containing a native (Com) or mutated (mCom) promoter that cannot be bound by OsMYBc. In contrast to wild-type (WT) or Com lines, the mCom lines were not able to recover the salt-sensitive phenotype of oshkt1;1. The OsMYBc-overexpressing plants were more tolerant to salt stress than WT plants. A yeast two-hybrid screen using the OsMYBc N-terminus as bait identified a rice MYBc stress-related RING finger protein (OsMSRFP). OsMSRFP is an active E3 ligase that ubiquitinated OsMYBc in vitro and mediated 26S proteasome-mediated degradation of OsMYBc under semi-in vitro and in vivo conditions. OsMSRFP attenuated OsMYBc-mediated OsHKT1;1 expression, and knockout of OsMSRFP led to rice salt tolerance. These findings uncover a regulatory mechanism of salt response that fine-tunes OsHKT1;1 transcription by ubiquitination of OsMYBc.

Review of the Pathophysiologic and Clinical Aspects of Hypokalemia in Children and Young Adults: an Update.

This article examines the regulatory function of the skeletal muscle, renal, and adrenergic systems in potassium homeostasis. The pathophysiologic bases of hypokalemia, systematic approach for an early diagnosis, and therapeutic strategy to avert life-threatening complications are highlighted. By promoting skeletal muscle uptake, intense physical exercise (post), severe trauma, and several toxins produce profound hypokalemia. Hypovolemia due to renal and extra-renal fluid losses and ineffective circulation activate secondary aldosteronism causing urinary potassium wasting. In addition to hypokalemic alkalosis, primary aldosteronism causes low-renin hypertension. Non-aldosterone mineralocorticoid activation leading to low-renin and low-aldosterone hypertension occurs in Liddle’s syndrome and apparent mineralocorticoid excess. Although there is enzymatic inhibition of cortisol synthesis in congenital adrenal hyperplasia, precursors of aldosterone produce low-renin hypokalemic hypertension. In addition to the glucocorticoid effect, hypercortisolism activates mineralocorticoid receptors in Cushing’s syndrome. Genetic mutations involving furosemide-sensitive Na+-K+-2Cl− co-transporters and thiazide-sensitive Na+-Cl− transporters result in (non-hypertensive) salt-wasting nephropathy. Proximal and distal renal tubular acidosis is associated with hypokalemia. Eating disorders causing hypokalemia include bulimia, laxative abuse, and diuretic misuse. Low urinary potassium (<15 mmol/day) and/or low urinary chloride (<20 mol/L) suggest a gastrointestinal pathology. Co-morbidity of hypokalemia with chronic pulmonary and cardiovascular diseases may increase the fatality rate.

Contribution of Exogenous Proline to Abiotic Stresses Tolerance in Plants: A Review.

Abiotic stresses are the major environmental factors that play a significant role in decreasing plant yield and production potential by influencing physiological, biochemical, and molecular processes. Abiotic stresses and global population growth have prompted scientists to use beneficial strategies to ensure food security. The use of organic compounds to improve tolerance to abiotic stresses has been considered for many years. For example, the application of potential external osmotic protective compounds such as proline is one of the approaches to counteract the adverse effects of abiotic stresses on plants. Proline level increases in plants in response to environmental stress. Proline accumulation is not just a signal of tension. Rather, according to research discussed in this article, this biomolecule improves plant resistance to abiotic stress by rising photosynthesis, enzymatic and non-enzymatic antioxidant activity, regulating osmolyte concentration, and sodium and potassium homeostasis. In this review, we discuss the biosynthesis, sensing, signaling, and transport of proline and its role in the development of various plant tissues, including seeds, floral components, and vegetative tissues. Further, the impacts of exogenous proline utilization under various non-living stresses such as drought, salinity, high and low temperatures, and heavy metals have been extensively studied. Numerous various studies have shown that exogenous proline can improve plant growth, yield, and stress tolerance under adverse environmental factors.

MO324: Serum Potassium Trajectory During AKI and Mortality Risk

Abstract BACKGROUND AND AIMS Kidneys play a primary role in potassium homeostasis. The association between potassium (sK+) level and mortality or the need for kidney replacement therapy (KRT) during acute kidney injury (AKI) has not been adequately explored. METHOD In this prospective cohort study, AKI patients admitted to the Hospital Civil de Guadalajara were enrolled from August 2017 to June 2021 with AKI. We divided patients into eight groups based on the serum potassium level trajectories up to 10 days following hospitalization: (1) normokalemia (normoK), defined as sK + values between 3.5 and 5.5 mEq/L; (2) corrected hyperkalemia (hyperK), sK+ &amp;gt; 5.5 mEq/L on hospital admission and decreased to normoK; (3) corrected hypokalemia (hypoK), sK+ &amp;lt; 3.5 mEq/L on hospital admission and increased to normoK; (4) fluctuating potassium, sK + increased/decreased in and out of normoK parameters; (5) uncorrected hypoK, sK+ &amp;lt; 3.5 mEq/L; (6) normoK to hypoK, sK + that were normal on hospital admission and decreased to hypoK and never went back to normal; (7) normoK to hyperK, sK + that were normal on hospital admission and increased to hyperK and never went back to normal; and (8) uncorrected hyperK, sK+ &amp;gt; 5.5 mEq/L. We assessed the association of serum potassium trajectories with mortality and the need for KRT (secondary objective). RESULTS A total of 311 AKI patients were included. The mean age was 52.6 years, and 182 (58.6%) were male. AKI stage 3 was present in 199 (63.9%). KRT started in 112 (36%) patients, and 66 patients (21.2%) were died. After adjusting for confounders, 10-day hospital mortality was significantly higher in group 7 and 8 (OR 1.37 and 1.63; P = &amp;lt; .05 for both, respectively), and KRT initiation was higher only in group 8 (OR 1.40; P = &amp;lt; .05) compared with group 1. Mortality in different subgroups of patients in group 8 did not change the primary results. CONCLUSION In our prospective cohort, most patients with AKI had alterations in sK + . NormoK to hyperK and uncorrected hyperK were associated with death, while only uncorrected hyperK was correlated with the need for KRT.

Candida albicans Potassium Transporters.

Potassium is basic for life. All living organisms require high amounts of intracellular potassium, which fulfils multiple functions. To reach efficient potassium homeostasis, eukaryotic cells have developed a complex and tightly regulated system of transporters present both in the plasma membrane and in the membranes of internal organelles that allow correct intracellular potassium content and distribution. We review the information available on the pathogenic yeast Candida albicans. While some of the plasma membrane potassium transporters are relatively well known and experimental data about their nature, function or regulation have been published, in the case of most of the transporters present in intracellular membranes, their existence and even function have just been deduced because of their homology with those present in other yeasts, such as Saccharomyces cerevisiae. Finally, we analyse the possible links between pathogenicity and potassium homeostasis. We comment on the possibility of using some of these transporters as tentative targets in the search for new antifungal drugs.

Severe Hypokalemic Myopathy With Very High Creatine Kinase as the First Manifestation of Primary Hyperaldosteronism - An Unusual Presentation of a Rare Disorder

Hypokalemia is one of the most common electrolyte imbalances to be encountered in clinical practice. The kidney is the primary actor that maintains long term potassium homeostasis and regulates serum level around a narrow range of 3.5-5.5mmol/L. There is a long list of common causes for hypokalemia; apart from these, rare diseases should not slip our mind while treating such a case. Regarding clinical features, muscular weakness accounts for a common one; however occasionally, severe hypokalemia can cause myopathy and/or rhabdomyolysis. Here, we present the case of a middle-aged man, who brought up to us with severe muscular weakness owing tohypokalemia; which was later found to be the rare clinical entity of a rare disorder - primary hyperaldosteronism (PH). In this article, we as well focused on the pathophysiological basis ofPH and hypokalemia leading to myopathy. Bangladesh J Medicine 2022; 33: 224-228