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Background: Potassium (K) is an essential nutrient for plant growth and development. Maize (Zea mays) is a widely planted crops in the world and requires a huge amount of K fertilizer. Arbuscular mycorrhizal fungi (AMF) are closely related to the K uptake of maize. Genetic improvement of maize K utilization efficiency will require elucidating the molecular mechanisms of maize K uptake through the mycorrhizal pathway. Here, we employed transcriptome and gene family analysis to elucidate the mechanism influencing the K uptake and utilization efficiency of mycorrhizal maize. Methods and results: The transcriptomes of maize were studied with and without AMF inoculation and under different K conditions. AM symbiosis increased the K concentration and dry weight of maize plants. RNA sequencing revealed that genes associated with the activity of the apoplast and nutrient reservoir were significantly enriched in mycorrhizal roots under low-K conditions but not under high-K conditions. Weighted gene correlation network analysis revealed that three modules were strongly correlated with K content. Twenty-one hub genes enriched in pathways associated with glycerophospholipid metabolism, glycerolipid metabolism, starch and sucrose metabolism, and anthocyanin biosynthesis were further identified. In general, these hub genes were upregulated in AMF-colonized roots under low-K conditions. Additionally, the members of 14 gene families associated with K obtain were identified (ARF: 38, ILK: 4, RBOH: 12, RUPO: 20, MAPKK: 89, CBL: 14, CIPK: 44, CPK: 40, PIN: 10, MYB: 174, NPF: 79, KT: 19, HAK/HKT/KUP: 38, and CPA: 8) from maize. The transcript levels of these genes showed that 92 genes (ARF:6, CBL:5, CIPK:13, CPK:2, HAK/HKT/KUP:7, PIN:2, MYB:26, NPF:16, RBOH:1, MAPKK:12 and RUPO:2) were upregulated with AM symbiosis under low-K conditions. Conclusions: This study indicated that AMF increase the resistance of maize to low-K stress by regulating K uptake at the gene transcription level. Our findings provide a genome-level resource for the functional assignment of genes regulated by K treatment and AM symbiosis in K uptake-related gene families in maize. This may contribute to elucidate the molecular mechanisms of maize response to low K stress with AMF inoculation, and provided a theoretical basis for AMF application in the crop field. [ABSTRACT FROM AUTHOR]

We aimed to evaluate the utility of simple, cost-effective, and non-invasive strategies alternative to BIPSS and peripheral CRH stimulation in differential diagnosis of ACTH-dependent CS. First, we performed ROC analysis to evaluate the performance of various tests for differential diagnosis of ACTH-dependent CS in our cohort (CD, n=76 and EAS, n=23) and derived their optimal cut-offs. Subsequently, combining various demographic (gender), clinical (hypokalemia), biochemical (plasma ACTH, HDDST, peripheral CRH stimulation) and imaging (MRI pituitary) parameters, we derived non-invasive models with 100% PPV for CD. Patients with pituitary macroadenoma (n=14) were excluded from the analysis involving non-invasive models. Relative percent ACTH (AUC: 0.933) and cortisol (AUC: 0.975) increase on peripheral CRH stimulation demonstrated excellent accuracy in discriminating CD from EAS. Best cut-offs for CD were plasma ACTH<97.3 pg/ml, HDDST≥57% cortisol suppression, CRH stimulation≥77% ACTH increase and≥11% cortisol increase. We derived six models that provided 100% PPV for CD and precluded the need for BIPPS in 35/85 (41.2%) patients with ACTH-dependent CS and no macroadenoma (in whom BIPSS would have otherwise been recommended). The first three models included basic parameters and avoided both peripheral CRH stimulation and BIPSS in 19 (22.4%) patients, while the next three models included peripheral CRH stimulation and avoided BIPSS in another 16 (18.8%) patients. Using simple and non-invasive alternative strategies, BIPSS can be avoided in 41% and peripheral CRH stimulation in 22% of patients with ACTH-dependent CS and no macroadenoma; such patients can be directly referred for a pituitary surgery. [ABSTRACT FROM AUTHOR]

Aim: This study was designed to investigate the association between Charlson Comorbidity Index (CCI) and in‐hospital mortality and other clinical outcomes among patients with hyperglycemic crises. Method: This retrospective cohort study was conducted using data from electric medical records. A total of 1668 diabetic patients with hyperglycemic crises from six tertiary hospitals met the inclusion criteria. CCI < 4 was defined as low CCI and CCI ≥ 4 was defined as high CCI. Propensity score matching (PSM) with the 1:1 nearest neighbour matching method and the caliper value of 0.02 was used to match the baseline characteristics of patients with high CCI and low CCI to reduce the confounding bias. In‐hospital mortality, ICU admission, hypoglycemia, hypokalemia, acute kidney injury, length of stay (LOS), and hospitalisation expense between low CCI and high CCI were compared and assessed. Univariate and multivariate regression were applied to estimate the impact of CCI on in‐hospital and other clinical outcomes. Outcome: One hundred twenty‐one hyperglycemic crisis (HC) patients died with a mortality rate of 7.3%. After PSM, compared with low CCI, patients with high CCI suffered higher in‐hospital mortality, ICU admission, LOS, and hospitalisation expenses. After multivariate regression, age (aOR: 1.12, 95% confidence interval [CI]: 1.06−1.18, p < 0.001), CCI(aOR: 4.42, 95% CI: 1.56−12.53, p = 0.005), uninsured (aOR: 22.32, 95% CI: 4.26−116.94, p < 0.001), shock (aOR: 10.57, 95% CI: 1.41−79.09, p = 0.022), mechanical ventilation (aOR: 75.29, 95% CI: 12.37−458.28, p < 0.001), and hypertension (aOR: 4.34, 95% CI: 1.37−13.82, p = 0.013) were independent risk factors of in‐hospital mortality of HC patients. Besides, high CCI was an independent risk factor for higher ICU Admission (aOR: 5.91, 95% CI: 2.31−15.08, p < 0.001), hypoglycemia (aOR: 2.19, 95% CI:1.01−4.08, p = 0.049), longer LOS (aOR: 1.23, 95% CI: 1.19−2.27, p = 0.021), and higher hospitalisation expense (aOR: 2089.97, 95% CI: 193.33−3988.61, p = 0.031) of HC patients. Conclusion: CCI is associated with in‐hospital mortality, ICU admission, hypoglycemia, LOS, and hospitalisation expense of HC patients. CCI could be an ideal indicator to identify, monitor, and manage chronic comorbidities among HC patients. [ABSTRACT FROM AUTHOR]

Objective: Rare disease. Background: Gitelman syndrome (GS) is an uncommon autosomal recessive inherited disease caused by inactivating mutations in the SLC12A3 gene located on chromosome 16q13, resulting in distal tubular dysfunction. Most cases are detected during routine examinations in adulthood, due to hypokalemia and alkalosis. GS needs to be distinguished from diseases that cause hypokalemia, such as Classic Bartter syndrome and hyperthyroidism. In individual cases, GS and hyperthyroidism occur simultaneously, which is prone to misdiagnosis. Case Report: A 51-year-old woman with intermittent palpitations and lower limb fatigue for 4 years received a diagnosis of hypokalemia at a local hospital. Treatment with potassium supplementation did not improve the patient's palpitations and fatigue. After coming to our hospital for examination, it was found that the patient had hyperthyroidism. After receiving treatment of hyperthyroidism remission and sufficient potassium replacement, the patient's serum potassium level remained low. Meanwhile, the patient had hypomagnesemia and metabolic alkalosis. Subsequently, according to our suggestion, the patient continued to take oral supplements of potassium and magnesium, while also started on spironolactone. We convinced the patient to undergo genetic testing and discovered compound heterozygous mutations in the SLC12A3 gene, which presented a definitive diagnosis of GS. In the following 3 months, the patient's serum potassium level was within the normal range, and the dose of methimazole was reduced. Conclusion: As a rare disease, GS may have only mild or occasional manifestations, making it prone to misdiagnosis. GS remains therapeutically challenging, and future progress in treatment will depend on further research of the disease. [ABSTRACT FROM AUTHOR]

This article provides a comprehensive overview of electrolyte and water homeostasis in pediatric patients, focusing on some of the common serum electrolyte abnormalities encountered in clinical practice. Understanding pathophysiology, taking a detailed history, performing comprehensive physical examinations, and ordering basic laboratory investigations are essential for the timely proper management of these conditions. We will discuss the pathophysiology, clinical manifestations, diagnostic approaches, and treatment strategies for each electrolyte disorder. This article aims to enhance the clinical approach to pediatric patients with electrolyte imbalance-related emergencies, ultimately improving patient outcomes. Trial registration This manuscript does not include a clinical trial; instead, it provides an updated review of literature. [ABSTRACT FROM AUTHOR]

This report describes a suspected case of paraneoplastic syndrome of inappropriate antidiuretic hormone (SIADH) in a 5‐year‐old male entire Australian Kelpie associated with a gastric adenocarcinoma. The dog had a history of chronic vomiting and presented with hyponatraemia, hypokalaemia, hypochloraemia and increased urinary sodium. Computed tomography identified the presence of a gastric tumour and histopathology confirmed a pyloric gastric adenocarcinoma. Removal of the tumour via a Billroth I procedure resulted in rapid resolution of electrolyte derangements. The dog was still alive six months postoperatively with no recurrence of either SIADH or tumour at the time of publication. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to describe the successful identification and treatment of severe hyperkalemia, cardiac arrhythmia, rhabdomyolysis, and acute kidney injury (AKI) in a domestic cat that underwent general anesthesia for abdominal exploratory surgery. The definitive underlying cause remains unknown; however, a reaction to propofol is suspected. Case summary: A 6-month-old intact male domestic short-hair cat underwent general anesthesia and developed severe intraoperative rhabdomyolysis, hyperkalemia, ventricular fibrillation, and AKI during surgery despite a documented mild hypokalemia and normal creatinine before inducing anesthesia. Propofol was administered as part of the anesthetic protocol. The patient was resuscitated successfully and responded well to advanced medical intervention. The hyperkalemia and AKI were resolved within less than 24 h from surgery and rhabdomyolysis was resolved at the time of recheck 5 days later. New or unique information provided: While previously suspected in dogs, to the authors' knowledge, propofol-related infusion syndrome (PRIS) has not been reported in domestic cats. Veterinary professionals should be aware that drug-induced intraoperative rhabdomyolysis and hyperkalemia can develop unexpectedly and should remain a differential for acute cardiac arrhythmias or cardiac arrest and AKI. [ABSTRACT FROM AUTHOR]

Cystic fibrosis (CF) is the most common life-threatening genetic disease in the United States and among people of European descent. Despite the widespread distribution of the cystic fibrosis transmembrane conductance regulator (CFTR) along kidney tubules, specific renal phenotypes attributable to CF have not been well documented. Recent studies have demonstrated the downregulation of the apical Cl-/HCO3 - exchanger pendrin (Slc26a4) in kidney B-intercalated cells of CF mouse models. These studies have shown that kidneys of both mice and humans with CF have an impaired ability to excrete excess HCO3 -, thus developing metabolic alkalosis when subjected to excess HCO3 - intake. The purpose of this minireview is to discuss the latest advances on the role of pendrin as a molecule with dual critical roles in acid base regulation and systemic vascular volume homeostasis, specifically in CF. Given the immense prevalence of vascular volume depletion, which is primarily precipitated via enhanced chloride loss through perspiration, we suggest that the dominant presentation of metabolic alkalosis in CF is due to the impaired function of pendrin, which plays a critical role in systemic vascular volume and acid base homeostasis. [ABSTRACT FROM AUTHOR]

Background: Hypokalemic rhabdomyolysis is a rare clinical manifestation of primary aldosteronism, making its diagnosis challenging, particularly when it becomes the primary presenting symptom. Herein, we present a case of primary aldosteronism with hypokalemic rhabdomyolysis and conduct a related literature review. Case presentation: We report the case of a 54-year-old Chinese male patient who presented with intermittent weakness over the past year and was admitted with sudden limb paralysis for 2 days. The final diagnosis was primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. By reviewing the related Chinese and English literature, we noticed that only a few cases were published since 1978. After excluding irrelevant literatures, we summarized and analyzed 43 patients of with primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. All patients showed good recovery, with normalized blood potassium levels, and a majority achieved normalized blood pressure. Some patients still required medication for blood pressure control. Conclusions: Primary aldosteronism rarely causes rhabdomyolysis; the occurrence of severe hypokalemia and rhabdomyolysis should prompt consideration of primary aldosteronism in the differential diagnosis. Early detection and treatment are crucial for determining patient prognosis. [ABSTRACT FROM AUTHOR]

Background: Syndrome of apparent mineralocorticoid excess (AME) is characterized by excessive MR stimulation despite low levels of aldosterone. 11Beta-hydroxysteroid dehydrogenase-2 (11βDSH-2) inactivates cortisol to cortisone, preventing cortisol-induced MR activation. Genetic defects in 11βDSH-2 cause AME through accumulation of cortisol in the distal nephron, leading to MR activation induced hypertension, hypokalemia and metabolic alkalosis. Acquired AME can occur due to the ingestion of glycyrrhizic acid, found in licorice root, which inhibits 11βDSH-2 and has additional effects on cortisol homeostasis through inhibition of 11βDSH-1. Case report: We present a case of acquired AME with a hyperadrenergic symptoms induced by ingestion of Advanced Liver Support, a nutritional supplement produced by Advanced BioNutritionals(R), in a 65-year-old Caucasian female who presented with accelerated hypertension, hypokalemia, metabolic alkalosis and adrenergic symptoms. Cessation of the licorice-containing supplement resulted in complete resolution of the patient's hypertension, symptoms and abnormal lab values. To our knowledge this is the first reported case of AME from this supplement, and the first to describe accompanying hyperadrenergic symptoms. Conclusions: Glycyrrhizic acid is increasingly being found in unregulated nutritional supplements and has the potential to induce a reversable syndrome of AME. Acquired AME should be suspected in individuals who present with hypertension along with hypokalemia, metabolic alkalosis and low plasma renin and serum aldosterone levels. [ABSTRACT FROM AUTHOR]

• Patients with HypoPP can have impaired quality of life. • Patients with HypoPP can suffer from fatigue and pain. • Attention should be given to muscle weakness and fatigue in patients with HypoPP. Primary hypokalemic periodic paralysis (HypoPP) is a skeletal muscle channelopathy most commonly caused by pathogenic variants in the calcium channel gene, CACNA1S. HypoPP can present with attacks of paralysis and/or permanent muscle weakness. Previous studies have shown that patients with HypoPP can have impaired quality of life (QoL). In this cross-sectional study, we aimed to describe the QoL in patients with HypoPP caused by pathogenic variants in CACNA1S using The Individualized Neuromuscular Quality of Life (INQoL) questionnaire, a validated tool to measure the QoL of patients with neuromuscular diseases (higher score, worse QoL). We showed that muscle weakness and fatigue were the symptoms with the greatest impact on participants' lives and that "activities", in the life domain of the INQoL, was most affected by HypoPP. Furthermore, we showed that the total INQoL score increased with age. Low QoL was primarily driven by progressive permanent muscle weakness and not attacks of paralysis, although half of the participants reported that attacks of paralysis challenged their daily life. The results suggest that special attention should be given to muscle weakness and fatigue in patients with HypoPP. [ABSTRACT FROM AUTHOR]

Sustainable management of potassium nutrition in alfalfa crop production is one of the major key factors for achieving optimum seed and biomass yields. An inappropriate supply of mineral potassium nutrition in alfalfa production could result in a decrease in biomass and grain yield production, leading to luxury consumption with cost implications. Alfalfa (Medicago sativa L.) is a perennial leguminous forage crop known for its high protein content, nutritive value, biomass yield production, soil-improving abilities, and livestock feed. Potassium nutrition plays a crucial role in alfalfa production by influencing several physiological processes essential for biomass yield, growth, development, photosynthesis, nutrient uptake, and stress tolerance. Although several studies have been conducted regarding the role of potassium nutrition in agriculture productivity, only limited research has focused on crop-specific impacts. Therefore, this paper reviews (i) the significant role potassium nutrition plays in alfalfa production along with its implications for quality, yield, growth, and resistance to abiotic stress; (ii) the factors affecting the availability, absorption, and transport of potassium; (iii) the source of potassium and the consequences of inadequate availability; and (iv) highlights some strategies for mitigating potassium nutrient deficiency to optimize alfalfa productivity and sustainability in agricultural systems. [ABSTRACT FROM AUTHOR]

Objective: To identify patients presenting to an acute medical hospital with common signs and symptoms that occur in people with eating disorders (EDs), and determine by retrospective file audit if these are diagnosed cases of an ED. Method: The investigators screened electronic medical records of people 16 years and older for common signs and symptoms of an ED such as hypokalemia, in patients presenting to an acute hospital in Sydney, Australia from 2018 to 2020. Cases where the clinical finding was unexplained had their file audited. Cases with a known ED diagnosis or coded with an ED were also retrieved to audit. Results: Investigators identified 192 definite ED cases with a total of 598 episodes of care from 2018 to 2020 presenting to the hospital. Eighty‐three cases were identified as possible EDs due to unexplained clinical signs consistent with an ED, but were not confirmed cases due to lack of clinical history in the file. Only 19.1% of presentations were diagnostically coded with an ED in the electronic medical record. Discussion: Our study revealed a large number of definite ED cases presenting to an acute medical hospital via the emergency department, who were not recognized as having an ED. Greater awareness of clinical signs and symptoms of an ED, such as unexplained low body mass index and hypokalemia, is necessary among acute care clinicians. Correctly identifying EDs in those seeking somatic care should be a public health priority, to facilitate timely and equitable access to diagnostic assessment and evidence based treatment. Public significance: People with eating disorders (EDs) present to acute care settings and have a relatively high utilization of generalist health services with nonspecific problems such as abdominal pain. An enhanced understanding of healthcare utilization by people with EDs, who may not disclose their symptoms, is crucial for improving access to treatment. [ABSTRACT FROM AUTHOR]

Potassium deficiency in wheat can significantly influence the accumulation of other macronutrients and affect various yield traits. Understanding the genetic factors controlling wheat macronutrient accumulation and yield attributes is important for improved nutritional wheat quality and human health under potassium deficiency This study investigated a set of 111 wheat accessions to assess their response to potassium deprivation. The accessions were subjected to two different levels of potassium treatment: moderate (K1) and low (K2). The wheat grains were analyzed for four macronutrients, mainly magnesium (Mg), calcium (Ca), potassium (K), and phosphorus (P), as well as yield attributes, under both treatments. A statistically significant decrease was observed for all assessed minerals and yield traits in wheat accessions under low potassium. Genome-wide association study (GWAS) analysis identified 366 SNP markers that were significantly linked with all assessed macronutrients and yield parameters, regardless of the potassium treatments. Remarkably, 14 genomic regions were identified that exhibited highly significant relationships with all evaluated characteristics under both treatments. Interestingly, the TraesCS1B02G359800 gene was located on chromosome 3B and annotated as protein kinases that harbor the variation of NGS, P, Mg_K2, and Mg_K1. Protein kinases can modulate the activity of ion transporters and channels, such as the High-Affinity K+ Transporter (HKT) family, to enhance the uptake and redistribution of potassium and other macronutrient. Therefore, integrating these genetic insights with modern breeding techniques holds the promise of developing superior wheat varieties that can meet the challenges of global food security. [ABSTRACT FROM AUTHOR]

Key Clinical Message: In managing Sjogren's syndrome, a thorough patient history, proper lab tests, and imaging are crucial. Clinicians should prioritize checking electrolyte levels in cases of muscle weakness, as early detection of hypokalemia can prevent severe complications. Proactive monitoring can avert renal tubular acidosis and improve patient outcomes. Distal renal tubular acidosis (dRTA) occurs in approximately one‐third of patients with Sjogren's syndrome, a systemic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands, leading to dryness of mucous membranes. Hypokalemic paralysis, a well‐documented but rare complication of dRTA, typically manifests as symmetric proximal muscle weakness of the extremities. We present the case of a 38‐year‐old woman with a history of Sjogren's syndrome diagnosed 3 years prior, who ceased her medication without medical supervision. She presented with quadriplegia, initially beginning unilaterally. This particular presentation is seldom documented in the literature. Laboratory investigations revealed hypokalemia and normal anion gap metabolic acidosis, consistent with dRTA‐induced hypokalemic paralysis. Intravenous potassium chloride was administered, resulting in complete recovery of muscle strength. Hypokalemic paralysis associated with dRTA is typically reversible; however, delays in diagnosis and treatment can lead to life‐threatening complications such as respiratory failure and arrhythmias. Therefore, clinicians should maintain a high index of suspicion for this condition in patients presenting with muscle weakness. Prompt and precise history takingand screening, and initiating appropriate management to prevent adverse outcomes. [ABSTRACT FROM AUTHOR]

Background: This study aimed to analyze genotype–phenotype correlations in children with Gitelman syndrome (GS). Methods: This multicenter retrospective study included 50 Korean children diagnosed with SLC12A3 variants in one or both alleles and the typical laboratory findings of GS. Genetic testing was performed using the Sanger sequencing except for one patient. Results: The median age at the diagnosis was 10.5 years (interquartile range, 6.8;14.1), and 41 patients were followed up for a median duration of 5.4 years (interquartile range, 4.1;9.6). A total of 30 different SLC12A3 variants were identified. Of the patients, 34 (68%) had biallelic variants, and 16 (32%) had monoallelic variants on examination. Among the patients with biallelic variants, those (n = 12) with the truncating variants in one or both alleles had lower serum chloride levels (92.2 ± 3.2 vs. 96.5 ± 3.8 mMol/L, P = 0.002) at onset, as well as lower serum potassium levels (3.0 ± 0.4 vs. 3.4 ± 0.3 mMol/L, P = 0.016), and lower serum chloride levels (96.1 ± 1.9 vs. 98.3 ± 3.0 mMol/L, P = 0.049) during follow-up than those without truncating variants (n = 22). Patients with monoallelic variants on examination showed similar phenotypes and treatment responsiveness to those with biallelic variants. Conclusions: Patients with GS who had truncating variants in one or both alleles had more severe electrolyte abnormalities than those without truncating variants. Patients with GS who had monoallelic SLC12A3 variants on examination had almost the same phenotypes, response to treatment, and long-term prognosis as those with biallelic variants. [ABSTRACT FROM AUTHOR]

Pseudohypoparathyroidism (PHP) comprises a cluster of heterogeneous diseases characterized by hypocalcemia and hyperphosphatemia due to parathyroid hormone (PTH) resistance. PHP type 1B (PHP1B) is caused by heterozygous maternal deletions within GNAS or STX16. STX16 exon 2–6 deletion is commonly observed in autosomal dominant (AD)-PHP1B, while sporadic PHP1B commonly results from methylation abnormalities of maternal differentially methylated regions and remains unclear at the molecular level. A 39-year-old male patient with PHP1B, who had his first seizure at 15 years of age, presented to our hospital. The methylation-specific multiplex ligation-dependent probe amplification results showed a half-reduced copy number of STX16 exon 5–7 and loss of methylation at GNAS exon A/B. His mother also had a half-reduced copy number of STX16 exon 5–7 but with normal methylation of GNAS. His father has a normal copy number of STX16 and normal methylation of GNAS. For the recognition and early diagnosis of this kind of disease, here we report the clinical symptoms, auxiliary examinations, genetic testing characteristics, and treatment of the patient. [ABSTRACT FROM AUTHOR]

Context Primary aldosteronism (PA) is a common cause of hypertension (HT). However, diagnosis is often delayed, leading to poorer clinical outcomes. Hypokalemia with HT is characteristic of PA, and is an indication for screening. Objective We evaluated if patients with PA had prolonged hypokalemia before diagnosis, the subsequent biochemical/clinical control, and factors associated with delayed diagnosis. Methods Our study included all PA patients with hypokalemia diagnosed between 2001 and 2022. Delayed diagnosis was defined as duration of hypokalemia of more than 1 year from first occurrence to first evaluation by a PA specialist. Patients were reassessed post adrenalectomy using the Primary Aldosteronism Surgery Outcomes criteria. We performed multivariable analysis to assess for factors associated with delayed diagnosis. Results Among 240 patients with PA who presented with hypokalemia, 122 (51%) patients had delayed diagnosis, with prolonged hypokalemia of median duration 4.5 years (range, 2.4-7.5 years). Patients with delayed diagnosis were older, had longer duration of HT, higher pill burden, lower renal function, and more prevalent cardiovascular disease. Factors associated with delayed diagnosis included older age, presence of hyperlipidemia, and less severe hypokalemia (serum potassium >3.0 mmol/L). Compared to patients with early diagnosis, a lower proportion of those with delayed diagnosis underwent adrenal vein sampling (73% vs 58%) (P <.05). Sixty of 118 (50.8%) nondelayed, and 39 of 122 (32.0%) patients with delayed diagnosis, underwent surgery. Conclusion Despite manifestation of hypokalemia, many patients with PA fail to be promptly screened. Greater emphasis in HT guidelines, and efforts to improve awareness of PA among primary care physicians, are urgently needed. [ABSTRACT FROM AUTHOR]

Background: Type III Bartter syndrome (BS) is an autosomal recessive renal tubular disease caused by the mutation of the chloride voltage-gated channel Kb (CLCNKB) gene. This condition is characterized by renal sodium loss, hypokalemia, metabolic alkaliosis, high renin, and high aldosterone levels. Methods: We report a case of adult type III BS caused by a novel complex heterozygous mutation of the CLCNKB gene. The peripheral blood was extracted for whole genome DNA extraction, and the genome exon region of BSrelated genes, was predicted by high-throughput sequencing and protein function prediction software. The selected mutation sites were verified by sequencing with Sanger method. Results: The new complex heterozygous mutations of CLCNKB include heterozygous deletion of exon 2 - 20 of CLCNKB and nonsense mutation of exon 19, c.2010G>A (p.W670X). This complex heterozygous mutation has not been reported in humans. Conclusions: For patients with high clinical suspicion of BS, a clear diagnosis should be made through genetic testing to improve patients' quality of life and provide genetic guidance. [ABSTRACT FROM AUTHOR]

Background: Clostridioides difficile infection is associated with antibiotic use and manifests as diarrhea; however, emerging cases of fulminant diarrhea caused by binary toxin-producing C. difficile unrelated to prior antibiotic exposure have been reported. Although fulminant colitis caused by C. difficile has been documented, instances of intussusception remain scarce. Here, we present a case of adult intussusception with severe hypokalemia and pneumonia resulting from a community-acquired C. difficile infection in Japan. Case presentation: An 82-year-old male presented with dizziness, progressive weakness, and diarrhea. Initial vital signs indicated severe respiratory and circulatory distress, and laboratory findings revealed hypokalemia, pneumonia, and septic shock. Imaging confirmed intussusception of the ascending colon. Although colonoscopy suggested a potential tumor, no malignancy was found. The C. difficile rapid test result was positive, indicating community-acquired C. difficile infection. Treatment with vancomycin was initiated; however, intussusception relapsed. Surgical intervention was successful and led to clinical improvement. The patient's complex pathophysiology involved community-acquired C. difficile-induced severe diarrhea, hypokalemia, hypermetabolic alkalosis, and subsequent intussusception. Although adult intussusception is uncommon, this case was uniquely linked to binary toxin-producing C. difficile. The identified strain, SUH1, belonged to a novel sequence type (ST1105) and clade 3, suggesting a highly virulent clone. Resistome analysis aligned with phenotypic susceptibility to metronidazole and vancomycin, confirming their treatment efficacy. Conclusion: This case report highlights a binary toxin-producing C. difficile that caused intussusception. The consideration of community-acquired C. difficile in the differential diagnosis of severe enteritis is necessary, even in Japan. [ABSTRACT FROM AUTHOR]

Chicory is a food with high nutritional. The use of beneficial elements in plants, such as sodium (Na) and silicon (Si), may be important to mitigate nutritional disorders, such as potassium (K) deficiency, but research is lacking on this topic. The objective was to evaluate the effects of sodium and nano-silicon on the nutritional, physiological, growth, and quality parameters of chicory under K deficiency and sufficiency. We used a concentration for sufficient K (3.0 mmol L−1), K-deficiency (1.5 mmol L−1), combined with the lack or presence of Na (2.0 mmol L−1) and Si (2.0 mmol L−1). The experiment was carried out in a greenhouse with six treatments corresponding to K sufficiency, K-sufficiency with Na, K-sufficiency with Si, K deficiency, K-deficiency with Na, and K-deficiency with Si, with six replications. The following growth variables were evaluated: (i) plant height, (ii) stem diameter, (iii) number of leaves, (iv) leaf area, and (v) plant biomass. Potassium and Si contents in the above ground part and K utilization efficiency were assessed, and the accumulation of K, Na, and Si was calculated. The efficiency of the quantum yield of photosystem II (Fv/Fm) and the photosynthetic pigments was determined. Electrolyte leakage index and relative water content, as well as phenolic compounds, ascorbic acid, and leaf firmness index were also determined. We found that supplying nano-Si and Na to a K-deficient nutrient solution increased K accumulation by 60% and 50% and K use efficiency by 79% and 62% compared to plants without supply of those elements. Nano-Si reduced electrolyte leakage, being 41% less than Na in K-deficient chicory. However, when Na was added to a nutrient solution with sufficient potassium, the K use efficiency decreased by 48% compared to sufficient potassium without Na. Under the same condition of sufficient supply of potassium and Na, K accumulation decreased by 20% in chicory compared to sufficient potassium without Na, and the photosynthetic pigments—total chlorophyll and carotenoids—were reduced by 5% and 10%, respectively. Our findings contribute to improve cultivation systems with low supply of K as the supply of Na and nano-Si mitigates the damage caused to the metabolism of chicory under K deficiency. [ABSTRACT FROM AUTHOR]

We investigated the clinical characteristics of primary aldosteronism (PA) screened from patients with hypertension in China. The participants were hypertensive patients who were suspected of PA and registered in the China Primary Aldosteronism Prospective Study. Plasma aldosterone‐to‐renin ratio (ARR) was used as the screening test. In patients screened positive for PA, that is, an ARR exceeding the thresholds and plasma aldosterone concentration (PAC) > 100 pg/mL, a confirmatory test was performed for diagnosis. Patients with PA underwent a CT scan and adrenal venous sampling for subtyping. Of the 1497 screened patients, 754 (50.4%) had an ARR exceeding the diagnostic threshold and 637 (84.5% of those eligible) were registered. These registered hypertensive patients with suspected PA had a mean (standard deviation) age of 52.6 ± 12.1 years, and included 442 (58.6%) women. In multiple stepwise logistic regression, the significant odds ratios for the presence of diagnosed (n = 490) versus suspected and non‐diagnosed PA (n = 147) were 4.54 (95% CI: 2.78‐7.39) for a history of hypokalemia, 0.79 (95% CI: 0.64‐0.98) for a 0.9 mmol/l higher serum total cholesterol, and 2.25 (95% CI: 1.63‐3.10) for a doubling of PAC in the supine or standing/sitting position. In multiple stepwise logistic regression, the significant odds ratios for the presence of unilateral (n = 135) versus bilateral PA (n = 53) were 3.04 (95% CI: 1.90‐4.87) for a 0.4 mmol/l lower minimum serum potassium concentration and 1.86 (95% CI: 1.20‐2.86) for a 0.3 mmol/l higher serum high‐density lipoprotein cholesterol. PA might be a biochemical continuum in the adrenal hypersecretion of aldosterone as well as hypokalemia. [ABSTRACT FROM AUTHOR]

Soil potassium deficiency is a common issue limiting agricultural productivity. Potassium-solubilizing bacteria (KSB) show significant potential in mitigating soil potassium deficiency, improving soil quality, and enhancing plant growth. However, different KSB strains exhibit diverse solubilization mechanisms, environmental adaptability, and growth-promoting abilities. In this study, we isolated a multifunctional KSB strain ZHS-1, which also has phosphate-solubilizing and IAA-producing capabilities. 16S rDNA sequencing identified it as Pantoea vagans. Scanning electron microscopy (SEM) showed that strain ZHS-1 severely corroded the smooth, compact surface of potassium feldspar into a rough and loose state. The potassium solubilization reached 20.3 mg/L under conditions where maltose was the carbon source, sodium nitrate was the nitrogen source, and the pH was 7. Organic acid metabolism profiling revealed that strain ZHS-1 primarily utilized the EMP-TCA cycle, supplemented by pathways involving pantothenic acid, glyoxylic acid, and dicarboxylic acids, to produce large amounts of organic acids and energy. This solubilization was achieved through direct solubilization mechanisms. The strain also secreted IAA through a tryptophan-dependent metabolic pathway. When strain ZHS-1 was inoculated into the rhizosphere of rice, it demonstrated significant growth-promoting effects. The rice plants exhibited improved growth and root development, with increased accumulation of potassium and phosphorus. The levels of available phosphorus and potassium in the rhizosphere soil also increased significantly. Additionally, we observed a decrease in the relative abundance of Actinobacteria and Proteobacteria in the rice rhizosphere soil, while the relative abundance of genera associated with acid production and potassium solubilization, such as Gemmatimonadota, Acidobacteria, and Chloroflexi, as well as Cyanobacteria, which are beneficial to plant growth, increased. These findings contribute to a deeper understanding of the potassium solubilization mechanisms of strain ZHS-1 and highlight its potential as a plant growth-promoting rhizobacteria. [ABSTRACT FROM AUTHOR]

Background: The diagnosis of primary aldosteronism (PA) is comprehensive, which includes case-detection testing, case confirmation followed by subtype classification. In certain instances, such as in the setting of spontaneous hypokalemia, suppressed renin activity (PRA) plus plasma aldosterone concentration (PAC) of > 15 ng/dL, one may not proceed with confirmatory tests. However, the quality of evidence behind this approach is very low. This study sought to evaluate the proposed "simplified confirmatory pathway" that can spare confirmatory testing for primary aldosteronism by evaluating the diagnostic performances of the various pre-specified PAC thresholds in combination with findings of suppressed renin and spontaneous hypokalemia. Methods: This is a multi-center, retrospective diagnostic accuracy cohort-selected cross-sectional study. A total of 133 participants aged 18 years and above underwent saline infusion test between January 2010 to March 2024. The outcome measures comprise of the diagnostic performances of the different index test combinations (baseline PAC, baseline PRA and presence of spontaneous hypokalemia): sensitivity, specificity, negative predictive value, positive predictive value, positive likelihood ratio, negative likelihood ratio, and diagnostic accuracy. Data analysis was performed using SPSS 29.0.1.0 & MedCalc 20.218. Results: Of the 133 patients who underwent saline infusion test, 88 (66.17%) were diagnosed with PA. A PAC of > 25 ng/dL plus PRA < 1.0 ng/dL/hr with spontaneous hypokalemia showed the highest specificity at 100% (95% CI 90.51%, 100.00%) and positive predictive value at 100% (85.18 – 100.00%). The minimum acceptable combination criteria were determined to be a PAC of > 20 ng/dL plus PRA < 0.6 ng/dL/hr, and presence of spontaneous hypokalemia. It has high specificity (94.59%; 95% CI 81.81%, 99.34%), positive predictive value (93.55%, 95% CI 78.49%, 98.29%), and moderate positive likelihood ratio (LR+) (6.39, 95% CI 1.61, 25.38) Conclusion: A hypertensive patient with spontaneous hypokalemia and screening findings of PAC > 20 ng/dL and suppressed PRA of < 0.6 ng/ml/hr, may be classified as "overt primary aldosteronism confirmed" and may not need to proceed with dynamic confirmatory testing. Protocol registration number: SRCTN34186253 [ABSTRACT FROM AUTHOR]

Introduction: This systematic review and meta-analysis aimed to determine the safety of liposomal amphotericin B (L-AMB) compared to other antifungal agents for secondary prophylaxis. Method: We conducted a comprehensive search across international databases and reference lists of articles to compile all relevant published evidence evaluating the efficacy and safety of L-AMB versus other antifungals (NLAMB) for secondary prophylaxis against invasive fungal infections. Pooled estimates were calculated after data transformation to evaluate mortality, breakthrough infections, and the frequency of adverse effects, including hypokalemia and nephrotoxicity. Comparisons of breakthrough fungal infection and mortality between the L-AMB and NLAMB groups were performed. Result: We identified 10 studies. The cumulative frequency of patients using L-AMB was 148, compared to 341 patients in the NLAMB group. The mortality rates in the L-AMB and NLAMB groups were 10% and 0%, respectively. However, based on the odds ratio, the mortality in the L-AMB group was lower than that in the NLAMB group. No significant difference was observed in breakthrough invasive fungal infections between the L-AMB and NLAMB groups. The frequencies of nephropathy and hypokalemia in the L-AMB group were 36% and 18%, respectively. Conclusion: Our findings indicate a lower incidence of mortality in the L-AMB group compared to the NLAMB group. No statistically significant difference was observed in the incidence of breakthrough infection between the two groups. L-AMB administration is associated with nephropathy and hypokalemia. However, the refusal to continue treatment due to adverse effects is not significantly high. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury (AKI) and hypokalaemia are common adverse events after treatment with liposomal amphotericin B (L‐AMB). Objectives: Because excess potassium (K) leakage occurs during renal tubular injury caused by L‐AMB, measuring the decrease in rate of serum K concentration might be more useful to assess the renal impact of L‐AMB than hypokalaemia identified from a one‐point measurement. The effects of a decrease in K concentration and duration of hypokalaemia on AKI were investigated. Methods: A ≥ 10% decrease in K concentration from the reference concentration within a 7‐day timeframe was evaluated. The hypokalaemia index, which combines the duration of K concentration lower than the reference and a marked low K concentration, was calculated from the area over the concentration curve. Results: Eighty‐six patients were included in the study. The incidences of AKI and decrease in K concentration were 36.0% and 63.9%, respectively. Of patients who developed both adverse events, a decrease in K concentration occurred first in 22 of 26 patients, followed by AKI 7 days later. Hypokalaemia did not increase AKI risk whereas a decrease in K concentration was an independent risk factor for AKI. The hypokalaemia index in patients with AKI was significantly higher than those without AKI (5.35 vs. 2.50 points, p = 0.002), and ≥3.45 points was a significant predictor for AKI. Conclusion: A ≥ 10% decrease in the K concentration was a significant factor for AKI in patients receiving L‐AMB therapy. In such patients, dose reduction or alternative antifungals could be considered based on the hypokalaemia index. [ABSTRACT FROM AUTHOR]

Background: On February 6th, 2023, two consecutive earthquakes struck southeastern Türkiye with magnitudes of 7.7 and 7.6, respectively. This study aimed to analyze the clinical and laboratory findings, as well as management of pediatric victims with Crush Syndrome (CS) and Acute Kidney Injury (AKI). Methods: The study included pediatric earthquake victims who were presented to Mersin University Hospital. Clinical and laboratory characteristics of the patients were collected retrospectively. Results: Among 649 patients, Crush injury (CI), CS and AKI was observed in 157, 59, and 17 patients, respectively. White blood cell count (12,870 [IQR: 9910–18700] vs. 10,545 [IQR: 8355–14057] /µL, P < 0.001), C-reactive protein (51.27 [IQR: 14.80–88.78] vs. 4.59 [1.04–18.25] mg/L, P < 0.001) and myoglobin levels (443.00 [IQR: 198.5–1759.35] vs. 17 [11.8–30.43] ng/ml) were higher in patients with CS, while their sodium (IQR: 134 [131–137] vs. 136 [134–138] mEq/L, P < 0.001) levels were lower compared to non-CS patients. An increase in myoglobin levels was identified as an independent risk factor for developing CS (OR = 1.017 [1.006–1.027]). Intravenous fluid replacement was administered to the patients with CS at a dose of 4000 cc/m2/day. Hypokalemia was observed in 51.9% of the CS patients on the third day. All patients with AKI showed improvement and no deaths were reported. Conclusions: Hyponatremia and increase in inflammation markers associated with CS may be observed. An increase in myoglobin levels was identified as a risk factor for CS. Hypokalemia may be seen as a complication of vigorous fluid therapy during hospitalization. [ABSTRACT FROM AUTHOR]

Diabetes is closely associated with K+ disturbances during disease progression and treatment. However, it remains unclear whether K+ imbalance occurs in diabetes with normal kidney function. In this study, we examined the effects of dietary K+ intake on systemic K+ balance and renal K+ handling in streptozotocin (STZ)-induced diabetic mice. The control and STZ mice were fed low or high K+ diet for 7 days to investigate the role of dietary K+ intake in renal K+ excretion and K+ homeostasis and to explore the underlying mechanism by evaluating K+ secretion-related transport proteins in distal nephrons. K+-deficient diet caused excessive urinary K+ loss, decreased daily K+ balance, and led to severe hypokalemia in STZ mice compared with control mice. In contrast, STZ mice showed an increased daily K+ balance and elevated plasma K+ level under K+-loading conditions. Dysregulation of the NaCl cotransporter (NCC), epithelial Naþ channel (ENaC), and renal outer medullary K+ channel (ROMK) was observed in diabetic mice fed either low or high K+ diet. Moreover, amiloride treatment reduced urinary K+ excretion and corrected hypokalemia in K+-restricted STZ mice. On the other hand, inhibition of SGLT2 by dapagliflozin promoted urinary K+ excretion and normalized plasma K+ levels in K+-supplemented STZ mice, at least partly by increasing ENaC activity. We conclude that STZ mice exhibited abnormal K+ balance and impaired renal K+ handling under either low or high K+ diet, which could be primarily attributed to the dysfunction of ENaC-dependent renal K+ excretion pathway, despite the possible role of NCC. NEW & NOTEWORTHY Neither low dietary K+ intake nor high dietary K+ intake effectively modulates renal K+ excretion and K+ homeostasis in STZ mice, which is closely related to the abnormality of ENaC expression and activity. SGLT2 inhibitor increases urinary K+ excretion and reduces plasma K+ level in STZ mice under high dietary K+ intake, an effect that may be partly due to the upregulation of ENaC activity. [ABSTRACT FROM AUTHOR]

Pseudohyperaldosteronism (PHA) is characterized by hypertension, hypokalemia, and a decrease in plasma renin and aldosterone levels. It can be caused by several causes, but the most frequent is due to excess intake of licorice. The effect is mediated by the active metabolite of licorice, glycyrrhetinic acid (GA), which acts by blocking the 11-hydroxysteroid dehydrogenase type 2 and binding to the mineralocorticoid receptor (MR) as an agonist. The management of licorice-induced PHA depends on several individual factors, such as age, gender, comorbidities, duration and amount of licorice intake, and metabolism. The clinical picture usually reverts upon licorice withdrawal, but sometimes mineralocorticoid-like effects can be critical and persist for several weeks, requiring treatment with MR blockers and potassium supplements. Through this case series of licorice-induced PHA, we aim to increase awareness about exogenous PHA, and the possible risk associated with excess intake of licorice. An accurate history is mandatory in patients with hypertension and hypokalemia to avoid unnecessary testing. GA is a component of several products, such as candies, breath fresheners, beverages, tobacco, cosmetics, and laxatives. In recent years, the mechanisms of action of licorice and its active compounds have been better elucidated, suggesting its benefits in several clinical settings. Nevertheless, licorice should still be consumed with caution, considering that licorice-induced PHA is still an underestimated condition, and its intake should be avoided in patients with increased risk of licorice toxicity due to concomitant comorbidities or interfering drugs. [ABSTRACT FROM AUTHOR]

Renin‐secreting tumours are rare causes of secondary hypertension and hypokalaemia. They are usually surgically curable, hence proper diagnostic work‐up and tumour localisation is essential. In this paper, we present three Swedish patients recently diagnosed with renin secreting tumours, two with reninomas and one with an extrarenal renin‐producing tumour, to illustrate diagnostic challenges. We also discuss the biochemical work‐up, the pros and cons of different imaging techniques (computer tomography [CT], magnetic resonance imaging and [18F]fluorodeoxyglucose‐positron emission tomography‐CT), as well as how renal vein sampling (RVC) may contribute to localisation of the tumour. [ABSTRACT FROM AUTHOR]

The majority of disorders that cause renal potassium wasting present with abnormalities in adrenal hormone secretion. While these findings frequently lead patients to seek endocrine evaluation, clinicians often struggle to accurately diagnose these conditions, delaying treatment and adversely impacting patient care. At the same time, growing insight into the genetic and molecular basis of these disorders continues to improve their diagnosis and management. In this review, we outline a practical integrated approach to the evaluation of renal hypokalemia syndromes that are seen in endocrine practice while highlighting recent advances in understanding of the genetics and pathophysiology behind them. [ABSTRACT FROM AUTHOR]

Abstract This article provides a comprehensive overview of electrolyte and water homeostasis in pediatric patients, focusing on some of the common serum electrolyte abnormalities encountered in clinical practice. Understanding pathophysiology, taking a detailed history, performing comprehensive physical examinations, and ordering basic laboratory investigations are essential for the timely proper management of these conditions. We will discuss the pathophysiology, clinical manifestations, diagnostic approaches, and treatment strategies for each electrolyte disorder. This article aims to enhance the clinical approach to pediatric patients with electrolyte imbalance-related emergencies, ultimately improving patient outcomes. Trial registration This manuscript does not include a clinical trial; instead, it provides an updated review of literature.

Abstract Background Hypokalemic rhabdomyolysis is a rare clinical manifestation of primary aldosteronism, making its diagnosis challenging, particularly when it becomes the primary presenting symptom. Herein, we present a case of primary aldosteronism with hypokalemic rhabdomyolysis and conduct a related literature review. Case presentation We report the case of a 54-year-old Chinese male patient who presented with intermittent weakness over the past year and was admitted with sudden limb paralysis for 2 days. The final diagnosis was primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. By reviewing the related Chinese and English literature, we noticed that only a few cases were published since 1978. After excluding irrelevant literatures, we summarized and analyzed 43 patients of with primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. All patients showed good recovery, with normalized blood potassium levels, and a majority achieved normalized blood pressure. Some patients still required medication for blood pressure control. Conclusions Primary aldosteronism rarely causes rhabdomyolysis; the occurrence of severe hypokalemia and rhabdomyolysis should prompt consideration of primary aldosteronism in the differential diagnosis. Early detection and treatment are crucial for determining patient prognosis.

Abstract Hypokalemia is a common issue in clinical settings, often indicating underlying systemic conditions that require careful evaluation. This study presents three cases where hypokalemic paralysis served as the initial symptom of systemic diseases. Key evaluation methods included clinical history, physical examination focusing on volume status, and acid–base assessment. The cases highlight the diverse etiologies of hypokalemia, including primary hyperaldosteronism, Sjogren’s syndrome, and Crohn’s disease.

Magdalena Stasiak,1 Przemys&lstrok;aw Witek,2 Emilia Adamska-Fita,1 Andrzej Lewi&nacute;ski1,3 1Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, Lodz, Poland; 2Department of Internal Medicine, Endocrinology and Diabetes, Medical University of Warsaw; Mazovian Brodnowski Hospital, Warszawa, Poland; 3Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, PolandCorrespondence: Magdalena Stasiak, Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, 281/289 Rzgowska Street, Lodz, 93-338, Poland, Tel +48502049292, Fax +48422711140, Email mstasiak33@gmail.comAbstract: Cushing’s disease (CD) is the most common cause of endogenous hypercortisolism. Osilodrostat was demonstrated to be efficient in treating CD, and the mean average dose required for CD control was < 11 mg/day. Potential differences in osilodrostat treatment between cortisol-producing adenoma (CPA) and CD have not been reported. The aim of this study was to present two patients with CPA in whom significant differences in the response to therapy compared to CD were found. We demonstrated a case of inverse response of cortisol levels with adrenal tumor progression during the initial dose escalation (Case 1). Simultaneously, severe exaggeration of hypercortisolism symptoms and life-threatening hypokalemia occurred. A further rapid dose increase resulted in the first noticeable cortisol response at a dose of 20 mg/day, and a full response at a dose of 45 mg/day. We also present a case that was initially resistant to therapy (Case 2). The doses required to achieve the first response and the full response were the same as those for Case 1. Our study demonstrated that osilodrostat therapy in patients with CPA may require a different approach than that in CD, with higher doses, faster dose escalation, and a possible initial inverse response or lack of response.Keywords: osilodrostat, adrenal adenoma, hypercortisolism, ACTH-independent, adverse events, hypokalemia

Objective: Congenital defects/diseases Background: Bartter syndrome is a rare, inherited salt-wasting tubulopathy caused by mutations in 1 of 6 genes that express ion transport channels in the thick ascending limb of nephrons. Excessive prostaglandin E2 and associated hyperreninemic hyperaldosteronism occurs, causing polyhydramnios, polyuria, prematurity, failure to thrive, and characteristic physical features. Hypokalemia, hypochloremic metabolic alkalosis, and, depending on the affected gene, hypercalciuria and nephrocalcinosis are hallmarks of Bartter syndrome. Case Reports: A 9-month-old male infant, born prematurely due to polyhydramnios, presented in the Emergency Department with dehydration due to incoercible vomiting and significant polyuria. A 6-year-old male infant with a previous history of prematurity due to polyhydramnios was referred to the Pediatric Endocrinology Department due to short stature and notable polydipsia and polyuria. Considering these marked symptoms, both cases triggered suspicion and started workup for arginine-vasopressin insufficiency/resistance. However, during the investigations, a broader clinical revision revealed that both had dysmorphic physical features (triangularly shaped face, prominent forehead, protruding ears, drooping mouth), poor growth, impaired weight gain, and typical biochemical findings (hypokalemic metabolic alkalosis, hypercalciuria, secondary hyperaldosteronism) of Bartter syndrome. Genetic testing confirmed the diagnosis of Bartter syndrome types 1 and type 2, respectively, and this diagnosis allowed proper treatment and significant clinical improvements, personalized follow-up, and genetic counseling for parents desiring further healthy pregnancies. Conclusions: Here, we present clinical and follow-up findings of 2 patients with Bartter syndrome types 1 and 2 discovered upon a broader clinical revision of suspected arginine-vasopressin insufficiency/resistance. We also review pertinent data on diagnosis and management of this challenging syndrome. [ABSTRACT FROM AUTHOR]

Hypokalemia is a common issue in clinical settings, often indicating underlying systemic conditions that require careful evaluation. This study presents three cases where hypokalemic paralysis served as the initial symptom of systemic diseases. Key evaluation methods included clinical history, physical examination focusing on volume status, and acid–base assessment. The cases highlight the diverse etiologies of hypokalemia, including primary hyperaldosteronism, Sjogren's syndrome, and Crohn's disease. [ABSTRACT FROM AUTHOR]

Background: The Stress Index (SI), calculated as the ratio of blood glucose to serum potassium levels, is a promising prognostic marker in various acute care settings. This study aimed to evaluate the utility of the SI for predicting mortality in patients with isolated moderate-to-severe traumatic brain injury (TBI). Methods: This retrospective cohort study included adult trauma patients (aged ≥ 20 years) with isolated moderate to severe TBI (Abbreviated Injury Scale ≥ 3 for only head region) treated from 2009–2022. The SI was computed from the initial glucose and potassium levels upon arrival at the emergency department. Logistic regression models were used to assess the association between the SI and mortality after adjusting for relevant covariates. The most effective threshold value of the SI for predicting mortality was identified using receiver operating characteristic (ROC) analysis. Results: Among the 4357 patients with isolated moderate and severe TBI, 463 (10.6%) died. Deceased patients had a significantly higher SI (61.7 vs. 44.1, p < 0.001). In multivariate analysis, higher SI independently predicted greater mortality risk (odds ratio (OR) 6.70, 95% confidence interval (CI) 1.66–26.99, p = 0.007). The optimal SI cutoff for predicting mortality was 48.50 (sensitivity 62.0%, specificity 71.4%, area under the curve 0.724). Patients with SI ≥ 48.5 had nearly two-fold higher adjusted mortality odds compared to those below the threshold (adjusted OR 1.94, 95% CI 1.51–2.50, p < 0.001). Conclusions: SI is a useful predictor of mortality in patients with isolated moderate-to-severe TBI. Incorporating SI with standard clinical assessments could enhance risk stratification and management approaches for this patient population. [ABSTRACT FROM AUTHOR]

This article discusses a case of a 23-year-old woman who had metabolic alkalosis and hypokalemia. The common causes of metabolic alkalosis are vomiting and diuretic use, but the patient did not have a history of these factors. Further investigation revealed a genetic defect called Gitelman syndrome, which affects the reabsorption of sodium chloride in the kidney. The patient was prescribed potassium chloride and magnesium oxide to manage her electrolyte abnormalities. The article also provides an overview of metabolic alkalosis and its causes, as well as information on how to diagnose and treat the condition. [Extracted from the article]

Hypokalemia is a common clinical condition that can lead to muscle weakness, difficulty breathing, malignant arrhythmias, and even death. This report describes two cases of severe hypokalemia resulting from the use of electronic cigarettes containing etomidate, both accompanied by varying degrees of adrenal hyperplasia. In both cases, the patients were admitted to the hospital with lower limb weakness and difficulty walking. Relevant examinations revealed low blood potassium, low cortisol, high adrenocorticotropic hormone, low renin, and low aldosterone levels in the patients, with Case 2 also having significant hypertension. In both cases, adrenal CT scans showed thickening of the adrenal glands. After the delivery of potassium supplementation in both cases, blood potassium levels gradually returned to normal and muscle strength gradually improved. The case reports are followed by a review of the literature on etomidate and its related mechanisms of action with discussion of its association with hypokalemia. [ABSTRACT FROM AUTHOR]

Identifying potassium (K+) deficiency in plants has traditionally been a difficult and expensive process. Traditional methods involve inspecting leaves for symptoms and conducting a laboratory analysis. These methods are not only time-consuming but also use toxic reagents. Additionally, the analysis is performed during the reproductive stage of growth, which does not allow enough time for corrective fertilization. Moreover, soybean growers do not have other tools to analyze the nutrition status during the earlier stages of development. Thus, this study proposes a quick approach for monitoring K+ in soybean crops using hyperspectral data through principal component analysis (PCA) and linear discriminant analysis (LDA) with a wavelength selection algorithm. The experiment was carried out at the Brazilian National Soybean Research Center in the 2017–2018, 2018–2019, and 2019–2020 soybean crop seasons, at the stages of development V4–V5, R1–R2, R3–R4, and R5.1–R5.3. Three treatments were evaluated that varied in K+ availability: severe potassium deficiency (SPD), moderate potassium deficiency (MPD), and an adequate supply of potassium (ASP). Spectral data were collected using an ASD Fieldspec 3 Jr. hyperspectral sensor. The results showed a variation in the leaf spectral signature based on the K+ availability, with SPD having higher reflectance in the visible region due to a lower concentration of pigments. PCA explained 100% of the variance across all stages and seasons, making it possible to distinguish SPD at an early development stage. LDA showed over 70% and 59% classification accuracies for discriminating a K+ deficiency in the simulation and validation stages. This study demonstrates the potential of the method as a rapid nondestructive and accurate tool for identifying K+ deficiency in soybean leaves. [ABSTRACT FROM AUTHOR]

Using the patch–clamp method in the whole-cell configuration, it was shown that external potassium ions play an important role in the regulation of calcium-activated chloride currents. A clear dependence of the amplitude of chloride currents on changes in the concentration of external potassium is shown. Changes in the concentration of sodium, magnesium, and calcium ions from outside the membrane have no significant effect, unlike the outside potassium ions. The effect of potassium on the amplitudes of chloride currents is significantly greater than the effect it has on other cell ionic currents—sodium, potassium, cation. There is reason to believe that a change in the amplitudes of chloride currents contributes to the pathophysiological processes characteristic of hypokalemia and hyperkalemia. [ABSTRACT FROM AUTHOR]

Background: The relationship of fibrin(ogen) degradation products (FDPs) and potassium with the functional outcomes of patients with aneurysmal subarachnoid hemorrhage (aSAH) is still uncertain. This study aims to evaluate the predictive value of a novel combination biomarker, the FDP-to-potassium ratio (FPR), for poor functional outcomes in patients with aSAH. Methods: A total of 425 consecutive patients with aSAH at a single center were retrospectively enrolled in our study. An unfavorable outcome was defined as a modified Rankin Scale (mRS) score of 3–6 at 3 months after discharge. Univariate analysis and multivariable logistic regression were performed for baseline information and laboratory parameters recorded at admission. In addition, the receiver operating characteristic curve was plotted, and propensity score matching was performed based on the FPR. Results: On the basis of mRS grade, 301 patients were classified as having favorable outcomes, and 124 patients were assessed as having unfavorable outcomes. FPR levels were significantly correlated with mRS grade (r[Spearman] = 0.410; P < 0.001). Multivariate logistic regression analysis showed that age (odds ratio [OR] 1.043, 95% confidence interval [CI] 1.016–1.071; P = 0.002), white blood cell count (OR 1.150, 95% CI 1.044–1.267; P = 0.005), potassium (OR 0.526, 95% CI 0.291–0.949; P = 0.033), World Federation of Neurosurgical Societies grade (OR 1.276, 95% CI 1.055–1.544; P = 0.012), and FPR (OR 1.219, 95% CI 1.102–1.349; P < 0.001) at admission were independently associated with poor functional outcomes. The DeLong test showed that the area under the receiver operating characteristic curve of FPR was higher than that of age, white blood cell count, potassium, World Federation of Neurosurgical Societies grade, or FDP alone, indicating that FPR had better predictive potential than these other variables. After 1:1 propensity score matching (FPR ≥ 1.45 vs. FPR < 1.45), the rate of poor prognosis was still significantly increased in the high-FPR group (48/121 [39.7%] vs. 16/121 [13.2%], P < 0.001). Conclusions: Fibrin(ogen) degradation product-to-potassium ratio is an independent predictor of poor outcomes for patients with aSAH and may be a promising tool for clinicians to evaluate patients' functional prognosis. [ABSTRACT FROM AUTHOR]

Objective The aim of the study is to explore the clinical and genetic characteristics of the combined oxidative phosphorylation defect type 21 (COXPD21) caused by the TARS2 compound heterozygous pathogenic variants, and to improve clinicians' awareness of the disease. Methods The proband was a girl of first birth, with repeated refractory hypokalemia, hearing impairment, developmental delay, intellectual disability, developmental retardation after infection, high limb muscle tension, and increased serum lactate as the clinical phenotype. The clinical performance, diagnosis, treatment process, and gene characteristics of COXPD21 caused by TARS2 of the case were analyzed, reviewed, and compared with the literature from the CNKI, Wanfang Data, and biomedical literature database (PubMed) until November 2021. Results The child was diagnosed with COXPD21 after two heterozygous variants in the TARS2 gene were found via whole exome sequencing. One of the variants was c.1679(exon14) A > C (p.Asp560Ala) missense, derived from the mother, and the other was c.1036(exon10)C > T (p.Arg346Cys) missense, derived from the father. The literature was searched and reviewed with the keywords "mitochondrial encephalomyopathy," "TARS2," and "combination oxidative phosphorylation deficiency type 21." A total of four complete domestic and foreign cases were collected from the literature search. Conclusion COXPD21 onset by a complex heterozygous variant of TARS2 causes refractory hypokalemia, which is rarely reported in China and abroad. [ABSTRACT FROM AUTHOR]

Background Insulin is a mainstay of treatment in diabetic ketoacidosis (DKA) however controversy remains over the optimal dose and administration. An initial bolus dose of insulin prior to a continuous infusion is utilized despite a lack of data showing clinical benefit and potential for complications. Objective This study was designed to evaluate the safety and efficacy of an initial insulin bolus in the treatment of DKA. Methods A retrospective chart review of patients with DKA was conducted. Fifty-nine patients met inclusion for the bolus group and 108 in the no-bolus group. The primary outcome was a composite of interruption of insulin infusion, hypoglycemia (BG <70 mg/dL), or hypokalemia (K+ <3.4 mEq/L) occurring within eight hours of starting insulin. Secondary outcomes included time to discontinuation of insulin infusion, as well as time to discharge from the ICU and the hospital. Results Baseline characteristics were similar between groups. The majority of patients were classified as having mild DKA. The primary outcome occurred significantly more frequently in the bolus group (45.8% vs 25%, P =.003) which was primarily driven by incidence of hypokalemia. Time to anion gap closure (6:39 vs 9:00, P =.063) was shorter with a bolus, although not significantly so. This finding carried forward to non-significant differences in time to stopping insulin infusion as well as ICU and hospital discharge. Conclusion An insulin bolus prior to initiation of an insulin infusion was associated with significantly more adverse effects early in therapy without a corresponding benefit in time to resolution of DKA. [ABSTRACT FROM AUTHOR]

SUMMARY: Potassium (K+), being an essential macronutrient in plants, plays a central role in many aspects. Root growth is highly plastic and is affected by many different abiotic stresses including nutrient deficiency. The Shaker‐type K+ channel Arabidopsis (Arabidopsis thaliana) K+ Transporter 1 (AKT1) is responsible for K+ uptake under both low and high external K+ conditions. However, the upstream transcription factor of AKT1 is not clear. Here, we demonstrated that the WRKY6 transcription factor modulates root growth to low potassium (LK) stress in Arabidopsis. WRKY6 showed a quick response to LK stress and also to many other abiotic stress treatments. The two wrky6 T‐DNA insertion mutants were highly sensitive to LK treatment, whose primary root lengths were much shorter, less biomass and lower K+ content in roots than those of wild‐type plants, while WRKY6‐overexpression lines showed opposite phenotypes. A further investigation showed that WRKY6 regulated the expression of the AKT1 gene via directly binding to the W‐box elements in its promoter through EMSA and ChIP‐qPCR assays. A dual luciferase reporter analysis further demonstrated that WRKY6 enhanced the transcription of AKT1. Genetic analysis further revealed that the overexpression of AKT1 greatly rescued the short root phenotype of the wrky6 mutant under LK stress, suggesting AKT1 is epistatic to WRKY6 in the control of LK response. Further transcriptome profiling suggested that WRKY6 modulates LK response through a complex regulatory network. Thus, this study unveils a transcription factor that modulates root growth under potassium deficiency conditions by affecting the potassium channel gene AKT1 expression. Significance Statement: This study has identified a WRKY‐type transcription factor WRKY6, which positively regulates potassium uptake, and mutants and overexpression lines showed opposite phenotypes. It exerts its role by directly binding to the promoter region of the potassium channel gene AKT1 and promoting its expression. [ABSTRACT FROM AUTHOR]

Introduction: New-onset Atrial Fibrillation (AF) carries significant morbidity and mortality risk for postoperative patients. Clinical practice guidelines aimed at preventing it are beneficial, with protocols in place to prevent deviations from the standard. Aim: To improve or strengthen the clinical practices that impact the incidence of new-onset AF after off-pump Coronary Artery Bypass Grafting (CABG). Materials and Methods: The present prospective clinical audit was conducted in the Department of Cardiac Anaesthesiology, Bhanubhai Madhuben Patel Cardiac Centre, Bhaikaka University, Anand, Gujarat, India, from January 2021 to June 2021. Study included 50 consecutive patients undergoing off-pump CABG surgery. The monitored standards included the continuation of betablocker therapy in the preoperative period, restarting them in the immediate postoperative period, and maintaining serum potassium (S.K+) within the range of 3.5-5.5 mEq/L. The incidence of AF was also noted. The data were analysed using Microsoft Excel. Results: The audit included a total of 50 patients, with 36 males with a mean age of 58.72 years, and 14 females with a mean age of 60.07 years. Preoperative beta-blocker/Calcium Channel Blocker (CCB) therapy on the day of surgery was administered to 45 (90%) patients, while restarting beta-blockers in the immediate postoperative period was done for 49 (98%) patients. S.K+ levels were maintained within the range in 31 (62%) patients. The last standard was reaudited, and compliance was achieved in 39 (78%) patients. New-onset AF occurred in 4 (8%) and 5 (10%) patients in the audit and reaudit samples, respectively. Conclusion: Clinical audit is a process that helps to identify the lacunae in clinical practices that affect patient outcomes. In the current study, clinical audits have aided in measuring compliance with different clinical practices, as per Institutional protocols. They have also assisted in increasing compliance with clinical practices where measured compliance was below the targeted goal. [ABSTRACT FROM AUTHOR]