Multi-omics strategies uncover the molecular mechanisms of nitrogen, phosphorus and potassium deficiency responses in Brassica napus.

BACKGROUND: Nitrogen (N), phosphorus (P) and potassium (K) are critical macronutrients in crops, such that deficiency in any of N, P or K has substantial effects on crop growth. However, the specific commonalities of plant responses to different macronutrient deficiencies remain largely unknown. METHODS: Here, we assessed the phenotypic and physiological performances along with whole transcriptome and metabolomic profiles of rapeseed seedlings exposed to N, P and K deficiency stresses. RESULTS: Quantities of reactive oxygen species were significantly increased by all macronutrient deficiencies. N and K deficiencies resulted in more severe root development responses than P deficiency, as well as greater chlorophyll content reduction in leaves (associated with disrupted chloroplast structure). Transcriptome and metabolome analyses validated the macronutrient-specific responses, with more pronounced effects of N and P deficiencies on mRNAs, microRNAs (miRNAs), circular RNAs (circRNAs) and metabolites relative to K deficiency. Tissue-specific responses also occurred, with greater effects of macronutrient deficiencies on roots compared with shoots. We further uncovered a set of common responders with simultaneous roles in all three macronutrient deficiencies, including 112 mRNAs and 10 miRNAs involved in hormonal signaling, ion transport and oxidative stress in the root, and 33 mRNAs and 6 miRNAs with roles in abiotic stress response and photosynthesis in the shoot. 27 and seven common miRNA-mRNA pairs with role in miRNA-mediated regulation of oxidoreduction processes and ion transmembrane transport were identified in all three macronutrient deficiencies. No circRNA was responsive to three macronutrient deficiency stresses, but two common circRNAs were identified for two macronutrient deficiencies. Combined analysis of circRNAs, miRNAs and mRNAs suggested that two circRNAs act as decoys for miR156 and participate in oxidoreduction processes and transmembrane transport in both N- and P-deprived roots. Simultaneously, dramatic alterations of metabolites also occurred. Associations of RNAs with metabolites were observed, and suggested potential positive regulatory roles for tricarboxylic acids, azoles, carbohydrates, sterols and auxins, and negative regulatory roles for aromatic and aspartate amino acids, glucosamine-containing compounds, cinnamic acid, and nicotianamine in plant adaptation to macronutrient deficiency. CONCLUSIONS: Our findings revealed strategies to rescue rapeseed from macronutrient deficiency stress, including reducing the expression of non-essential genes and activating or enhancing the expression of anti-stress genes, aided by plant hormones, ion transporters and stress responders. The common responders to different macronutrient deficiencies identified could be targeted to enhance nutrient use efficiency in rapeseed.

[The role of magnesium and potassium in preventive and therapeutic nutrition].

Due to the versatility of its functions and participation in all types of metabolism, magnesium can be considered the main cation in the human organism. Equally important is the role of the main intracellular ion - potassium, which is a synergist of magnesium, especially with regard to the effect on cardiovascular system function. In Russia, there is insufficient consumption of magnesium and potassium by the population. The purpose of the work was to assess the role of magnesium and potassium in ensuring public health. Material and methods. Literature search was carried out using PubMed, Google Scholar, ResearchGate, RISC systems mainly over the past 10 years, with the exception of works of fundamental importance, according to the keywords "magnesium", "bioavailability", "potassium", "efficiency". Results. Chronic hypomagnesemia and hypokalemia are involved in the pathogenesis of various metabolic disorders (metabolic syndrome, insulin resistance and type 2 diabetes mellitus, hypertension, hyperlipidemia and sluggish inflammation). Magnesium deficiency increases the risk of cardiovascular (arrhythmia, hypertension, heart failure), neurological diseases (stroke) and depression, as well as diseases of the respiratory system (bronchial asthma, chronic obstructive pulmonary disease). Potassium deficiency is also associated with pathology of the cardiovascular system. Adequate intake of magnesium and potassium with food and/or dietary supplements prevents the development of chronic metabolic complications. Various magnesium compounds used to correct its deficiency, have different bioavailability. Conclusion. The expediency of compensating for magnesium and potassium deficiency in nutrition has been proven both for preventive purposes in a healthy person and as part of diet therapy in a patient. Enrichment of the diet with magnesium and potassium is a reliable non-drug, economical and safe prevention of chronic deficiency and associated metabolic disorders.

Transcriptome analysis of sweet potato responses to potassium deficiency.

BACKGROUND: As one of three essential nutrients, potassium is regarded as a main limiting factor for growth and development in plant. Sweet potato (Ipomoea batatas L.) is one of seven major food crops grown worldwide, and is both a nutrient-rich food and a bioenergy crop. It is a typical 'K-favoring' crop, and the level of potassium ion (K+) supplementation directly influences its production. However, little is known about the transcriptional changes in sweet potato genes under low-K+ conditions. Here, we analyzed the transcriptomic profiles of sweet potato roots in response to K+ deficiency to determine the effect of low-K+ stress on this economically important crop. RESULTS: The roots of sweet potato seedlings with or without K+ treatment were harvested and used for transcriptome analyses. The results showed 559 differently expressed genes (DEGs) in low and high K+ groups. Among the DEGs, 336 were upregulated and 223 were downregulated. These DEGs were involved in transcriptional regulation, calcium binding, redox-signaling, biosynthesis, transport, and metabolic process. Further analysis revealed previously unknow genes involved in low-K+ stress, which could be investigated further to improve low K+ tolerance in plants. Confirmation of RNA-sequencing results using qRT-PCR displayed a high level of consistency between the two experiments. Analysis showed that many auxin-, ethylene- and jasmonic acid-related genes respond to K+ deficiency, suggesting that these hormones have important roles in K+ nutrient signaling in sweet potato. CONCLUSIONS: According to the transcriptome data of sweet potato, various DEGs showed transcriptional changes in response to low-K+ stress. However, the expression level of some kinases, transporters, transcription factors (TFs), hormone-related genes, and plant defense-related genes changed significantly, suggesting that they have important roles during K+ deficiency. Thus, this study identifies potential genes for genetic improvement of responses to low-K+ stress and provides valuable insight into the molecular mechanisms regulating low K+ tolerance in sweet potato. Further research is required to clarify the function of these DEGs under low-K+ stress.

Potassium deficiency stress tolerance in peanut (Arachis hypogaea) through ion homeostasis, activation of antioxidant defense, and metabolic dynamics: Alleviatory role of silicon supplementation.

Potassium (K) scarcity of arable land is one of the important factors that hamper the growth of the plants and reduce yield worldwide. In the current study, we examine the physiological, biochemical, and metabolome response of Arachis hypogaea (GG7 genotype: fast-growing, tall, early maturing, and high yielding) under low K either solitary or in combination with Si to elucidate the ameliorative role of Si. The reduced fresh and dry biomass of peanut and photosynthetic pigments content was significantly alleviated by Si. Si application did not affect the leaf and stem K+, although it enhanced root K+ in K-limitation, which is probably due to up-regulated expression of genes responsible for K uptake. Si improves the potassium use efficiency in K-limitation as compared to control. K-deficiency increased MDA, O2•-, and H2O2 levels in leaf and root of peanut. Si improved/maintained the activity of antioxidative enzymes, which significantly lowered the ROS accumulation in K-limitation. The AsA/DHA and GSH/GSSG ratio was approximately unaffected in both leaf and root, suggesting the maintained cellular redox potential in K-starved peanut. Si promotes accumulation of sugars and sugar alcohols, phytohormones indicating their probable involvement in signal transduction, osmotic regulation, and improvement of stress tolerance. Down-regulation of aspartic acid and glutamic acid while up-regulation of lysine, histidine, and arginine could maintain charge balance in K-deprived peanut. The significant accumulation of polyphenols under K limitation supplemented with Si suggests the role of polyphenols for ROS scavenging. Our results demonstrated that Si as a beneficial element can mitigate K-nutrient toxicity and improve KUE of peanut under K-limitation conditions. Moreover, our results demonstrate that Si application can improve crop yield, quality, and nutrient use efficiency under nutrient limitation conditions.

Expression of potential reference genes in response to macronutrient stress in rice and soybean.

Given the complexity of nutrient stress responses and the availability of a few validated reference genes, we aimed to identify robust and stable reference genes for macronutrient stress in rice and soybean. Ten potential reference genes were evaluated using geNorm, NormFinder, BestKeeper, Comparative ΔCt method, and RefFinder algorithms under low and completely starved conditions of nitrogen (N), phosphorus (P), potassium (K), and sulphur (S). Results revealed distinct sets of reference gene pairs, showing stable expression under different experimental conditions. The gene pairs TIP41/UBC(9/10/18) and F-box/UBC10 were most stable in rice and soybean, respectively under N stress. Under P stress, UBC9/UBC10 in rice and F-Box/UBC10 in soybean were most stable. Similarly, TIP41/UBC10 in rice and RING FINGER/UBC9 in soybean were the best gene pairs under K stress while F-Box/TIP41 in rice and UBC9/UBC10 in soybean were the most stable gene pairs under S stress. These reference gene pairs were validated by quantifying the expression levels of high-affinity transporters like NRT2.1/NRT2.5, PT1, AKT1, and SULTR1 for N, P, K, and S stress, respectively. This study reiterates the importance of choosing reference genes based on crop species and the experimental conditions, in order to obtain concrete answers to missing links of gene regulation in response to macronutrient deficiencies.

Potassium deficiency reconfigures sugar export and induces catecholamine accumulation in oil palm leaves.

Metabolic effects of potassium (K) deficiency have been described for nearly 70 years but specific effects of low K availability on sugar composition, sugar export rate and its relationship with other leaf metabolites are not very well documented. Having such pieces of information is nevertheless essential to identify metabolic signatures to monitor K fertilization. This is particularly true in oil-producing crop species such as oil palm (Elaeis guineensis), which is strongly K-demanding and involves high sugar dependence for fruit formation because of low carbon use efficiency in lipid synthesis. Here, we used metabolic analyses, measured sugar export rates with 13C isotopic labeling and examined the effects of K availability on both leaflet and rachis sugar metabolism in oil palm seedlings. We show that low K leads to a modification of sugar composition mostly in rachis and decreased sucrose and hexose export rates from leaflets. As a result, leaflets contained more starch and induced alternative pathways such as raffinose synthesis, although metabolites of the raffinose pathway remained quantitatively minor. The alteration of glycolysis by low K was compensated for by an increase in alternative sugar phosphate utilization by tyrosine metabolism, resulting in considerable amounts of tyramine and dopamine.

HAK/KUP/KT family potassium transporter genes are involved in potassium deficiency and stress responses in tea plants (Camellia sinensis L.): expression and functional analysis.

BACKGROUND: Tea plant is one of the most important non-alcoholic beverage crops worldwide. While potassium (K+) is an essential macronutrient and greatly affects the growth and development of plants, the molecular mechanism underlying K+ uptake and transport in tea plant root, especially under limited-K+ conditions, is still poorly understood. In plants, HAK/KUP/KT family members play a crucial role in K+ acquisition and translocation, growth and development, and response to stresses. Nevertheless, the biological functions of these genes in tea plant are still in mystery, especially their roles in K+ uptake and stress responses. RESULTS: In this study, a total of 21 non-redundant HAK/KUP/KT genes (designated as CsHAKs) were identified in tea plant. Phylogenetic and structural analysis classified the CsHAKs into four clusters (I, II, III, IV), containing 4, 8, 4 and 5 genes, respectively. Three major categories of cis-acting elements were found in the promoter regions of CsHAKs. Tissue-specific expression analysis indicated extremely low expression levels in various tissues of cluster I CsHAKs with the exception of a high root expression of CsHAK4 and CsHAK5, a constitutive expression of clusters II and III CsHAKs, and a moderate cluster IV CsHAKs expression. Remarkably, the transcript levels of CsHAKs in roots were significantly induced or suppressed after exposure to K+ deficiency, salt and drought stresses, and phytohormones treatments. Also notably, CsHAK7 was highly expressed in all tissues and was further induced under various stress conditions. Therefore, functional characterization of CsHAK7 was performed, and the results demostrated that CsHAK7 locates on plasma membrane and plays a key role in K+ transport in yeast. Taken together, the results provide promising candidate CsHAKs for further functional studies and contribute to the molecular breeding for new tea plants varieties with highly efficient utilization of K+. CONCLUSION: This study demonstrated the first genome-wide analysis of CsHAK family genes of tea plant and provides a foundation for understanding the classification and functions of the CsHAKs in tea plants.

Potassium Intake and Blood Pressure: A Dose-Response Meta-Analysis of Randomized Controlled Trials.

Background Epidemiologic studies, including trials, suggest an association between potassium intake and blood pressure (BP). However, the strength and shape of this relationship is uncertain. Methods and Results We performed a meta-analysis to explore the dose-response relationship between potassium supplementation and BP in randomized-controlled trials with a duration ≥4 weeks using the recently developed 1-stage cubic spline regression model. This model allows use of trials with at least 2 exposure categories. We identified 32 eligible trials. Most were conducted in adults with hypertension using a crossover design and potassium supplementation doses that ranged from 30 to 140 mmol/d. We observed a U-shaped relationship between 24-hour active and control arm differences in potassium excretion and BP levels, with weakening of the BP reduction effect above differences of 30 mmol/d and a BP increase above differences ≈80 mmol/d. Achieved potassium excretion analysis also identified a U-shaped relationship. The BP-lowering effects of potassium supplementation were stronger in participants with hypertension and at higher levels of sodium intake. The BP increase with high potassium excretion was noted in participants with antihypertensive drug-treated hypertension but not in their untreated counterparts. Conclusions We identified a nonlinear relationship between potassium intake and both systolic and diastolic BP, although estimates for BP effects of high potassium intakes should be interpreted with caution because of limited availability of trials. Our findings indicate an adequate intake of potassium is desirable to achieve a lower BP level but suggest excessive potassium supplementation should be avoided, particularly in specific subgroups.

The Cotton High-Affinity K+ Transporter, GhHAK5a, Is Essential for Shoot Regulation of K+ Uptake in Root under Potassium Deficiency.

Potassium (K) deficiency is a key limiting factor in cotton (Gossypium hirsutum) production. By grafting two contrasting cotton cultivars, CCRI41 (more susceptible to K+ deficiency) and SCRC22 (more tolerant of K+ deficiency), we established that cotton shoot plays a vital role in the regulation of root K+ uptake. To identify the genetic basis of this finding, we performed RNA sequencing (RNA-seq) of roots of CCRI41 self-grafts (CCRI41/CCRI41, scion/rootstock) and SCRC22/CCRI41 reciprocal-grafts exposed to K+ deficiency. We found that GhHAK5a, an orthologous of Arabidopsis thaliana high-affinity K+ transporter, AtHAK5, was significantly induced in the CCRI41 rootstock by the SCRC22 scion. This gene was mainly expressed in roots and was more highly induced by K+ deficiency in roots of SCRC22 than those of CCRI41. Agrobacterium-mediated virus-induced gene silencing and yeast complementary assay showed that GhHAK5a is a high-affinity K+ uptake transporter. Importantly, silencing of GhHAK5a in the CCRI41 rootstock almost completely inhibited the K+ uptake induced by SCRC22 scion in CCRI41 rootstock. We identified a key high-affinity K+ transporter, GhHAK5a in cotton, which is the essential target for shoot regulation of root K+ uptake under K+ deficiency.

Assessment of silt from sand and gravel processing as a suitable sub-soil material in land restoration: A glasshouse study.

Annually, sand and gravel processing generates approximately 20 million tonnes of non-commercial by-product as fine silt particles (<63 µm) which constitutes approximately 20% of quarry production in the UK. This study is significant as it investigated the use of quarry silt as a sub-soil medium to partially substitute soil-forming materials whilst facilitating successful post-restoration crop establishment. In a glasshouse pot experiment, top-soil and sub-soil layering was simulated, generating an artificial sub-soil medium by mixing two quarry non-commercial by-products, i.e. silt and overburden. These were blended in three ratios (100:0, 70:30, 50:50). Pots were packed to two bulk densities (1.3 and 1.5 g cm-3) and sown with three cover crops used in the early restoration process namely winter rye (Secale cereale), white mustard (Sinapis alba) and a grassland seed mixture (Lolium perenne, Phleum pratense, Poa pratensis, Festuca rubra). Three weeks into growth, the first signs of nitrogen (N) deficiency were observed in mustard plants, with phosphorus (P) and potassium (K) deficiencies observed at 35 days. Rye exhibited minor N deficiency symptoms four weeks into growth, whilst the grassland mixture showed no deficiency symptoms. The 70:30 silt:overburden sub-soil blend resulted in significantly higher Root Mass Densities of grassland seed mixture and rye in the sub-soil layer as compared with the other blends. The innovation in this work is the detailed physical, chemical and biological characterisation of silt:overburden blends and effects on root development of plants commonly used in early restoration to bio-engineer soil structural improvements.

Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial.

Background: Low potassium has been identified both as a risk factor for type 2 diabetes and as a mediator of the racial disparity in diabetes risk. Low potassium could be a potentially modifiable risk factor, particularly for African Americans.Objective: We sought to determine the effects of potassium chloride (KCl) supplements, at a commonly prescribed dose, on measures of potassium and glucose metabolism.Design: Among African-American adults with prediabetes, we conducted a double-blinded pilot randomized controlled trial that compared the effects of 40 mEq K/d as KCl supplements with a matching placebo, taken for 3 mo, on measures of potassium and glucose metabolism, with measures collected from frequently sampled oral-glucose-tolerance tests (OGTTs).Results: Twenty-seven of 29 recruited participants completed the trial. Participants had high adherence to the study medication (92% by pill count). Participants in both groups gained weight, with an overall mean ± SD weight gain of 1.24 ± 2.03 kg. In comparison with participants who received placebo, urine potassium but not serum potassium increased significantly among participants randomly assigned to receive KCl (P = 0.005 and 0.258, respectively). At the end of the study, participants taking KCl had stable or improved fasting glucose, with a mean ± SD change in fasting glucose of -1.1 ± 8.4 mg/dL compared with an increase of 6.1 ± 7.6 mg/dL in those who received placebo (P = 0.03 for comparison between arms). There were no significant differences in glucose or insulin measures during the OGTT between the 2 groups, but there was a trend for improved insulin sensitivity in potassium-treated participants.Conclusions: In this pilot trial, KCl at a dose of 40 mEq/d did not increase serum potassium significantly. However, despite weight gain, KCl prevented worsening of fasting glucose. Further studies in larger sample sizes, as well as with interventions to increase serum potassium more than was achieved with our intervention, are indicated to definitively test this potentially safe and inexpensive approach to reducing diabetes risk. This trial was registered at clinicaltrials.gov as NCT02236598.

Restoration of the growth of Escherichia coli under K+-deficient conditions by Cs+ incorporation via the K+ transporter Kup.

Biological incorporation of cesium ions (Cs+) has recently attracted significant attention in terms of the possible applications for bioremediation of radiocesium and their significant roles in biogeochemical cycling. Although high concentrations of Cs+ exhibit cytotoxicity on microorganisms, there are a few reports on the promotive effects of Cs+ on microbial growth under K+-deficient conditions. However, whether this growth-promoting effect is a common phenomenon remains uncertain, and direct correlation between growth promotion and Cs+ uptake abilities has not been confirmed yet. Here, we validated the growth promotive effects of Cs+ uptake under K+-deficient conditions using an Escherichia coli strain with an inducible expression of the Kup K+ transporter that has nonspecific Cs+ transport activities (strain kup-IE). The strain kup-IE exhibited superior growth under the Cs+-supplemented and K+-deficient conditions compared to the wild type and the kup null strains. The intracellular Cs+ levels were significantly higher in strain kup-IE than in the other strains, and were well correlated with their growth yields. Furthermore, induction levels of the kup gene, intracellular Cs+ concentrations, and the growth stimulation by Cs+ also correlated positively. These results clearly demonstrated that Cs+ incorporation via Kup transporter restores growth defects of E. coli under K+-deficient conditions.

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.

Angiotensin II (AngII) hypertension increases distal tubule Na-Cl cotransporter (NCC) abundance and phosphorylation (NCCp), as well as epithelial Na(+) channel abundance and activating cleavage. Acutely raising plasma [K(+)] by infusion or ingestion provokes a rapid decrease in NCCp that drives a compensatory kaliuresis. The first aim tested whether acutely raising plasma [K(+)] with a single 3-hour 2% potassium meal would lower NCCp in Sprague-Dawley rats after 14 days of AngII (400 ng/kg per minute). The potassium-rich meal neither decreased NCCp nor increased K(+) excretion. AngII-infused rats exhibited lower plasma [K(+)] versus controls (3.6±0.2 versus 4.5±0.1 mmol/L; P<0.05), suggesting that AngII-mediated epithelial Na(+) channel activation provokes K(+) depletion. The second aim tested whether doubling dietary potassium intake from 1% (A1K) to 2% (A2K) would prevent K(+) depletion during AngII infusion and, thus, prevent NCC accumulation. A2K-fed rats exhibited normal plasma [K(+)] and 2-fold higher K(+) excretion and plasma [aldosterone] versus A1K. In A1K rats, NCC, NCCpS71, and NCCpT53 abundance increased 1.5- to 3-fold versus controls (P<0.05). The rise in NCC and NCCp abundance was prevented in the A2K rats, yet blood pressure did not significantly decrease. Epithelial Na(+) channel subunit abundance and cleavage increased 1.5- to 3-fold in both A1K and A2K; ROMK (renal outer medulla K(+) channel abundance) abundance was unaffected by AngII or dietary K(+) In summary, the accumulation and phosphorylation of NCC seen during chronic AngII infusion hypertension is likely secondary to potassium deficiency driven by epithelial Na(+) channel stimulation.

Potassium Intake, Bioavailability, Hypertension, and Glucose Control.

Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid where it plays a key role in maintaining cell function. The gradient of potassium across the cell membrane determines cellular membrane potential, which is maintained in large part by the ubiquitous ion channel the sodium-potassium (Na+-K+) ATPase pump. Approximately 90% of potassium consumed (60-100 mEq) is lost in the urine, with the other 10% excreted in the stool, and a very small amount lost in sweat. Little is known about the bioavailability of potassium, especially from dietary sources. Less is understood on how bioavailability may affect health outcomes. Hypertension (HTN) is the leading cause of cardiovascular disease (CVD) and a major financial burden ($50.6 billion) to the US public health system, and has a significant impact on all-cause morbidity and mortality worldwide. The relationship between increased potassium supplementation and a decrease in HTN is relatively well understood, but the effect of increased potassium intake from dietary sources on blood pressure overall is less clear. In addition, treatment options for hypertensive individuals (e.g., thiazide diuretics) may further compound chronic disease risk via impairments in potassium utilization and glucose control. Understanding potassium bioavailability from various sources may help to reveal how specific compounds and tissues influence potassium movement, and further the understanding of its role in health.

A case report of Gitelman syndrome resulting from two novel mutations in SLC12A3 gene / El caso del síndrome de Gitelman causado por dos nuevas mutaciones en el gen SLC12A3

Introduction: Hypokalaemia is a common clinical problem. A potential but commonly overlooked cause of hypokalaemia is Gitelman syndrome. Material and methods: A 26-year-old man was admitted to the hospital due to syncope with general and muscular weakness and muscle cramps. The patient's history revealed previous recurrent syncope events associated to hypokalaemia with the lowest serum potassium value being 2.6mmol/l. At admission, blood pressure was normal and no changes were found at physical examination. Laboratory tests showed mild hypokalaemia (3.0mmol/l), hypomagnesaemia (1.36mg/dl), hypocalciuria (< 40mg/24h), and metabolic alkalosis (HCO3− 29.7mmol/l, BE 5.3mmol/l). Results: Further laboratory tests (FeK, TTKG) confirmed inappropriate kaliuresis. Conn's disease was excluded by hormonal and imaging assessments. Genetic testing was performed and two novel heterozygous mutations: c.35_36insA and c.1095+5G>A were found in transcriptNM_000339.2 in SLC12A3 gene. Conclusion: The patient was diagnosed with Gitelman syndrome and was treated with supplements of potassium and magnesium (AU)

Introducción: La hipopotasemia es un problema clínico común. El síndrome de Gitelman es una posible causa de hipopotasemia a veces no reconocida. Material y métodos: Un hombre de 26 años de edad ingresa en un hospital por causa de un síncope, debilidad generalizada y calambres musculares. La historia clínica del paciente reveló la incidencia del síncope con hipopotasemia recurrente con el valor más bajo de potasio en 2,6mmol/l. En el ingreso, el paciente presentaba una presión arterial normal y la exploración física no reveló ninguna enfermedad. La evaluación del laboratorio demostró una hipopotasemia leve (K+ 3,0mmol/l), hipomagnesemia (Mg 1,36mg/dl), hipocalciuria (<40mg/24h) y alcalosis metabólica (HCO3- 29,7mmol/l, exceso de base 5,3mmol/l). Resultados: Otras pruebas de laboratorio (FeK, TTKG) confirman una caliuresis inadecuada. La enfermedad de Conn fue excluida tras la evaluación hormonal y radiológica. Se realizaron las pruebas genéticas y 2 mutaciones heterocigóticas: c.35_36insA y c.1095+5G>A fueron encontradas en la transcripción NM_000339.2 del gen SLC12A3. Conclusión: El paciente fue diagnosticado con el síndrome de Gitelman y fue tratado con suplementos de potasio y magnesio (AU)

Achieving the Benefits of a High-Potassium, Paleolithic Diet, Without the Toxicity.

The average US dietary intake of K(+) is well below the current recommended nutritional requirements. This deficiency is even more striking when comparing our current intake with that of our ancestors, who consumed large amounts of dietary K(+). K(+) deficiency has been implicated in many diseases including cardiovascular disease, kidney stones, and osteoporosis. Importantly, dietary supplementation of K(+) has favorable effects on reducing blood pressure, decreasing the risk of stroke, improving bone health, and reducing the risk of nephrolithiasis. For this comprehensive review, we scanned the literature using PubMed and MEDLINE using the following search terms: potassium intake, renal potassium excretion, and prevention of hyperkalemia. Articles were selected for inclusion if they represented primary data or review articles published between 1980 and 2015 in high-impact journals. The normal kidney has the capacity to tightly regulate K(+) homoeostasis. We discuss new findings with respect to sensing mechanisms by which the kidney maintains K(+) homeostasis in the gastrointestinal tract and distal tubule. There are widely prescribed hypertensive medications that cause hyperkalemia and thus require dietary K(+) restriction. We conclude by discussing newly approved drugs capable of binding K(+) in the gastrointestinal tract and speculate that this new pharmacology might allow diet liberalization in patients at risk for hyperkalemia, affording them the numerous benefits of a K(+)-rich diet.

Effects of K+-deficient diets with and without NaCl supplementation on Na+, K+, and H2O transporters' abundance along the nephron.

Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) and H(2)O transporters' pool size regulation in response to removing K(+) from a diet containing 0.74% NaCl, as well as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet electrolytes. Sprague-Dawley rats (n = 5-6) were fed for 6 days with one of these diets: 2% KCl, 0.74% NaCl (2K1Na, control chow) compared with 0.03% KCl, 0.74% NaCl (0K1Na); or 2% KCl, 2%NaCl (2K2Na) compared with 0.03% KCl, 2% NaCl (0K2Na, Na(+) replete). In both 0K1Na and 0K2Na there were significant decreases in: 1) plasma [K(+)] (<2.5 mM); 2) urinary K(+) excretion (<5% of control); 3) urine osmolality and plasma [aldosterone], as well as 4) an increase in urine volume and medullary hypertrophy. The 0K2Na group had the lowest [aldosterone] (172.0 ± 17.4 pg/ml) and lower blood pressure (93.2 ± 4.9 vs. 112.0 ± 3.1 mmHg in 2K2Na). Transporter pool size regulation was determined by quantitative immunoblotting of renal cortex and medulla homogenates. The only differences measured in both 0K1Na and 0K2Na groups were a 20-30% decrease in cortical ß-ENaC, 30-40% increases in kidney-specific Ste20/SPS1-related proline/alanine-rich kinase, and a 40% increase in medullary sodium pump abundance. The following proteins were not significantly changed in both the 0 K groups: Na(+)/H(+) exchanger isoform 3; Na(+)-K(+)-Cl(-) cotransporter; Na(+)-Cl(-) cotransporter, oxidative stress response kinase-1; renal outer medullary K(+) channel; autosomal recessive hypercholesterolemia; c-Src, aquaporin 2 isoform; or renin. Thus, despite profound hypokalemia and renal K(+) conservation, we did not confirm many of the changes that were previously reported. We predict that changes in transporter distribution and activity are likely more important for conserving K(+) than changes in total abundance.

Dietary intake and nutritional deficiencies in patients with diabetic or idiopathic gastroparesis.

BACKGROUND & AIMS: Gastroparesis can lead to food aversion, poor oral intake, and subsequent malnutrition. We characterized dietary intake and nutritional deficiencies in patients with diabetic and idiopathic gastroparesis. METHODS: Patients with gastroparesis on oral intake (N = 305) were enrolled in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Registry and completed diet questionnaires at 7 centers. Medical history, gastroparesis symptoms, answers to the Block Food Frequency Questionnaire, and gastric emptying scintigraphy results were analyzed. RESULTS: Caloric intake averaged 1168 ± 801 kcal/day, amounting to 58% ± 39% of daily total energy requirements (TER). A total of 194 patients (64%) reported caloric-deficient diets, defined as <60% of estimated TER. Only 5 patients (2%) followed a diet suggested for patients with gastroparesis. Deficiencies were present in several vitamins and minerals; patients with idiopathic disorders were more likely to have diets with estimated deficiencies in vitamins A, B(6), C, K, iron, potassium, and zinc than diabetic patients. Only one-third of patients were taking multivitamin supplements. More severe symptoms (bloating and constipation) were characteristic of patients who reported an energy-deficient diet. Overall, 32% of patients had nutritional consultation after the onset of gastroparesis; consultation was more likely among patients with longer duration of symptoms and more hospitalizations and patients with diabetes. Multivariable logistic regression analysis indicated that nutritional consultation increased the chances that daily TER were met (odds ratio, 1.51; P = .08). CONCLUSIONS: Many patients with gastroparesis have diets deficient in calories, vitamins, and minerals. Nutritional consultation is obtained infrequently but is suggested for dietary therapy and to address nutritional deficiencies.