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Nephron. Physiology

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https://www.readbyqxmd.com/read/25632857/uk-renal-registry-17th-annual-report-chapter-4-demography-of-the-uk-paediatric-renal-replacement-therapy-population-in-2013
#1
Rishi Pruthi, Alexander J Hamilton, Catherine O'Brien, Anna Casula, Fiona Braddon, Carol Inward, Malcolm Lewis, Heather Maxwell, Jelena Stojanovic, Yincent Tse, Manish D Sinha
No abstract text is available yet for this article.
2015: Nephron. Physiology
https://www.readbyqxmd.com/read/25632856/uk-renal-registry-17th-annual-report-chapter-3-demographic-and-biochemistry-profile-of-kidney-transplant-recipients-in-the-uk-in-2013-national-and-centre-specific-analyses
#2
https://www.readbyqxmd.com/read/25632855/uk-renal-registry-17th-annual-report-chapter-2-uk-renal-replacement-therapy-prevalence-in-2013-national-and-centre-specific-analyses
#3
Anirudh Rao, Anna Casula, Clare Castledine
No abstract text is available yet for this article.
2015: Nephron. Physiology
https://www.readbyqxmd.com/read/25632854/uk-renal-registry-17th-annual-report-chapter-1-uk-renal-replacement-therapy-incidence-in-2013-national-and-centre-specific-analyses
#4
Julie Gilg, Rishi Pruthi, Damian Fogarty
No abstract text is available yet for this article.
2015: Nephron. Physiology
https://www.readbyqxmd.com/read/25471091/renal-oxygenation-characteristics-in-healthy-native-kidneys-assessment-with-blood-oxygen-level-dependent-magnetic-resonance-imaging
#5
Zhenfeng Zheng, Huilan Shi, Hui Ma, Fengtan Li, Jing Zhang, Yunting Zhang
OBJECTIVE: To explore the characteristics of blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) in healthy native kidneys. METHODS: Seventy-nine patients without chronic kidney disease underwent BOLD-MRI with T2* spoiled gradient recalled echo sequences. BOLD images were analyzed using R2*map software to produce an R2* pseudo-color map. Cortical and medullary R2* values were analyzed in both kidneys and in both sexes. Different regional R2* values in the cortex and medulla were also analyzed...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25377380/impact-of-aldosterone-on-osteoinductive-signaling-and-vascular-calcification
#6
REVIEW
Florian Lang, Eberhard Ritz, Ioana Alesutan, Jakob Voelkl
Vascular calcification is frequently found already in early stages of chronic kidney disease (CKD) patients and is associated with high cardiovascular risk. The process of vascular calcification is not considered a passive phenomenon but involves, at least in part, phenotypical transformation of vascular smooth muscle cells (VSMCs). Following exposure to excessive extracellular phosphate concentrations, VSMCs undergo a reprogramming into osteo-/chondroblast-like cells. Such 'vascular osteoinduction' is characterized by expression of osteogenic transcription factors and triggered by increased phosphate concentrations...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25377230/mineralocorticoid-and-sgk1-sensitive-inflammation-and-tissue-fibrosis
#7
REVIEW
Ferruh Artunc, Florian Lang
Effects of mineralocorticoids are not restricted to regulation of epithelial salt transport, extracellular volume and blood pressure; mineralocorticoids also influence a wide variety of seemingly unrelated functions such as inflammation and fibrosis. The present brief review addresses the role of mineralocorticoids in the orchestration of these latter processes. Mineralocorticoids foster inflammation as well as vascular, cardiac, renal and peritoneal fibrosis. Mechanisms involved in mineralocorticoid-sensitive inflammation and fibrosis include the serum- and glucocorticoid-inducible kinase 1 (SGK1), which is genomically upregulated by mineralocorticoids and transforming growth factor β (TGF-β), and stimulated by mineralocorticoid-sensitive phosphatidylinositide 3-kinase...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25377117/effect-of-mineralocorticoids-on-acid-base-balance
#8
REVIEW
Carsten A Wagner
Aldosterone is classically associated with the regulation of salt and potassium homeostasis but has also profound effects on acid-base balance. During acidosis, circulating aldosterone levels are increased and the hormone acts in concert with angiotensin II and other factors to stimulate renal acid excretion. Pharmacological blockade of aldosterone action as well as inherited or acquired syndromes of impaired aldosterone release or action impair the renal response to acid loading and cause hyperkalemic renal tubular acidosis...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25376974/genetic-molecular-and-clinical-determinants-for-the-involvement-of-aldosterone-and-its-receptors-in-major-depression
#9
REVIEW
Harald Murck, Matthias Büttner, Tilo Kircher, Carsten Konrad
Major depression (MDE) has metabolic and neuroendocrine correlates, which point to a biological overlap between MDE and cardiovascular diseases. Whereas the hypothalamic-pituitary-adrenocortical axis has long been recognized for its involvement in depression, the focus was mostly on cortisol/corticosterone, whereas aldosterone appears to be the 'forgotten' stress hormone. Part of the reason for this is that the receptors for aldosterone, the mineralocorticoid receptors (MR), were thought to be occupied by glucocorticoids in most parts of the brain...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25376899/mineralocorticoid-induced-sodium-appetite-and-renal-salt-retention-evidence-for-common-signaling-and-effector-mechanisms
#10
REVIEW
Yiling Fu, Volker Vallon
An increase in renal sodium chloride (salt) retention and an increase in sodium appetite are the body's responses to salt restriction or depletion in order to restore salt balance. Renal salt retention and increased sodium appetite can also be maladaptive and sustain the pathophysiology in conditions like salt-sensitive hypertension and chronic heart failure. Here we review the central role of the mineralocorticoid aldosterone in both the increase in renal salt reabsorption and sodium appetite. We discuss the working hypothesis that aldosterone activates similar signaling and effector mechanisms in the kidney and brain, including the mineralocorticoid receptor, the serum- and glucocorticoid-induced kinase SGK1, the ubiquitin ligase NEDD4-2, and the epithelial sodium channel ENaC...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25376771/on-the-pleotropic-actions-of-mineralocorticoids
#11
Florian Lang
Classical effects of mineralocorticoids include stimulation of Na(+) reabsorption and K(+) secretion in the kidney and other epithelia including colon and several glands. Moreover, mineralocorticoids enhance the excretion of Mg(2+) and renal tubular H(+) secretion. The renal salt retention following mineralocorticoid excess leads to extracellular volume expansion and hypertension. The increase of blood pressure following mineralocorticoid excess is, however, not only the result of volume expansion but may result from stiff endothelial cell syndrome impairing the release of vasodilating nitric oxide...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/25358339/insulin-receptor-and-the-kidney-nephrocalcinosis-in-patients-with-recessive-insr-mutations
#12
Arabella Simpkin, Elaine Cochran, Fergus Cameron, Mehul Dattani, Martin de Bock, David B Dunger, Gun Forsander, Tulay Guran, Julie Harris, Iona Isaac, Khalid Hussain, Robert Kleta, Catherine Peters, Velibor Tasic, Rachel Williams, Fabian Yap Kok Peng, Stephan O''Rahilly, Philipp Gorden, Robert K Semple, Detlef Bockenhauer
BACKGROUND/AIMS: Donohue and Rabson-Mendenhall syndrome are rare autosomal recessive disorders caused by mutations in the insulin receptor gene, INSR. Phenotypic features include extreme insulin resistance, linear growth retardation, paucity of fat and muscle, and soft tissue overgrowth. The insulin receptor is also expressed in the kidney, where animal data suggest it plays a role in glomerular function and blood pressure (BP) regulation, yet such a role in the human kidney is untested...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/24970544/ernest-henry-starling-1866-1927-on-the-glomerular-and-tubular-functions-of-the-kidney
#13
Leon G Fine
Around the turn of the 20th century, Ernest Henry Starling (1866-1927) made many fundamental contributions to the understanding of human physiology. With a deep interest in how fluid balance is regulated, he naturally turned to explore the intricacies of kidney function. Early in his career he focused upon the process of glomerular filtration and was able to substantiate the view of Carl Ludwig that this process can be explained entirely upon the basis of hydrostatic and oncotic pressure gradients across the glomerular capillary wall and that the process can be regulated by alterations in the tone of the afferent and efferent arterioles...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/24852245/ernest-henry-starling-1866-1927-on-the-formation-and-reabsorption-of-lymph
#14
Leon G Fine
Ernest Henry Starling laid the groundwork for our modern understanding of how the interstitial fluid, which he referred to as 'lymph', is regulated. Together with his colleague, William Bayliss, he provided the crucial insight into how fluid is driven out of the capillary to form interstitial fluid. That was to measure (estimate) the capillary pressure in different parts of the circulation and to relate changes in these pressures to altered lymph formation. In addressing how interstitial fluid re-enters the circulation, he was able to show that this occurs not only via the lymphatics, but also by re-entering the capillaries, mediated by the oncotic pressure of the plasma proteins...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/24576893/bolus-administration-of-intravenous-glucose-in-the-treatment-of-hyperkalemia-a-randomized-controlled-trial
#15
RANDOMIZED CONTROLLED TRIAL
Mogamat-Yazied Chothia, Mitchell L Halperin, Megan A Rensburg, Mogamat Shafick Hassan, Mogamat Razeen Davids
BACKGROUND: Hyperkalemia is a common medical emergency that may result in serious cardiac arrhythmias. Standard therapy with insulin plus glucose reliably lowers the serum potassium concentration ([K(+)]) but carries the risk of hypoglycemia. This study examined whether an intravenous glucose-only bolus lowers serum [K(+)] in stable, nondiabetic, hyperkalemic patients and compared this intervention with insulin-plus-glucose therapy. METHODS: A randomized, crossover study was conducted in 10 chronic hemodialysis patients who were prone to hyperkalemia...
2014: Nephron. Physiology
https://www.readbyqxmd.com/read/24335189/beyond-linear-methods-of-data-analysis-time-series-analysis-and-its-applications-in-renal-research
#16
REVIEW
Ashwani K Gupta, Andreea Udrea
Analysis of temporal trends in medicine is needed to understand normal physiology and to study the evolution of disease processes. It is also useful for monitoring response to drugs and interventions, and for accountability and tracking of health care resources. In this review, we discuss what makes time series analysis unique for the purposes of renal research and its limitations. We also introduce nonlinear time series analysis methods and provide examples where these have advantages over linear methods. We review areas where these computational methods have found applications in nephrology ranging from basic physiology to health services research...
2013: Nephron. Physiology
https://www.readbyqxmd.com/read/24296675/dynamics-of-renal-electrolyte-excretion-in-growing-mice
#17
Katharina Schmidt, Maria Ripper, Ines Tegtmeier, Evelyn Humberg, Christina Sterner, Markus Reichold, Richard Warth, Sascha Bandulik
Genetically modified mice represent important models for elucidating renal pathophysiology, but gene deletions frequently cause severe failure to thrive. In such cases, the analysis of the phenotype is often limited to the first weeks of life when renal excretory function undergoes dramatic physiological changes. Here, we investigated the postnatal dynamics of urinary ion excretion in mice. The profiles of urinary electrolyte excretion of mice were examined from birth until after weaning using an automated ion chromatography system...
2013: Nephron. Physiology
https://www.readbyqxmd.com/read/24247155/glutathione-is-a-low-affinity-substrate-of-the-human-sodium-dependent-dicarboxylate-transporter
#18
Lena Schorbach, Wolfgang Krick, Gerhard Burckhardt, Birgitta C Burckhardt
BACKGROUND/AIMS: During a single pass through the kidneys, more than 80% of glutathione (GSH) is excreted, indicating not only glomerular filtration, but also tubular secretion. The first step in tubular secretion is the uptake of a substance across the basolateral membrane of proximal tubule cells by sodium-dependent and -independent transporters. Due to the dicarboxylate-like structure, we postulated that GSH uptake across the basolateral membrane is mediated by the sodium-dependent dicarboxylate transporter 3 (NaDC3)...
2013: Nephron. Physiology
https://www.readbyqxmd.com/read/24193250/kcnj10-mutations-display-differential-sensitivity-to-heteromerisation-with-kcnj16
#19
Sophie Parrock, Sofia Hussain, Naomi Issler, Ann-Marie Differ, Nicholas Lench, Stefano Guarino, Michiel J S Oosterveld, Mandy Keijzer-Veen, Eva Brilstra, Hester van Wieringen, A Yvette Konijnenberg, Sarah Amin-Rasip, Simona Dumitriu, Enriko Klootwijk, Nine Knoers, Detlef Bockenhauer, Robert Kleta, Anselm A Zdebik
BACKGROUND/AIMS: Mutations in the inwardly-rectifying K(+)-channel KCNJ10/Kir4.1 cause autosomal recessive EAST syndrome (epilepsy, ataxia, sensorineural deafness and tubulopathy). KCNJ10 is expressed in the distal convoluted tubule of the kidney, stria vascularis of the inner ear and brain glial cells. Patients diagnosed clinically with EAST syndrome were genotyped and mutations in KCNJ10 were studied functionally. METHODS: Patient DNA was amplified and sequenced, and new mutations were identified...
2013: Nephron. Physiology
https://www.readbyqxmd.com/read/23887028/adenosine-effects-on-renal-function-in-the-rat-role-of-sodium-intake-and-cytochrome-p450
#20
Marta Kuczeriszka, Leszek Dobrowolski, Agnieszka Walkowska, Janusz Sadowski, Elżbieta Kompanowska-Jezierska
BACKGROUND/AIMS: Adenosine (ADO) causes vasodilation in most tissues. In the kidney it can induce vasoconstriction or vasodilation, depending on the prevailing stimulation of A1 or A2 receptors (A1R, A2R). ADO-induced alterations of renal excretion may be secondary to haemodynamic changes, or reflect a direct influence on tubular transport. This whole-kidney study explored renal excretory responses to ADO receptor stimulation as related to renal haemodynamics sodium intake and cytochrome P450 (CYP-450) activity...
2013: Nephron. Physiology
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