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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]

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]

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]

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]

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]

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]

Background: Levetiracetam is an anti-seizure medication (ASM) with an established safety profile. However, a potential safety signal of hypokalemia following levetiracetam use was published in the World Health Organization newsletter. Objective: To investigate the possible causal association between the use of levetiracetam and the development of hypokalemia. Method: This was a new-user, active-comparator retrospective cohort study using Real-world Evidence Research Network data at the Saudi Food and Drug Authority from 2016 to 2022. Adults (≥ 18 years old) with an incident prescription for either levetiracetam or carbamazepine were followed for up to 6 months from the prescription date. Hypokalemia was ascertained by using diagnostic code (i.e., E87.6) or by serum potassium level below 3.5 mmol/L. A Cox proportional hazards model, adjusted with stabilized inverse probability of treatment weight, was fitted to compare the hazard of hypokalemia between levetiracetam and carbamazepine exposed patients. Results: A total of 8,982 patients entered the study cohort. The incidence rate of hypokalemia was 303 cases per 10,000 patient-years in the levetiracetam-exposed cohort compared to 57 cases per 10,000 patient-years among carbamazepine users. Compared to carbamazepine users, patients exposed to levetiracetam had an adjusted hazard ratio related to induced hypokalemia of 1.99 (95% confidence interval, 0.88–4.49). Results of sensitivity analyses were comparable to the main analysis. Conclusion: The hazard ratio for hypokalemia with the use of levetiracetam versus carbamazepine was statistically comparable. However, the potential association between levetiracetam use and hypokalemia cannot be ruled out given the elevated hazard ratios from the main and sensitivity analyses. Further studies may provide a more precise assessment of this association. [ABSTRACT FROM AUTHOR]

Abiotic stresses limit the quantity and quality of rice grain production, which is considered a strategic crop in many countries. In this study, a meta-analysis of different microarray data at seedling stage was performed to investigate the effects of multiple abiotic stresses (drought, salinity, cold situation, high temperature, alkali condition, iron, aluminum, and heavy metal toxicity, nitrogen, phosphorus, and potassium deficiency) on rice. Comparative analysis between multiple abiotic stress groups and their control groups indicated 561 differentially expressed genes (DEGs), among which 422 and 139 genes were up-regulated and down-regulated, respectively. Gene Ontology analysis showed that the process of responding to stresses and stimuli was significantly enriched. In addition, pathways such as metabolic process and biosynthesis of secondary metabolites were identified by KEGG pathway analysis. Weighted correlation network analysis (WGCNA) uncovered 17 distinct co-expression modules. Six modules were significantly associated with genes involved in response to abiotic stresses. Finally, to validate the results of the meta-analysis, five genes, including TIFY9 (JAZ5), RAB16B, ADF3, Os01g0124650, and Os05g0142900 selected for qRT-PCR analysis. Expression patterns of selected genes confirmed the results of the meta-analysis. The outcome of this study could help introduce candidate genes that may be beneficial for use in genetic engineering programs to produce more tolerant crops or as markers for selection. [ABSTRACT FROM AUTHOR]

This study aims to investigate the potential correlation between the use of olanzapine, a psychopharmacological intervention commonly prescribed in Anorexia Nervosa treatment, and the occurrence of Refeeding Syndrome. Despite the acknowledged nutritional and biochemical impacts of olanzapine, the literature lacks information regarding its specific association with Refeeding Syndrome onset in individuals with Anorexia Nervosa. This is a naturalistic, retrospective, observational study, reporting the occurrence of Refeeding Syndrome in children and adolescents with Anorexia Nervosa, treated or untreated with olanzapine. Dosages and serum levels of olanzapine were assessed for potential associations with the occurrence of Refeeding Syndrome and specific variations in Refeeding Syndrome–related electrolytes. Overall, 113 patients were enrolled, including 46 (41%) who developed a Refeeding Syndrome. Mild (87%), moderate (6.5%), and severe (6.5%) Refeeding Syndrome was described, at a current average intake of 1378 ± 289 kcal/day (39 ± 7.7 kcal/kg/die), frequently associated with nasogastric tube (39%) or parenteral (2.2%) nutrition. Individuals receiving olanzapine experienced a more positive phosphorus balance than those who did not (F(1,110) = 4.835, p = 0.030), but no difference in the occurrence of Refeeding Syndrome was documented. The mean prescribed doses and serum concentrations of olanzapine were comparable between Refeeding Syndrome and no-Refeeding Syndrome patients. Conclusion: The present paper describes the occurrence of Refeeding Syndrome and its association with olanzapine prescriptions in children and adolescents with Anorexia Nervosa. Olanzapine was associated with a more positive phosphorus balance, but not with a different occurrence of Refeeding Syndrome. Further, longitudinal studies are required. What is Known: • Refeeding Syndrome (RS) is a critical complication during refeeding in malnourished patients, marked by electrolyte (phosphorus, magnesium, potassium) imbalances. • Olanzapine, an atypical antipsychotic with nutritional and biochemical impacts, is used in Anorexia Nervosa (AN) treatment, however data concerning its association with RS are lacking. What is New: • The study observed RS in 46/113 (41%) young patients with AN. • Olanzapine-treated individuals showed a higher improvement in serum phosphate levels than untreated ones, although no impact on the occurrence of Refeeding Syndrome was observed. [ABSTRACT FROM AUTHOR]

The inland saline waters were continuously observed to have low potassium concentrations compared to their seawater counterpart of the same salinity. We hypothesize that the toxic effect of sulfate may manifest in low potassium saline (LPSW) waters compared to brackish water of the same salinity. Thus, LC50 trials were performed in GIFT (genetically improved farmed tilapia) fry (0.5 ± 0.02 g) to determine the acute sulfate toxicity in freshwater (FW, 0.5 g L−1), artificial seawater (ASW, 10 g L−1), and LPSW (10 g L−1). The median lethal concentrations (96h LC50) of sulfate ion in FW, LPSW, and ASW for the GIFT were 5.30 g L−1, 2.56 g L−1, and 2.98 g L−1, respectively. A second experiment was conducted for 21 days, exposing fish to a sub-lethal level of sulfate ion (SO42−) concentration (1000 mg L−1, one-fifth of FW LC50) with different types of waters (FW, freshwater, 0.5 g L−1; ASW, artificial seawater, 10 g L−1; LPSW, low potassium saline water, 10 g L−1) with and without sulfate inclusion to constitute the treatments as follows, (FW, FW + SO4, ASW, ASW + SO4, LPSW, LPSW + SO4). The effect of sulfate on GIFT reared in sulfate-rich potassium-deficient medium saline water was evaluated by focusing on the hematological adjustments, stress-induced oxidative damage, and osmoregulatory imbalances. The survival was not altered due to the sulfate concentration and K+ deficiency; however, there were significant changes in branchial NKA (Na+/K+-ATPase) activity and osmolality. The increase in NKA was highest in LPSW treatment, suggesting that internal ionic imbalance was triggered due to an interactive effect of sulfate and K+ deficiency. The cortisol levels showed a pronounced increase due to sulfate inclusion irrespective of K+ deficiency. The antioxidant enzymes, i.e., SOD (superoxide dismutase), catalase, GST (glutathione-S-transferase), and GPX (glutathione peroxidase), reflected a similar pattern of increment in the gills and liver of the LPSW + SO4 groups, suggesting a poor antioxidant status of the exposed group. The hepatic peroxidation status, i.e. TBARS (thiobarbituric acid reactive substances), and the peroxide values were enhanced due to both K+ deficiency and sulfate inclusion, suggesting a possible lipid peroxidation in the liver due to handling the excess sulfate anion concentration. The hematological parameters, including haemoglobin, total erythrocyte count, and hematocrit level, reduced significantly in the LPSW + SO4 group, indicating a reduced blood oxygen capacity due to the sulfate exposure and water potassium deficiency. The hepatic acetylcholine esterase activity was suppressed in all the treatments with sulfate inclusion, while the highest suppression was observed in the LPSW + SO4 group. Thus, it is concluded that sulfate-induced physiological imbalances manifest more in potassium-deficient water, indicating that environmental sulfate is more detrimental to inland saline water than freshwater or brackish water of the same salinity. [ABSTRACT FROM AUTHOR]

Approximately 1% of all patients with Sjögren's syndrome (SS) are children. Unlike the adult form, in which sicca syndrome is the main presentation, in children, the most common clinical finding is recurrent enlargement of the salivary glands. In pediatric SS, extraglandular manifestations represent a significant feature and, among these, kidney manifestations are relevant. Kidney involvement is observed in 5–20.5% of children with SS, most frequently tubulointerstitial nephritis. This injury can lead to serious phenotypes, including distal kidney tubular acidosis with the development of severe hypokalemia, which can lead to ECG abnormalities, weakness, and hypokalemic periodic paralysis. Kidney implications in pediatric SS also include nephrolithiasis, nephrocalcinosis, and various types of glomerular damage, which often require immunosuppressive therapies. Laboratory findings are usually comparable to adults, including hyperglobulinemia and high rates of antinuclear antibodies (ANA, 63.6–96.2%), and anti-Ro/SSA (36.4–84.6%). The current classification criteria for SS are inaccurate for the pediatric population, and more specific criteria are needed to improve the diagnostic rate. Due to the rarity of the disease, strong recommendations for treatment are lacking, and several therapeutic strategies have been reported, mostly based on glucocorticoids and disease-modifying antirheumatic drugs, with different outcomes. The aim of this paper is to provide an overview of the kidney implications of pediatric SS based on the latest evidence of the medical literature. [ABSTRACT FROM AUTHOR]

Introduction: This study will test the hypothesis that primary aldosteronism (PA) involves alterations in Na+, K+, and water content in the skin that are corrected by adrenalectomy. Aim and Methods: In skin biopsies, we will measure the content of Na+, K+, water, by physical-chemical methods and the osmotic-stress-responsive transcription factor Tonicity-responsive Enhancer Binding Protein (TonEBP, NFAT5) mRNA copy number by droplet digital PCR, in sex-balanced cohorts of 18 -75-year-old consecutive consenting patients with unilateral and bilateral PA, primary (essential) hypertension, and normotension. Before surgery, the patients with unilateral PA will receive the mineralocorticoid receptor antagonist (MRA) canrenone at doses that correct hypokalemia and high blood pressure values. They will be reassessed in an identical way one month after surgical cure, while off MRA. PA patients not selected for adrenalectomy will similarly be assessed at diagnosis and follow-up while on stable MRA treatment. Since a pilot study showed a direct correlation of dry weight (DW) with skin electrolytes and water content and significant differences of biopsy DW between surgery and follow-up, meaningful comparison of the skin cations and water content and TonEBP mRNA copy number, between specimen obtained at different time points, will require DW- and total mRNA-adjustment, respectively. Conclusion: This study will provide novel information on the skin Na+, K+ and water content in PA, the paradigm of salt-dependent hypertension, and novel knowledge on the effect of surgical cure of hyperaldosteronism. The TonEBP-mediated regulation of Na+, K+ and water content in the skin will also be unveiled. Trail Registry: Trial Registration number: NCT06090617. Date of Registration: 2023-10-19. [ABSTRACT FROM AUTHOR]

Objective: To estimate the incidence rates (IR) of prespecified outcomes of interest in pediatric patients (1 month to < 1 year) treated with intravenous (IV) pantoprazole using Optum's longitudinal electronic health records database (Optum Market Clarity) from the United States (US). Methods: This real-world, non-interventional, retrospective cohort study was conducted from 01 January 2007 to 31 December 2020 in patients who received IV pantoprazole. Premature patients and those weighing < 2.36 kg were excluded. Patients were categorized based on diagnosis of gastroesophageal reflux disease (GERD) and erosive esophagitis (EE) into: Subgroup 1 (GERD and EE), Subgroup 2 (GERD and no EE), and Subgroup 3 (absence of GERD and EE). Overall IRs (per 1000 person-years [PY]) and 95% confidence intervals (CI) of outcomes were estimated (overall and subgroups) and stratified by duration of IV pantoprazole treatment (< 4 days versus ≥ 4 days). Results: Of 1879 eligible patients, none were identified in Subgroup 1; 851 (45.3%) and 1028 (54.7%) patients were identified in Subgroups 2 and 3, respectively. IRs of outcomes of interest ranged from 0.0 to 742.8 per 1000 PY. IRs were highest for vomiting (742.80), diarrhea (377.77), abdominal distension (214.31), hyponatremia (204.99), and hypokalemia (203.49). IRs were comparable between Subgroups 2 and 3. For most outcomes, IRs were higher among patients treated with IV pantoprazole for ≥ 4 days versus those treated for < 4 days. Conclusion: These results are consistent with the known safety profile of pantoprazole and emphasize the utility of using real-world data from pediatric populations for assessment of safety outcomes. [ABSTRACT FROM AUTHOR]

We investigated the effectiveness of antibiotics (amikacin, bedaquiline, linezolid, moxifloxacin, and rifampicin) on metabolically inert M. abscessus obtained under conditions of potassium deficiency in vitro. It was found that bedaquiline led to a significant decrease in the ability of bacteria to form colonies on dense media, but did not lead to their death, since it was shown that during cultivation in a liquid medium, they reverted to a state of active division and growth. Moxifloxacin had a bactericidal effect against metabolically inert bacteria, irreversibly and significantly reducing the number of viable cells in culture, which emphasizes the effectiveness of its use for the treatment of infections caused by M. abscessus. [ABSTRACT FROM AUTHOR]

The soybean grain yield is affected by several factors, among them, the nutritional deficiency caused by low levels of potassium (K+) is one of the main responsible for the reduction in grain yield both in Brazil and worldwide. Traditional methods of nutrient determination involve leaf collection and laboratory procedures with toxic reagents, which is a destructive, time-consuming, expensive, and environmentally unfriendly method. In this context, the use of hyperspectral data and machine learning regression models can be a powerful tool in the nutritional diagnosis of plants. However, the comparison among different machine learning algorithms for K+ estimation in soybean leaves from hyperspectral reflectance data is yet to be reported. From this, the goal of this research was to obtain K+ prediction models in soybean leaves at different stages of development using hyperspectral data and machine learning regression models with wavelength selection algorithms. The experiment was carried out at the National Soybean Research Centre (Embrapa Soja) in the 2017/2018, 2018/2019 and 2019/2020 soybean crop season, at the stages of development V4–V5, R1–R2, R3–R4 and R5.1–R5.3. The experimental plots were managed to obtain different conditions of K+ availability for the plants, from severe deficiency level to the appropriate level of nutrient, under the following experimental treatments: severe potassium deficiency, moderate potassium deficiency and adequate supply of potassium. Spectral data were obtained by the ASD Fieldspec 3 Jr. hyperspectral sensor in the visible/near-infrared spectral range (400–1000 nm) and correlated to leaf K+ through ten machine learning methods: Partial Least Square Regression (PLSR), interval Partial Least Squares (iPLS), Genetics Algorithm (GA), Competitive Adaptive Reweighted Sampling (CARS), Random Frog (RF, Frog), Variable combination population analysis (VCPA), Principal Component Regression (PCR), Support Vector Machine (SVM), Successive projections algorithm (SPA), and Stepwise. The results showed that K+ deficiency significantly reduce grain yield and nutrient content in the leaf, making enabling the clustering separation of all treatments by Tukey's test. Among the 601 wavelengths obtained by the sensor, the algorithms selected from 1 to 33.28%, largely distributed in the regions of red, green, blue, red-edge and NIR. In all stages of development, it was possible to quantify the nutrient with high accuracy (R2 ≅ 0.88). The multivariate regression models from the selection of variables contributed to increase the accuracy (R2) in about 7.65% for the calibration step and 6.45% for the cross-validation step, when compared to the model using the full spectra. The results obtained demonstrate that the monitoring of K+ in soybean leaves is possible and has the potential to determine the nutritional content in the early stages of plant development. [ABSTRACT FROM AUTHOR]

Background: Oral Abiraterone acetate is a novel antineoplastic agent approved by the FDA for the treatment of metastatic prostate cancer. Abiraterone is an irreversible inhibitor of the 17α-hydroxylase (CYP17) enzyme complex resulting in a reduction of androgens and corticosteroids. It may cause mineralocorticoid excess syndrome; hence, it is prescribed with steroids. Here we describe a case of postoperative severe hypokalemia with unusual presentation in a patient after spine surgery in which abiraterone with prednisolone was continued preoperatively. Anesthetic concerns about the perioperative administration of abiraterone have not been reported in the literature. Case presentation: An 80-year-old male with a known case of metastatic prostate cancer was posted for spine surgery under general anesthesia. Surgery was uneventful and the patient was extubated after ensuring adequate muscle power and respiratory parameters. Postoperatively, the patient developed aphonia, quadriparesis, and respiratory distress leading to reintubation. After evaluation, severe grade 4 hypokalemia was found to be the causative factor. The patient recovered well after potassium and steroid supplementation. Low potassium and cortisol levels indicate a diagnosis of abiraterone-induced hypokalemia. Conclusion: Patients on abiraterone require more stringent and vigilant monitoring of potassium and cortisol levels. In such circumstances, it might be advantageous to add additional steroids or substitute alternative steroids. [ABSTRACT FROM AUTHOR]

Purpose: Information regarding frequency, details of neurological signs and recovery patterns of patients with secondary hypokalaemic paralysis (HP) is limited. This study aimed to analyse the frequency, aetiology, clinical features and recovery patterns of patients with secondary HP. Methods: The clinical and laboratory records of 18 consecutive patients with secondary HP aged ≥ 18 years admitted to our hospital between April 2011 and March 2022 were reviewed. Patients with inherited hypokalaemic periodic paralysis were excluded. Results: Of the 18 patients, 16 had a common aetiology: chronic alcoholism, diarrhoea or an imbalanced diet. Initial symptoms, such as fatigue, were often atypical. Three patients had prominent asymmetric limb weakness and four had predominant upper limb weakness. On admission, the mean serum potassium and creatine kinase (CK) levels of the patients were 1.90 mmol/L and 4488 U/mL, respectively. Ten patients (56%) had decreased potassium levels after admission, despite potassium replacement treatment (rebound hypokalaemia). Twelve patients presented with increased CK levels even after 2–5 days (delayed hyperCKaemia). Low serum magnesium levels significantly correlated with rebound hypokalaemia. Conclusions: Secondary HP can be caused by a variety of conditions, but mainly occurs due to lifestyle conditions/disorders. Secondary HP often presents with atypical symptoms, and the initial symptoms can be non-specific. Rebound hypokalaemia and delayed hyperCKaemia are common in secondary HP, despite potassium replacement. As such, careful serial monitoring is needed for patients with secondary HP. [ABSTRACT FROM AUTHOR]

Potassium (K) deficiency in maize plants damages the nutritional functions of K. However, few studies have investigated the influence of K on C:N:P stoichiometry, the nutritional efficiency of these nutrients, and whether the mitigating effect of Si in plants under stress could act on these nutritional mechanisms involved with C, N, and P to mitigate K deficiency. Therefore, this study aimed to evaluate the impact of K deficiency in the absence and presence of Si on N and P uptake, C:N:P stoichiometric homeostasis, nutritional efficiency, photosynthetic rate, and dry matter production of maize plants. The experiment was conducted under controlled conditions using a 2 × 2 factorial scheme comprising two K concentrations: potassium deficiency (7.82 mg L−1) and potassium sufficiency (234.59 mg L−1). These concentrations were combined with the absence (0.0 mg L−1) and presence of Si (56.17 mg L−1), arranged in randomized blocks with five replicates. Potassium deficiency decreased stoichiometric ratios (C:N and C:P) and the plant's C, N, and P accumulation. Furthermore, it decreased the use efficiency of these nutrients, net photosynthesis, and biomass of maize plants. The results showed that Si supply stood out in K-deficient maize plants by increasing the C, N, and P accumulation. Moreover, it decreased stoichiometric ratios (C:N, C:P, N:P, C:Si, N:Si, and P:Si) and increased the efficiencies of uptake, translocation, and use of nutrients, net photosynthesis, and dry matter production of maize plants. Therefore, the low nutritional efficiency of C, N, and P caused by K deficiency in maize plants can be alleviated with the supply of 56.17 mg L−1 of Si in the nutrient solution. It changes C:N:P stoichiometry and favors the use efficiency of these nutrients, which enhances the photosynthesis and sustainability of maize. [ABSTRACT FROM AUTHOR]

Background: Hyperkalemia and hypokalemia are associated with mortality in patients undergoing hemodialysis. However, there are few reports on the association between potassium level fluctuations and mortality. We retrospectively investigated the association between serum potassium level variability and mortality in patients undergoing hemodialysis. Methods: This study was conducted at a single center. Variability in serum potassium levels was evaluated using the standard deviation of potassium level from July 2011 to June 2012, and its association with prognosis was examined by following up the patients for 5 years. Serum potassium variability was assessed as the coefficient of variation, and the statistical analysis was performed after log transformation. Results: Among 302 patients (mean age 64.9 ± 13.3; 57.9% male; and median dialysis vintage 70.5 months [interquartile range, IQR 34–138.3]), 135 died during the observation period (median observation period 5.0 years [2.3–5.0]). Although the mean potassium level was not associated with prognosis, serum potassium level variability was associated with prognosis, even after adjustments for confounding factors such as age and dialysis time (hazard ratio: 6.93, 95% confidence interval [Cl] 1.98–25.00, p = 0.001). After the adjustments, the coefficient of variation of potassium level in the highest tertile (T3) showed a higher relative risk for prognosis than that in T1 (relative risk: 1.98, 95% CI 1.19–3.29, p = 0.01). Conclusions: Variability in serum potassium levels was associated with mortality in patients undergoing hemodialysis. Careful monitoring of potassium levels and their fluctuations is necessary for this patient population. [ABSTRACT FROM AUTHOR]

Salinity is one of the most constraining environmental factors that limits plant growth and productivity because it disturbs mineral nutrition by triggering interactions at the interface soil roots. It implies a notable competition between sodium (Na+) and potassium (K+), with this last mineral being a key nutrient for plants. Using the halophyte Cakile maritima as a model plant grown in hydroponic conditions, this study was aimed to analyze how the simultaneous stressful conditions of high salinity (400 mM NaCl) and K+ deficiency (0 mM) for 15 days affect plant growth, ion balance, and antioxidant and NADPH-generating systems. Among the parameters analyzed, the most remarkable changes were observed in leaves, with drastic increases in the Na+/K+, Na+/Ca2+ and Na+/Mg2+ ratios, an enhanced accumulation of anthocyanins, and the induction of 3 new copper/zinc superoxide dismutase (CuZnSOD) isozymes in plants simultaneously exposed to both stresses. Taken together, the data revealed that the combination of both, high salinity and K+ deficiency, caused oxidative stress and modulated the whole antioxidative response of C. maritima in leaves and roots. Besides the differential response underwent by both organs, considering the different parameters analyzed under these stressful conditions, the most notable traits were that the effect of both stresses seems to be not additive and that salinity appears to improve C. maritima response to K+, a behavior not manifested in glycophyte species. Taken together our data support that, under extreme conditions that lead to an excess of ROS production, the induction of several CuZn-SODs in C. maritima may be one of the most outstanding strategies for the adaptation of this plant species to survive. [ABSTRACT FROM AUTHOR]

Background: Valproic acid is prescribed for epilepsy and as prophylaxis for bipolar disorder and migraine headaches. It has also been implicated as a cause of a kidney tubular injury. Methods: We undertook a review of the literature to characterize the biochemical and histopathological features of the overt kidney tubular injury and to evaluate the possible existence of a pauci-symptomatic injury. The pre-registered review (CRD42022360357) was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology. Searches were conducted in Excerpta Medica, the National Library of Medicine, and Web of Science. The gray literature was also considered. Results: For the final analysis, we retained 36 articles: 28 case reports documented 48 individuals with epilepsy on valproic acid for 7 months or more and presenting with features consistent with an overt kidney tubular injury. The following disturbances were noted: hypophosphatemia (N = 46), normoglycemic glycosuria (N = 46), total proteinuria (N = 45), metabolic acidosis (N = 36), hypouricemia (N = 27), tubular proteinuria (N = 27), hypokalemia (N = 23), and hypocalcemia (N = 8). A biopsy, obtained in six cases, disclosed altered proximal tubular cells with giant and dysmorphic mitochondria. Eight case series addressed the existence of a pauci- or even asymptomatic kidney injury. In the reported 285 subjects on valproic acid for 7 months or more, an isolated tubular proteinuria, mostly N-acetyl-β-glucosaminidase, was often noted. Conclusions: Valproic acid may induce an overt kidney tubular injury, which is associated with a proximal tubular mitochondrial toxicity. Treatment for 7 months or more is often associated with a pauci- or oligosymptomatic kidney tubular injury. [ABSTRACT FROM AUTHOR]

The treatment of patients with acute myeloid leukemia (AML) who are intolerable to intensive chemotherapy remains to be further explored. Recent studies have shown that venetoclax combined with hypomethylating agents (HMAs) or low-dose cytarabine (LDAC) may have a good effect on these patients. Given the lack of a comprehensive analysis of the efficacy and safety of such treatment, the aim of this review was to assess the efficacy and safety of venetoclax plus HMAs or LDAC for untreated AML patients who are ineligible for intensive chemotherapy. A systematic literature review was conducted in the PubMed, Embase, and Cochrane databases up to April 30, 2021. A total of four clinical trials including 440 patients were eligible for this meta-analysis. The pooled complete remission (CR) and complete remission plus complete remission with incomplete blood count recovery (CR/CRi) rates were 0.40 (95% CI 0.26–0.55) and 0.64 (95% CI 0.49–0.77), respectively. The median overall survival time was 11.7 (95% CI 10.15–14.18) months. The most common adverse events (AEs) of any grade were nausea (57%), diarrhea (42%), and hypokalemia (36%). The most common AEs of grade ≥ 3 were febrile neutropenia (38%) and thrombocytopenia (35%). The pooled 30-day mortality rate in our study was 5%. The improved remission rate and tolerance make venetoclax combined with HMAs or LDAC an attractive induction therapy option for untreated AML patients who are unsuitable for intensive chemotherapy. [ABSTRACT FROM AUTHOR]

Patients with cirrhosis are prone to electrolyte disorders, including hypokalaemia. The available evidence suggests that hypokalaemia facilitates hyperammonaemia and thus increases the risk for hepatic encephalopathy (HE). In case studies, plasma potassium decrements were followed by plasma ammonia increments and HE progression, which was reversed by potassium supplementation. The explanation to the hyperammonaemia may be that hypokalaemia both stimulates renal ammonia production and reduces hepatic ammonia elimination by urea synthesis. Further, hypokalaemia eases the entrance of the increased ammonia into the central nervous system because the lower potassium ion concentration favours the competition of NH4+ ions for potassium transporters across the blood brain barrier, and because hypokalaemia-induced metabolic alkalosis increases the amount of gaseous ammonia, which freely passes the barrier. Potassium depletion thus seems to be a mechanistic contributor to HE, supporting the clinical notion of routinely correcting low potassium in patients with cirrhosis. [ABSTRACT FROM AUTHOR]

HLX22 is a novel monoclonal antibody targeting human epidermal growth factor receptor 2 (HER2). This first-in-human, phase 1 dose-escalation study aimed to evaluate the safety, pharmacokinetics, pharmacodynamics, and preliminary efficacy of HLX22 in patients with advanced solid tumors who had failed or were intolerant to standard therapies. Enrolled patients aged 18 to 75 years with histologically confirmed HER2-overexpressing advanced or metastatic solid tumors received intravenous HLX22 once every 3 weeks at 3, 10, and 25 mg/kg. Primary endpoints were safety and the maximum tolerated dose (MTD). Secondary endpoints included pharmacokinetics, pharmacodynamics, immunogenicity, and efficacy. Between July 31, 2019, and December 27, 2021, 11 patients were enrolled to receive HLX22 at 3 (n = 5), 10 (n = 3), and 25 (n = 3) mg/kg doses. The most common treatment-emergent adverse events were lymphocyte count decreased (45.5%), white blood cell count decreased (36.4%), and hypokalemia (36.4%). No serious adverse events or dose-limiting toxicities occurred during the treatment period, and the MTD was determined at 25 mg/kg once every 3 weeks. Systemic exposure of HLX22 increased with escalating dose levels. No patients achieved a complete or partial response, and four (36.4%) had stable disease. The disease control rate and median progression-free survival were 36.4% (95% confidence interval [CI], 7.9–64.8) and 44.0 days (95% CI, 41.0–170.0), respectively. HLX22 was well tolerated in patients with advanced solid tumors overexpressing HER2 after failure of standard therapies. The study results support further investigation of HLX22 in combination with trastuzumab and chemotherapy. [ABSTRACT FROM AUTHOR]

Background: Few studies describe acute kidney injury (AKI) burden during paediatric cisplatin therapy and post-cisplatin kidney outcomes. We determined risk factors for and rate of (1) AKI during cisplatin therapy, (2) chronic kidney disease (CKD) and hypertension 2–6 months post-cisplatin, and (3) whether AKI is associated with 2–6-month outcomes. Methods: This prospective cohort study enrolled children (aged < 18 years at cancer diagnosis) treated with cisplatin from twelve Canadian hospitals. AKI during cisplatin therapy (primary exposure) was defined based on Kidney Disease: Improving Global Outcomes (KDIGO) serum creatinine criteria (≥ stage one). Severe electrolyte abnormalities (secondary exposure) included ≥ grade three hypophosphatemia, hypokalemia, or hypomagnesemia (National Cancer Institute Common Terminology Criteria for Adverse Events v4.0). CKD was albuminuria or decreased kidney function for age (KDIGO guidelines). Hypertension was defined based on the 2017 American Academy of Pediatrics guidelines. Results: Of 159 children (median [interquartile range [IQR]] age: 6 [2–12] years), 73/159 (46%) participants developed AKI and 55/159 (35%) experienced severe electrolyte abnormalities during cisplatin therapy. At median [IQR] 90 [76–110] days post-cisplatin, 53/119 (45%) had CKD and 18/128 (14%) developed hypertension. In multivariable analyses, AKI was not associated with 2–6-month CKD or hypertension. Severe electrolyte abnormalities during cisplatin were associated with having 2–6-month CKD or hypertension (adjusted odds ratio (AdjOR) [95% CI]: 2.65 [1.04–6.74]). Having both AKI and severe electrolyte abnormalities was associated with 2–6-month hypertension (AdjOR [95% CI]: 3.64 [1.05–12.62]). Conclusions: Severe electrolyte abnormalities were associated with kidney outcomes. Cisplatin dose optimization to reduce toxicity and clear post-cisplatin kidney follow-up guidelines are needed. [ABSTRACT FROM AUTHOR]

Kidney tubules are responsible for the preservation of fluid, electrolyte and acid-base homeostasis via passive and active mechanisms. These physiological processes can be disrupted by inherited or acquired aetiologies. The net result is a tubulopathy. It is important to make a prompt and accurate diagnosis of tubulopathies in children and young adults. This allows timely and appropriate management, including disease-specific therapies, and avoids complications such as growth failure. Tubulopathies can present with a variety of non-specific clinical features which can be diagnostically challenging. In this review, we build from this common anatomical and physiological understanding to present a tangible appreciation of tubulopathies as they are likely to be clinically encountered among affected children and young adults. [ABSTRACT FROM AUTHOR]

The clinical manifestations of primary distal renal tubular acidosis usually begin in childhood, but the disease is caused by a genetic defect that persists throughout life. This review focuses on the complications of distal tubular acidosis that occur or remain long-term such as nephrocalcinosis and urolithiasis, growth impairment, bone mineralization, severe hypokalemia, kidney cysts, and progressive kidney failure, as well as other persistent manifestations that occur independent of acidosis but are associated with some inherited forms of the disease. The pathogenic factors responsible for kidney failure are discussed in particular because it is a complication to which different publications have recently drawn attention and which affects a high percentage of adults with primary distal renal tubular acidosis. The need to maintain optimal metabolic control of the disease and scheduled clinical follow-up throughout life and the importance of organizing protocols for the transition of patients to adult nephrology services are emphasized. [ABSTRACT FROM AUTHOR]

We describe an unusual clinical presentation of autoimmune Bartter syndrome in a patient with primary hypothyroidism. A 65-year-old female patient was admitted with neuromuscular weakness associated with hypokalemia and metabolic alkalosis. She had a suboptimal response to potassium supplementation and potassium-sparing diuretic resulting in re-hospitalization with the same symptoms. A detailed serum and urinary biochemistry analysis in the absence of other causes of potassium wasting helped diagnose Bartter syndrome, a rare entity in adults. An autoimmune profile showed anti-Scl-70 antibody to be positive, although she did not develop other systemic features of the disease. Our patient responded to a steroid-based regimen potassium supplement, Indomethacin, and aldosterone antagonist with remarkable resolution of symptoms and correction of electrolyte derangement. We reviewed the literature to search for similar cases and included twenty-seven full-length publications on acquired and autoimmune causes of Bartter syndrome. Our case highlights the fact that hypokalemia with metabolic alkalosis in an adult patient should prompt clinicians to evaluate for common and uncommon conditions. While assessing for abnormal conditions, acquired Bartter syndrome should be considered if a patient has an underlying autoimmune, endocrine, or connective tissue disease. [ABSTRACT FROM AUTHOR]

Background: Hypokalemic paralysis is characterized by episodic attacks of flaccid muscle weakness of variable duration and severity associated with hypokalemia. Overall, there is a scarcity of data regarding hypokalemic paralysis from Indian subcontinent particularly from rural areas. Methods: A total of 50 consecutive patients of hypokalemic paralysis who were admitted in our hospital were recruited in this study. Results: Fifty patients of hypokalemic paralysis were admitted to our department over a period of 4 years. Forty-two (84%) patients presented with classic acute onset quadriparesis, while eight patients had atypical presentation. Five patients had paraparesis, two had hemiparesis and one patient presented with isolated neck muscle weakness without any limb weakness. Thirty-two patients had primary hypokalemic periodic paralysis (HoPP) and 18 had secondary hypokalemic paralysis. There was no significant difference in severity of weakness (p = 0.53), number of episodes of weakness (p = 0.66) and serum CPK levels (p = 0.36) between primary and secondary hypokalemic paralysis. Secondary cases required significantly prolonged time for recovery as well as higher potassium supplements as compared to the primary HoPP. The severity of weakness of proximal muscles measured in MRC grading showed a significant correlation with serum potassium levels (p = 0.010), but did not show any correlation with CPK Levels (p = 0.86). Conclusion: Hypokalemic paralysis is an important cause of acute flaccid paralysis in the Emergency Room that often improves dramatically with potassium supplements. While secondary cases often require treatment of underlying etiology, primary hypokalemic paralysis often requires chronic treatment with acetazolamide and/or potassium-sparing diuretics. Key Message: Hypokalemic paralysis is an important differential diagnosis of acute flaccid paralysis that rapidly recovers with treatment. Most of the cases are primary, usually a calcium channel disorder (Type I) or very rarely a sodium channel disorder (Type II). However, secondary causes should be evaluated for and reasonably excluded before labeling the disorder as primary hypokalemic paralysis. [ABSTRACT FROM AUTHOR]

Gitelman syndrome represents the clinical manifestations of inactivation of the Slc12a3 genes encoding the thiazide-sensitive sodium chloride cotransporter and the Trpm6-Mg genes encoding the magnesium transporters in the distal convoluted tubule. In fact, the biochemical findings resemble those with thiazide diuretics such as hypokalemia, hypomagnesaemia, hypocalciuria, metabolic alkalosis, and low normal blood pressure. He is usually associated with calcium pyrophosphate deposition. Serum uricemia level is rarely affected in Gitelman syndrome. We aimed to report a rare association of chronic gout with Gitelman syndrome, hence the interest of our case. We describe a 29-year-old male patient with a history of Gitelman syndrome associated with articular gout including pelvic localization. We provided pictorial evidence of extensive and diffuse monosodium urate deposition in articular and periarticular structures to confirm the gout origin. A literature review illustrates 4 reported cases of Gitelman syndrome associated with gout. The gender distribution was equal with a mean age of 40 years. Key Points • Gouty arthritis and Gitelman syndrome is a rare association. • Gitelman syndrome may be a new risk factor for the development of gout, due to its thiazide-like effect. [ABSTRACT FROM AUTHOR]

The dysfunction of Na+-Cl− cotransporter (NCC) caused by mutations in solute carrier family12, member 3 gene (SLC12A3) primarily causes Gitelman syndrome (GS). In identifying the pathogenicity of R158Q and G212S variants of SLC12A3, we evaluated the pathogenicity by bioinformatic, expression, and localization analysis of two variants from a patient in our cohort. The prediction of mutant protein showed that p.R158Q and p.G212S could alter protein's three-dimensional structure. Western blot showed a decrease of mutant Ncc. Immunofluorescence of the two mutations revealed a diffuse positive staining below the plasma membrane. Meanwhile, we conducted a compound heterozygous model—Ncc R156Q/G210S mice corresponding to human NCC R158Q/G212S. NccR156Q/G210S mice clearly exhibited typical GS features, including hypokalemia, hypomagnesemia, and increased fractional excretion of K+ and Mg2+ with a normal blood pressure level, which made NccR156Q/G210S mice an optimal mouse model for further study of GS. A dramatic decrease and abnormal localization of the mutant Ncc in distal convoluted tubules contributed to the phenotype. The hydrochlorothiazide test showed a loss of function of mutant Ncc in NccR156Q/G210S mice. These findings indicated that R158Q and G212S variants of SLC12A3 were pathogenic variants of GS. [ABSTRACT FROM AUTHOR]

A clinical quiz on a case of a child patient with growth retardation and late-onset hypertension is presented.

Neonatal hypokalemia (defined as a serum potassium level <3.5 mEq/L) is the most common electrolyte disorder encountered in clinical practice. In addition to common secondary causes, primary genetic etiologies are also closely associated with hypokalemia. Currently, a systematic characterization of these genetic disorders is lacking, making early recognition challenging and clinical management uncertain. This review will aid clinicians by summarizing the genetic background of neonatal hypokalemia from two aspects: (1) increased excretion of K+, whereby genetic factors primarily lead to increased renal Na+ influx, decreased H+ efflux, or reduced Cl− influx, ultimately resulting in increased K+ efflux; and (2) decreased extracellular distribution of K+, whereby genetic factors result in abnormalities in transmembrane ion channels, reducing outward potassium currents or generating inward cation leak currents. We describe over ten genetic diseases associated with neonatal hypokalemia, which involve pathogenic variants in dozens of genes and affect multiple target organs, including the kidneys, intestines, and skeletal muscle. For example, in the renal tubules, pathogenic variants in the SLC12A1 gene encoding the Na+-K+-2Cl- cotransporter lead to renal K+ loss, causing Bartter syndrome type I; in intestinal epithelial cells, pathogenic variants in the SLC26A3 gene result in a defective Cl⁻-HCO₃⁻ exchanger, causing congenital chloride diarrhea; and in skeletal muscle, pathogenic variants in the CACNA1S gene impact membrane calcium ion channels resulting in hypokalemic periodic paralysis. Given the wide variety of organs and genetic alterations that can contribute to neonatal hypokalemia, we believe this review will provide valuable insights for clinical diagnosis and treatment.A higher resolution version of the Graphical abstract is available as Supplementary informationA higher resolution version of the Graphical abstract is available as Supplementary informationGraphical abstract: Neonatal hypokalemia (defined as a serum potassium level <3.5 mEq/L) is the most common electrolyte disorder encountered in clinical practice. In addition to common secondary causes, primary genetic etiologies are also closely associated with hypokalemia. Currently, a systematic characterization of these genetic disorders is lacking, making early recognition challenging and clinical management uncertain. This review will aid clinicians by summarizing the genetic background of neonatal hypokalemia from two aspects: (1) increased excretion of K+, whereby genetic factors primarily lead to increased renal Na+ influx, decreased H+ efflux, or reduced Cl− influx, ultimately resulting in increased K+ efflux; and (2) decreased extracellular distribution of K+, whereby genetic factors result in abnormalities in transmembrane ion channels, reducing outward potassium currents or generating inward cation leak currents. We describe over ten genetic diseases associated with neonatal hypokalemia, which involve pathogenic variants in dozens of genes and affect multiple target organs, including the kidneys, intestines, and skeletal muscle. For example, in the renal tubules, pathogenic variants in the SLC12A1 gene encoding the Na+-K+-2Cl- cotransporter lead to renal K+ loss, causing Bartter syndrome type I; in intestinal epithelial cells, pathogenic variants in the SLC26A3 gene result in a defective Cl⁻-HCO₃⁻ exchanger, causing congenital chloride diarrhea; and in skeletal muscle, pathogenic variants in the CACNA1S gene impact membrane calcium ion channels resulting in hypokalemic periodic paralysis. Given the wide variety of organs and genetic alterations that can contribute to neonatal hypokalemia, we believe this review will provide valuable insights for clinical diagnosis and treatment.A higher resolution version of the Graphical abstract is available as Supplementary informationA higher resolution version of the Graphical abstract is available as Supplementary information [ABSTRACT FROM AUTHOR]

Background and aims: Potassium (K+) deficiency is a major abiotic stress that severely hampers plant growth and development. Hydrogen sulfide (H2S), a signal molecule regulating several critical functions in plants, is involved in plant tolerance to various environmental stresses. However, its involvement in the alleviation of K+ deficiency is not yet elucidated. The objective of the present work was to study the effects of K+ deficiency-H2S interaction on Brassica napus (rapeseed).Plants were grown under two potassium regimes (K+ control C, 3 mM) and (K+ deficient KD, 20 µM) in the absence or the presence of 200 µM NaHS (H2S donor).Results demonstrated that K+ deficiency reduced plant growth, pigment and soluble sugar concentrations, as well as diminished photosynthetic activity. Notably, photosystem II (PSII) was more affected than photosystem I (PSI), as indicated by modulated chlorophyll measurements. The exogenous application of NaHS significantly alleviated these negative effects induced by K+ deficiency. This amelioration was associated with increased activity of L/D-cysteine desulfhydrase (LCD and DCD) enzymes, which contributed to maintaining adequate endogenous H2S and nitric oxide (NO) concentrations. These balanced levels of H2S and NO improved rapeseed plants' ability to cope with K+ deficiency stress.This study suggests a synergistic action of H2S and NO in mitigating K+ deficiency stress by enhancing plant growth, photosynthetic capacity, and energy conversion in both photosystems. This research implies that H2S could serve as a sustainable solution to boost plant growth and productivity, potentially ensuring food security, particularly in underdeveloped economies.Methods: Potassium (K+) deficiency is a major abiotic stress that severely hampers plant growth and development. Hydrogen sulfide (H2S), a signal molecule regulating several critical functions in plants, is involved in plant tolerance to various environmental stresses. However, its involvement in the alleviation of K+ deficiency is not yet elucidated. The objective of the present work was to study the effects of K+ deficiency-H2S interaction on Brassica napus (rapeseed).Plants were grown under two potassium regimes (K+ control C, 3 mM) and (K+ deficient KD, 20 µM) in the absence or the presence of 200 µM NaHS (H2S donor).Results demonstrated that K+ deficiency reduced plant growth, pigment and soluble sugar concentrations, as well as diminished photosynthetic activity. Notably, photosystem II (PSII) was more affected than photosystem I (PSI), as indicated by modulated chlorophyll measurements. The exogenous application of NaHS significantly alleviated these negative effects induced by K+ deficiency. This amelioration was associated with increased activity of L/D-cysteine desulfhydrase (LCD and DCD) enzymes, which contributed to maintaining adequate endogenous H2S and nitric oxide (NO) concentrations. These balanced levels of H2S and NO improved rapeseed plants' ability to cope with K+ deficiency stress.This study suggests a synergistic action of H2S and NO in mitigating K+ deficiency stress by enhancing plant growth, photosynthetic capacity, and energy conversion in both photosystems. This research implies that H2S could serve as a sustainable solution to boost plant growth and productivity, potentially ensuring food security, particularly in underdeveloped economies.Results: Potassium (K+) deficiency is a major abiotic stress that severely hampers plant growth and development. Hydrogen sulfide (H2S), a signal molecule regulating several critical functions in plants, is involved in plant tolerance to various environmental stresses. However, its involvement in the alleviation of K+ deficiency is not yet elucidated. The objective of the present work was to study the effects of K+ deficiency-H2S interaction on Brassica napus (rapeseed).Plants were grown under two potassium regimes (K+ control C, 3 mM) and (K+ deficient KD, 20 µM) in the absence or the presence of 200 µM NaHS (H2S donor).Results demonstrated that K+ deficiency reduced plant growth, pigment and soluble sugar concentrations, as well as diminished photosynthetic activity. Notably, photosystem II (PSII) was more affected than photosystem I (PSI), as indicated by modulated chlorophyll measurements. The exogenous application of NaHS significantly alleviated these negative effects induced by K+ deficiency. This amelioration was associated with increased activity of L/D-cysteine desulfhydrase (LCD and DCD) enzymes, which contributed to maintaining adequate endogenous H2S and nitric oxide (NO) concentrations. These balanced levels of H2S and NO improved rapeseed plants' ability to cope with K+ deficiency stress.This study suggests a synergistic action of H2S and NO in mitigating K+ deficiency stress by enhancing plant growth, photosynthetic capacity, and energy conversion in both photosystems. This research implies that H2S could serve as a sustainable solution to boost plant growth and productivity, potentially ensuring food security, particularly in underdeveloped economies.Conclusion: Potassium (K+) deficiency is a major abiotic stress that severely hampers plant growth and development. Hydrogen sulfide (H2S), a signal molecule regulating several critical functions in plants, is involved in plant tolerance to various environmental stresses. However, its involvement in the alleviation of K+ deficiency is not yet elucidated. The objective of the present work was to study the effects of K+ deficiency-H2S interaction on Brassica napus (rapeseed).Plants were grown under two potassium regimes (K+ control C, 3 mM) and (K+ deficient KD, 20 µM) in the absence or the presence of 200 µM NaHS (H2S donor).Results demonstrated that K+ deficiency reduced plant growth, pigment and soluble sugar concentrations, as well as diminished photosynthetic activity. Notably, photosystem II (PSII) was more affected than photosystem I (PSI), as indicated by modulated chlorophyll measurements. The exogenous application of NaHS significantly alleviated these negative effects induced by K+ deficiency. This amelioration was associated with increased activity of L/D-cysteine desulfhydrase (LCD and DCD) enzymes, which contributed to maintaining adequate endogenous H2S and nitric oxide (NO) concentrations. These balanced levels of H2S and NO improved rapeseed plants' ability to cope with K+ deficiency stress.This study suggests a synergistic action of H2S and NO in mitigating K+ deficiency stress by enhancing plant growth, photosynthetic capacity, and energy conversion in both photosystems. This research implies that H2S could serve as a sustainable solution to boost plant growth and productivity, potentially ensuring food security, particularly in underdeveloped economies. [ABSTRACT FROM AUTHOR]

The article presents the discussion on Hypokalemia resulting from inadequate potassium intake, shifting of potassium (K) from the extracellular to the intracellular space. Topics include Bartter syndrome being an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, normomagnesemia; and Gitelman syndrome being an autosomal recessive disorder presenting with hypokalemia.

Aims: Potassium (K+) deficiency is one of the most abiotic constraints reducing plant growth and productivity. The use of silicon (Si) has been reported to alleviate abiotic stresses in plants. However, data regarding the roles played by this element in mediating K+ deficiency are still scarce. Therefore, the present work was carried out to investigate the possible involvement of Si in mitigating the negative impact of K+ deficiency on cultivated barley Hordeum vulgare L. (var. Rihane). Methods: Plants were hydroponically grown either under K+ sufficient nutrient solution containing 3 mM K+ or in K+-deficient medium containing 10 µM K+ without or with Si (1 mM). Shoot growth, shoot water content, leaf osmotic potential, shoot K+ concentration, photosynthetic activity, chlorophyll fluorescence, soluble sugar concentrations, and shoot phenolic compound contents and their antioxidant properties were determined. Results: Results showed that shoot growth, shoot K+ concentration, and gaseous exchange were reduced by K+ deficiency. Photosynthesis decrease was mainly linked to sugar accumulation in leaves. Except for K+ concentration, a beneficial effect of Si was observed. A modulation in the accumulation of polyphenols and their antioxidant capacities has been observed. Conclusions: Overall, the data indicate that the beneficial effects of Si on barley plants grown under K+ deficient medium were mainly due to increased growth and photosynthetic activity but not through an improvement of shoot K+ concentration and phenolic compound accumulation and related antioxidant capacity suggesting a possible use of Si as a fertilizer to correct the deleterious effects of nutritional stress. [ABSTRACT FROM AUTHOR]

Monogenic disorders of hypertension are a distinct group of diseases causing dysregulation of the renin–angiotensin–aldosterone system and are characterized by low plasma renin activity. These can chiefly be classified as causing (i) excessive aldosterone synthesis (familial hyperaldosteronism), (ii) dysregulated adrenal steroid metabolism and action (apparent mineralocorticoid excess, congenital adrenal hyperplasia, activating mineralocorticoid receptor mutation, primary glucocorticoid resistance), and (iii) hyperactivity of sodium and chloride transporters in the distal tubule (Liddle syndrome and pseudohypoaldosteronism type 2). The final common pathway is plasma volume expansion and catecholamine/sympathetic excess that causes urinary potassium wasting; hypokalemia and early-onset refractory hypertension are characteristic. However, several single gene defects may show phenotypic heterogeneity, presenting with mild hypertension with normal electrolytes. Evaluation is based on careful attention to family history, physical examination, and measurement of blood levels of potassium, renin, and aldosterone. Genetic sequencing is essential for precise diagnosis and individualized therapy. Early recognition and specific management improves prognosis and prevents long-term sequelae of severe hypertension. [ABSTRACT FROM AUTHOR]

The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, − 0.16 to − 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses. [ABSTRACT FROM AUTHOR]

Electrolytes, particularly sodium and potassium, are highly paramount for the uptake of nutrients that are required for the proliferation, differentiation and survival of Plasmodium falciparum in the host. Sequel to this essential role, information on the interplay between electrolytes and nutrients would add to the current understanding of the malarial infection pathophysiology. To this end, we carried out a hospital-based cross-sectional study and estimated the serum levels of sodium, potassium, glucose, cholesterol and total protein in both P. falciparum-infected patients and apparently healthy patients. Our results showed that the levels of sodium, potassium, glucose, cholesterol and total protein were significantly (p < 0.05) reduced compared to their respective control groups. In addition, glucose, cholesterol and total protein had a non-significant (p > 0.05) association with the sodium and potassium, respectively, in P. falciparum-infected patients. Evidence from the present study demonstrated that P. falciparum-induced depletion in sodium and potassium seems not to play a significant role in the alterations of glucose, cholesterol and total protein during P. falciparum infection. [ABSTRACT FROM AUTHOR]

Background: Indapamide can cause hypokalaemia and hyponatraemia. Rhabdomyolysis associated with these electrolyte abnormalities has been reported. Objective: The aim of this study was to assess causal association between the use of indapamide and the occurrence of rhabdomyolysis using the Bradford Hill criteria. Methods: Variables in the rhabdomyolysis case reports and literature were reviewed. Bradford Hill criteria were used in the assessment of causal association. Results: Up to 11 November 2020, there were 28 unique cases in VigiBase from 13 countries reporting indapamide-associated rhabdomyolysis. In 18 of these cases, hypokalaemia (n = 14) or hyponatremia (n = 8) was a co-reported event, including four cases where both of these events were reported. Indapamide was the only suspected drug in nine of these 18 cases and positive dechallenge was mentioned in 13 of them. In addition, there were risk factors such as falls, concomitant drugs with risk of hypokalaemia, or muscle injury. In two cases, liquorice (containing glycyrrhizin) was concomitantly used with indapamide before hypokalaemia and rhabdomyolysis occurred. Thiazide diuretics, known to cause hypokalaemia, showed similar disproportionality patterns as indapamide regarding rhabdomyolysis and myopathy, while calcium channel blockers (not causing hypokalaemia), had lower disproportionality values than indapamide. Conclusions: Based on the review of case series and causality assessment using Bradford Hill criteria, indapamide may cause rhabdomyolysis due to hypokalaemia or hyponatremia. Considering the seriousness of the reported cases, health care professionals should be aware of this potential risk following indapamide intake, particularly when there are risk factors for hypokalaemia and hyponatremia such as excessive liquorice consumption. A similar risk of muscle injuries may apply to thiazide diuretics as well. [ABSTRACT FROM AUTHOR]

Pulmonary edema is a leading cause of hospital admissions, morbidity, and mortality in heart failure (HF) patients. A point-of-care lung ultrasound (LUS) is a useful tool to detect subclinical pulmonary edema. We performed a comprehensive literature search of multiple databases for studies that evaluated the clinical utility of LUS-guided management versus standard care for HF patients in the outpatient setting. The primary outcome of interest was HF hospitalization. The secondary outcomes were all-cause mortality, urgent visits for HF worsening, acute kidney injury (AKI), and hypokalemia rates. Pooled risk ratio (RR) and corresponding 95% confidence intervals (CIs) were calculated and combined using random-effect model meta-analysis. A total of 3 randomized controlled trials including 493 HF patients managed in the outpatient setting (251 managed with LUS plus physical examination (PE)–guided therapy vs. 242 managed with PE-guided therapy alone) were included in the final analysis. The mean follow-up period was 5 months. There was no significant difference in HF hospitalization rate between the two groups (RR 0.65; 95% CI 0.34–1.22; P = 0.18). Similarly, there was no significant difference in all-cause mortality (RR 1.39; 95% CI 0.68–2.82; P = 0.37), AKI (RR 1.27; 95% CI 0.60–2.69; P = 0.52), and hypokalemia (RR 0.72; 95% CI 0.21–2.44; P = 0.59). However, LUS-guided therapy was associated with a lower rate for urgent care visits (RR 0.32; 95% CI 0.18–0.59; P = 0.0002). Our study demonstrated that outpatient LUS-guided diuretic therapy of pulmonary congestion reduces urgent visits for worsening symptoms of HF. Further studies are needed to evaluate LUS utility in the outpatient treatment of HF. [ABSTRACT FROM AUTHOR]

Background: Available information about prognostic implications of potassium levels alteration in the setting of acute heart failure (AHF) is scarce. Objectives: We aim to describe the prevalence of dyskalemia (hypo or hyperkalemia), its dynamic changes during AHF-hospitalization, and its long-term clinical impact after hospitalization. Methods: We analyzed 1779 patients hospitalized with AHF who were included in the REDINSCOR II registry. Patients were classified in three groups, according to potassium levels both on admission and discharge: hypokalemia (potassium < 3.5 mEq/L), normokalemia (potassium = 3.5–5.0 mEq/L and, hyperkalemia (potassium > 5 mEq/L). Results: The prevalence of hypokalemia and hyperkalemia on admission was 8.2 and 4.6%, respectively, and 6.4 and 2.7% at discharge. Hyperkalemia on admission was associated with higher in-hospital mortality (OR = 2.32 [95% CI: 1.04–5.21] p = 0.045). Among patients with hypokalemia on admission, 79% had normalized potassium levels at discharge. In the case of patients with hyperkalemia on admission, 89% normalized kalemia before discharge. In multivariate Cox regression, dyskalemia was associated with higher 12-month mortality, (HR = 1.48 [95% CI, 1.12–1.96], p = 0.005). Among all patterns of dyskalemia persistent hypokalemia (HR = 3.17 [95% CI: 1.71–5.88]; p < 0.001), and transient hyperkalemia (HR = 1.75 [95% CI: 1.07–2.86]; p = 0.023) were related to reduced 12-month survival. Conclusions: Potassium levels alterations are frequent and show a dynamic behavior during AHF admission. Hyperkalemia on admission is an independent predictor of higher in-hospital mortality. Furthermore, persistent hypokalemia and transient hyperkalemia on admission are independent predictors of 12-month mortality. [ABSTRACT FROM AUTHOR]

Cancer continues to be the most dangerous disease around the world; it causes electrolyte imbalance as well as metabolic changes. There is a complicated relationship between electrolyte disorder and cancer. Cancer patients commonly pass with abnormalities in serum electrolyte levels such as hypokalemia, hyperkalemia, hyponatremia, and hypercalcemia. So, these electrolyte imbalances indicate the existence of paraneoplastic processes and help come to a more informed prognosis. Hypokalemia is defined as a serum potassium concentration below 3.5 mmol/L and it is the second common electrolyte imbalance seen in patients with malignant diseases. In this paper, the contribution of serum potassium concentration to tumor progression was studied by applying a promising and non-invasive technique called laser-induced breakdown spectroscopy (LIBS). It was found that there is a correlation between hypokalemia and the colorectal cancer problem. Also, significant serum potassium concentration differences were detected among two different stages of the same cancer and also between two groups of the same stage of a cancer held in common but one of them suffers from hypercalcemia. In addition, the optimum conditions of LIBS setup were arranged such that it will be suitable to work with serum samples on glass substrate. [ABSTRACT FROM AUTHOR]

In plants, the HAK/KUP/KT family is the largest group of potassium transporters, and it plays an important role in mineral element absorption, plant growth, environmental stress adaptation, and symbiosis. Although these important genes have been investigated in many plant species, limited information is currently available on the HAK/KUP/KT genes for Pepper (Capsicum annuum L.). In the present study, a total of 20 CaHAK genes were identified from the pepper genome and the CaHAK genes were numbered 1 – 20 based on phylogenetic analysis. For the genes and their corresponding proteins, the physicochemical properties, phylogenetic relationship, chromosomal distribution, gene structure, conserved motifs, gene duplication events, and expression patterns were analyzed. Phylogenetic analysis divided CaHAK genes into four cluster (I–IV) based on their structural features and the topology of the phylogenetic tree. Purifying selection played a crucial role in the evolution of CaHAK genes, while whole-genome triplication contributed to the expansion of the CaHAK gene family. The expression patterns showed that CaHAK proteins exhibited functional divergence in terms of plant K+ uptake and salt stress response. In particular, transcript abundance of CaHAK3 and CaHAK7 was strongly and specifically up-regulated in pepper roots under low K+ or high salinity conditions, suggesting that these genes are candidates for high-affinity K+ uptake transporters and may play crucial roles in the maintenance of the Na+/K+ balance during salt stress in pepper. In summary, the results not only provided the important information on the characteristics and evolutionary relationships of CaHAKs, but also provided potential genes responding to potassium deficiency and salt stress. [ABSTRACT FROM AUTHOR]