293 results match your criteria Nephron Physiology[Journal]


Renal Oxygenation Characteristics in Healthy Native Kidneys: Assessment with Blood Oxygen Level-Dependent Magnetic Resonance Imaging.

Nephron Physiol 2014 27;128(3-4):47-54. Epub 2014 Nov 27.

Department of Nephrology, General Hospital of Tianjin Medical University, Tianjin, PR China.

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. Read More

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http://dx.doi.org/10.1159/000366448DOI Listing
November 2014
4 Reads

Impact of aldosterone on osteoinductive signaling and vascular calcification.

Nephron Physiol 2014 6;128(1-2):40-5. Epub 2014 Nov 6.

Department of Physiology, University of Tübingen, Tübingen, Germany.

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. Read More

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http://dx.doi.org/10.1159/000368268DOI Listing
August 2015
3 Reads

Mineralocorticoid and SGK1-sensitive inflammation and tissue fibrosis.

Nephron Physiol 2014 6;128(1-2):35-9. Epub 2014 Nov 6.

Department of Internal Medicine, University of Tübingen, Tübingen, Germany.

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. Read More

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http://dx.doi.org/10.1159/000368267DOI Listing
August 2015
5 Reads

Effect of mineralocorticoids on acid-base balance.

Authors:
Carsten A Wagner

Nephron Physiol 2014 6;128(1-2):26-34. Epub 2014 Nov 6.

Institute of Physiology, University of Zurich, Zurich, Switzerland.

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. Read More

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http://dx.doi.org/10.1159/000368266DOI Listing
August 2015
2 Reads

Genetic, molecular and clinical determinants for the involvement of aldosterone and its receptors in major depression.

Nephron Physiol 2014 6;128(1-2):17-25. Epub 2014 Nov 6.

Covance Inc., Princeton, N.J., USA.

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. Read More

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http://dx.doi.org/10.1159/000368265DOI Listing
August 2015
7 Reads

Mineralocorticoid-induced sodium appetite and renal salt retention: evidence for common signaling and effector mechanisms.

Nephron Physiol 2014 6;128(1-2):8-16. Epub 2014 Nov 6.

Department of Medicine, University of California San Diego, La Jolla, Calif., USA.

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. Read More

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http://dx.doi.org/10.1159/000368264DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275376PMC
August 2015
13 Reads

On the pleotropic actions of mineralocorticoids.

Authors:
Florian Lang

Nephron Physiol 2014 5;128(1-2):1-7. Epub 2014 Nov 5.

Department of Physiology, Eberhard Karls University of Tübingen, Tübingen, Germany.

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. Read More

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http://dx.doi.org/10.1159/000368263DOI Listing
August 2015
1 Read

Insulin Receptor and the Kidney: Nephrocalcinosis in Patients with Recessive INSR Mutations.

Nephron Physiol 2014 24;128(3-4):55-61. Epub 2014 Oct 24.

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. Read More

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http://dx.doi.org/10.1159/000366225DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369119PMC
October 2014
34 Reads

Ernest Henry Starling (1866-1927) on the glomerular and tubular functions of the kidney.

Authors:
Leon G Fine

Nephron Physiol 2014 26;126(4):19-28. Epub 2014 Jun 26.

Department of Biomedical Sciences, Cedars-Sinai Medical Center and University of California Los Angeles, Los Angeles, Calif., USA.

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. Read More

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http://dx.doi.org/10.1159/000363302DOI Listing
April 2015
5 Reads

Ernest Henry Starling (1866-1927) on the formation and reabsorption of lymph.

Authors:
Leon G Fine

Nephron Physiol 2014 16;126(3):9-17. Epub 2014 May 16.

Department of Biomedical Sciences, Cedars-Sinai Medical Center and University of California Los Angeles, Los Angeles, Calif., USA.

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. Read More

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http://dx.doi.org/10.1159/000362620DOI Listing
February 2015
8 Reads

Bolus administration of intravenous glucose in the treatment of hyperkalemia: a randomized controlled trial.

Nephron Physiol 2014 22;126(1):1-8. Epub 2014 Feb 22.

Division of Nephrology, Department of Medicine, Stellenbosch University and Tygerberg Hospital, Cape Town, South Africa.

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. Read More

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http://dx.doi.org/10.1159/000358836DOI Listing
November 2014
25 Reads
6 Citations
1.545 Impact Factor

Beyond linear methods of data analysis: time series analysis and its applications in renal research.

Nephron Physiol 2013 10;124(3-4):14-27. Epub 2013 Dec 10.

Department of Nephrology, University of Florida, Jacksonville, Fla., USA.

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. Read More

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http://dx.doi.org/10.1159/000356382DOI Listing
October 2014
1 Read

Dynamics of renal electrolyte excretion in growing mice.

Nephron Physiol 2013 26;124(3-4):7-13. Epub 2013 Nov 26.

Medical Cell Biology, University of Regensburg, Regensburg, Germany.

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. Read More

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http://dx.doi.org/10.1159/000356816DOI Listing
October 2014
5 Reads

Glutathione is a low-affinity substrate of the human sodium-dependent dicarboxylate transporter.

Nephron Physiol 2013 14;124(1-2):1-5. Epub 2013 Nov 14.

Institute of Systemic Physiology and Pathophysiology, University Medical Center Göttingen, Göttingen, Germany.

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). Read More

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http://dx.doi.org/10.1159/000356419DOI Listing
July 2014
12 Reads

KCNJ10 mutations display differential sensitivity to heteromerisation with KCNJ16.

Nephron Physiol 2013 2;123(3-4):7-14. Epub 2013 Nov 2.

Department of Neuroscience, Physiology and Pharmacology, University College London, London, UK.

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. Read More

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http://dx.doi.org/10.1159/000356353DOI Listing
June 2014
21 Reads

Adenosine effects on renal function in the rat: role of sodium intake and cytochrome P450.

Nephron Physiol 2013 25;123(1-2):1-5. Epub 2013 Jul 25.

Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

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. Read More

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http://dx.doi.org/10.1159/000353705DOI Listing
February 2014
4 Reads

Variations of dietary salt and fluid modulate calcium and magnesium transport in the renal distal tubule.

Nephron Physiol 2012 11;122(3-4):19-27. Epub 2013 Jun 11.

Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang-Gung Memorial Hospital, Chang-Gung University College of Medicine, Kaohsiung, Taiwan.

Background: The renal distal tubule fine-tunes renal epithelial calcium transport. Dietary intake of salt and fluid varies day-to-day and the kidney adapts accordingly to maintain homeostasis. The alternations in salt and fluid balance affect calcium and magnesium transport in the distal tubule, but the mechanisms are not fully understood. Read More

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http://dx.doi.org/10.1159/000353199DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007268PMC
January 2014
33 Reads

Non-natriuretic doses of furosemide: potential use for decreasing the workload of the renal outer medulla with minimal magnesium wasting in the rat.

Nephron Physiol 2012 15;122(1-2):7-12. Epub 2013 Mar 15.

Department of Anesthesia, Division of Nephrology, University of Toronto, St. Michael's Hospital, Keenan Research Centre in the Li Ka Shing Knowledge Institute, Toronto, Ont., Canada.

Background/aims: Since furosemide (FS) inhibits active Na(+) reabsorption by medullary thick ascending limb (mTAL) in the renal outer medulla, it may decrease its work during periods of low O2 supply to deep in the renal outer medulla. This study was designed to demonstrate that there may be a dose of FS would reduce its metabolic work while preventing the excessive loss of magnesium (Mg(2+)). Mg(2+) is important because the ATP needed to perform work must have bound Mg(2+) to it. Read More

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http://dx.doi.org/10.1159/000346741DOI Listing
October 2013
2 Reads

Nephrocalcinosis (enamel renal syndrome) caused by autosomal recessive FAM20A mutations.

Nephron Physiol 2012 23;122(1-2):1-6. Epub 2013 Feb 23.

Centre for Nephrology, University College London, London, UK.

Background/aims: Calcium homeostasis requires regulated cellular and interstitial systems interacting to modulate the activity and movement of this ion. Disruption of these systems in the kidney results in nephrocalcinosis and nephrolithiasis, important medical problems whose pathogenesis is incompletely understood.

Methods: We investigated 25 patients from 16 families with unexplained nephrocalcinosis and characteristic dental defects (amelogenesis imperfecta, gingival hyperplasia, impaired tooth eruption). Read More

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http://dx.doi.org/10.1159/000349989DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3782194PMC
October 2013
55 Reads

Assessment of the effect of 24-hour aldosterone administration on protein abundance in fluorescence-sorted mouse distal renal tubules by mass spectrometry.

Nephron Physiol 2012 14;121(3-4):p9-15. Epub 2013 Feb 14.

Department of Biomedicine and the Water and Salt Research Center, Aarhus University - Health, Aarhus, Denmark.

Background/aims: Aldosterone exerts multiple long-term effects on the distal renal tubules. The aim of this study was to establish a method for identifying proteins in these tubules that change in abundance by only 24-hour aldosterone administration.

Methods: Mice endogenously expressing green fluorescent protein (eGFP) in the connecting tubule and cortical collecting ducts were treated with a subcutaneous injection of 2. Read More

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http://dx.doi.org/10.1159/000346832DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648998PMC
July 2013
4 Reads

Response of the renal inner medulla to hypoxia: possible defense mechanisms.

Nephron Physiol 2012 30;121(1-2):p1-7. Epub 2012 Nov 30.

Department of Anesthesia, Keenan Research Centre of Li Ka Shing Knowledge Institute, University of Toronto, St. Michael's Hospital, Toronto, Ontario, Canada.

Background/aims: Owing to the precarious blood supply to the renal medulla and the high metabolic requirement of the medullary thick ascending limb of Henle's loop, this nephron segment should be especially vulnerable when its supply of O(2) declines.

Methods: Rats were exposed to 8 or 21% O(2) at different time points up to 5 h, and samples were collected for urine flow rate, urine (U(osm)) and renal papillary (RP(osm)) osmolality, urinary excretion of Na(+), Cl(-), K(+) and Mg(2+), blood gases, erythropoietin and vasopressinase activity in plasma. Other groups of rats were pretreated with desmopressin acetate (dDAVP) or underwent bilateral nephrectomy (BNX) 1 h prior to the exposure. Read More

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http://dx.doi.org/10.1159/000345516DOI Listing
May 2013
9 Reads

Extracellular pyrophosphate in the kidney: how does it get there and what does it do?.

Nephron Physiol 2012 12;120(4):p33-8. Epub 2012 Oct 12.

UCL Centre for Nephrology Royal Free, Royal Free London NHS Foundation Trust, London, UK. smoochhala @ nhs.net

Pyrophosphate (PPi) is well known as a regulator of calcification, and the ANKH (ANK in mouse) protein has a role in the membrane transport of PPi. Earlier work concentrated on bones and joints, but ANKH is also likely to have important roles in the kidney, with newer studies focusing on vascular calcification in renal failure. Renal calcification can occur due to a naturally occurring ANK mouse mutation, yet other ANK mutations do not cause a renal phenotype. Read More

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http://dx.doi.org/10.1159/000341597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5166521PMC
February 2014
1 Read

An intact kidney slice model to investigate vasa recta properties and function in situ.

Nephron Physiol 2012 20;120(3):p17-31. Epub 2012 Jul 20.

Medway School of Pharmacy, The Universities of Kent and Greenwich at Medway, Chatham, UK.

Background: Medullary blood flow is via vasa recta capillaries, which possess contractile pericytes. In vitro studies using isolated descending vasa recta show that pericytes can constrict/dilate descending vasa recta when vasoactive substances are present. We describe a live kidney slice model in which pericyte-mediated vasa recta constriction/dilation can be visualized in situ. Read More

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http://dx.doi.org/10.1159/000339110DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5166522PMC
January 2013
6 Reads

An acute infusion of lactic acid lowers the concentration of potassium in arterial plasma by inducing a shift of potassium into cells of the liver in fed rats.

Nephron Physiol 2012 28;120(2):p7-15. Epub 2012 Apr 28.

Division of Nephrology, St. Michael's Hospital, Toronto, Ont., Canada.

Background: Potassium (K(+)) input occurs after meals or during ischemic exercise and is accompanied by a high concentration of L-lactate in plasma (P(L-lactate)).

Methods: We examined whether infusing 100 μmol L-lactic acid/min for 15 min would lead to a fall in the arterial plasma K(+) concentration (P(K)). We also aimed to evaluate the mechanisms involved in normal rats compared with rats with acute hyperkalemia caused by a shift of K(+) from cells or a positive K(+) balance. Read More

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http://dx.doi.org/10.1159/000336321DOI Listing
September 2012
3 Reads

Electrolyte-free water clearance versus modified electrolyte-free water clearance: do the results justify the effort?

Nephron Physiol 2012 6;120(1):p1-5. Epub 2012 Mar 6.

Department of Emergency Medicine, Inselspital, University of Bern, Bern, Switzerland.

Background: Calculation of electrolyte-free water clearance (EFWC) allows for quantification of renal losses of free water and was shown to be helpful in the differential diagnosis of dysnatremias and might help in the correction of the electrolyte disorders. A modified EFWC formula (MEFWC) was described to be more accurate than the conventional one; however, it has never been evaluated clinically.

Methods: In order to evaluate the performance of MEFWC compared to EFWC under clinical circumstances, we gathered data from a total of 912 patient days of 138 critically ill patients. Read More

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https://www.karger.com/Article/FullText/336550
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http://dx.doi.org/10.1159/000336550DOI Listing
August 2012
31 Reads

Weight, age and coefficients of variation in renal solute excretion.

Nephron Physiol 2012 19;122(1-2):13-8. Epub 2013 Mar 19.

Department of Medicine, SUNY Upstate Medical University, Syracuse, NY 13210, USA.

Background: Homoscedasticity (constant variance over axes or among statistical factors) is an integral assumption of most statistical analyses. However, a number of empirical studies in model organisms and humans demonstrate significant differences in residual variance (that component of phenotype unexplained by known factors) or intra-individual variation among genotypes. Our work suggests that renal traits may be particularly susceptible to randomization by genetic and non-genetic factors, including endogenous variables like age and weight. Read More

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http://dx.doi.org/10.1159/000346148DOI Listing
October 2013
3 Reads

Renal stone disease: a commentary on the nature and significance of Randall's plaque.

Nephron Physiol 2011 21;119(4):p49-53. Epub 2011 Sep 21.

Indiana University School of Medicine, Indianapolis, IN 46202-5120, USA.

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http://dx.doi.org/10.1159/000330255DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701452PMC
February 2012
1 Read

KCNJ10 mutations disrupt function in patients with EAST syndrome.

Nephron Physiol 2011 18;119(3):p40-8. Epub 2011 Aug 18.

Centre for Nephrology, University College London, Royal Free Hospital, London, UK.

Background/aims: Mutations in the inwardly-rectifying K+ channel KCNJ10/Kir4.1 cause an autosomal recessive disorder characterized by epilepsy, ataxia, sensorineural deafness and tubulopathy (EAST syndrome). KCNJ10 is expressed in the kidney distal convoluted tubule, cochlear stria vascularis and brain glial cells. Read More

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http://dx.doi.org/10.1159/000330250DOI Listing
April 2014
17 Reads

Familial autosomal recessive renal tubular acidosis: importance of early diagnosis.

Nephron Physiol 2011 18;119(3):p31-9. Epub 2011 Aug 18.

Department of Pediatrics, Talpiot Medical Leadership Program, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Background And Aims: Untreated renal tubular acidosis (RTA) can result in severe complications. We reviewed the clinical features of patients with mutations in two genes causing RTA and evaluated their developmental expression assuming that timing, symptom severity and complications may be related to its occurrence.

Methods: Clinical data from 16 patients with RTA due to mutations in either ATP6V1B1 or CAII were retrospectively reviewed. Read More

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http://dx.doi.org/10.1159/000329668DOI Listing
April 2014
13 Reads

Senile nephrosclerosis--does it explain the decline in glomerular filtration rate with aging?

Nephron Physiol 2011 10;119 Suppl 1:p6-11. Epub 2011 Aug 10.

Division of Nephrology and Hypertension and Division of Epidemiology, Rochester, MN 55905, USA. rule.andrew @ mayo.edu

Nephrosclerosis can be defined by the presence of glomerulosclerosis, tubular atrophy, interstitial fibrosis, and arteriosclerosis on renal biopsy. Chronic kidney disease is identified clinically by a reduction in glomerular filtration rate (GFR) and has been characterized histologically by nephrosclerosis. Many relatively healthy older adults have been diagnosed with chronic kidney disease because of a decline in GFR with normal aging. Read More

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http://dx.doi.org/10.1159/000328012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280422PMC
May 2012
5 Reads

Aging and physiological changes of the kidneys including changes in glomerular filtration rate.

Nephron Physiol 2011 10;119 Suppl 1:p1-5. Epub 2011 Aug 10.

Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.

In addition to the structural changes in the kidney associated with aging, physiological changes in renal function are also found in older adults, such as decreased glomerular filtration rate, vascular dysautonomia, altered tubular handling of creatinine, reduction in sodium reabsorption and potassium secretion, and diminished renal reserve. These alterations make aged individuals susceptible to the development of clinical conditions in response to usual stimuli that would otherwise be compensated for in younger individuals, including acute kidney injury, volume depletion and overload, disorders of serum sodium and potassium concentration, and toxic reactions to water-soluble drugs excreted by the kidneys. Additionally, the preservation with aging of a normal urinalysis, normal serum urea and creatinine values, erythropoietin synthesis, and normal phosphorus, calcium and magnesium tubular handling distinguishes decreased GFR due to normal aging from that due to chronic kidney disease. Read More

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http://dx.doi.org/10.1159/000328010DOI Listing
May 2012
2 Reads

Potential role of serine proteases in modulating renal sodium transport in vivo.

Nephron Physiol 2011 11;119(2):p22-9. Epub 2011 Aug 11.

UCL Centre for Nephrology, Royal Free Hospital, University College London, Medical School, London, UK.

The maintenance of sodium (Na+) homeostasis is an essential function of the kidney. It is achieved by a variety of transport processes localized all along the highly specialised segments of the nephron. Impairment of these transport mechanisms, and thereby Na+ handling, is associated with disturbed Na+ and water balance, leading to hypertension and oedema. Read More

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http://dx.doi.org/10.1159/000328926DOI Listing
February 2012
1 Read

Hypertonic stress promotes the upregulation and phosphorylation of zonula occludens 1.

Nephron Physiol 2011 7;119(2):p11-21. Epub 2011 Jul 7.

Department of Internal Medicine II, University Medical Center, Regensburg, Germany.

Tight junction molecules form a barrier between adjacent cells and mediate the cells' ability to develop membranes that constitute boundaries of different compartments within the body. Membranes with selective ion and water passage are important for the electrolyte and water homeostasis in the kidney. Due to their role in the urinary concentration process, renal medullary cells are exposed to hyperosmotic stress. Read More

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http://dx.doi.org/10.1159/000327567DOI Listing
February 2012
2 Reads

Proteomic approaches in understanding a detected relationship between chemotherapy-induced nephrotoxicity and cell respiration in HK-2 cells.

Nephron Physiol 2011 9;119(1):p1-10. Epub 2011 Jun 9.

Nephrology Division, Department of Medicine, Federal University of São Paulo, São Paulo, Brazil.

Background/aims: Nephrotoxicity is a prominent component of the profile of chemotherapeutic agents and to date proteomics has represented the main technique to identify protein profiles in response to xenobiotic exposure.

Methods: We made use of two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight analysis to evaluate chemotoxicity effects of cisplatin (CPT) and carboplatin (CB) on proteins from human renal proximal tubule epithelial cells (HK-2).

Results: Tandem mass spectrometry analysis showed that ATP synthase subunit α and serine hydroxymethyltransferase were only expressed in HK-2 cells exposed to CPT. Read More

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http://dx.doi.org/10.1159/000327575DOI Listing
February 2012
4 Reads

New evidence of a dihydropyridine-activated cationic channel in the MDCK cell line.

Nephron Physiol 2011 18;118(4):p73-81. Epub 2011 Apr 18.

Departamento de Farmacia, Escuela Nacional de Ciencias Biológicas del Instituto Politécnico Nacional, México, Mexico.

Newborn rat distal cells express an apical Ca2+ channel activated by dihydropyridine drugs. Similarly, in Madin-Darby canine kidney (MDCK) cells, nifedipine increased Ca2+i in a concentration-dependent manner (IC50=4 μM) in fura-2-loaded cells. Response to nifedipine was abolished by EGTA, suggesting that it depends on extracellular calcium. Read More

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http://dx.doi.org/10.1159/000325467DOI Listing
May 2012
2 Reads

Unexplained hyponatremia: seek and you will find.

Nephron Physiol 2011 7;118(3):p66-71. Epub 2011 Jan 7.

Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands. ejhoorn @ gmail.com

Background: Hyponatremia is a common diagnostic challenge.

Methods: An index case is presented to discuss the diagnostic approach to chronic and unexplained hyponatremia.

Results: The index case concerns a 60-year-old man with chronic hepatitis C and previous alcohol use who was referred because of weight loss, poor dietary intake, dizzy spells, and unexplained hyponatremia (serum sodium 124-129 mmol/l). Read More

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https://www.karger.com/Article/FullText/322240
Publisher Site
http://dx.doi.org/10.1159/000322240DOI Listing
January 2012
3 Reads

Amelogenesis imperfecta and nephrocalcinosis syndrome: a case report and review of the literature.

Nephron Physiol 2011 7;118(3):p62-5. Epub 2011 Jan 7.

Stomatology Clinic, Dental School, State University of Montes Claros, Brazil.

Amelogenesis imperfecta (AI) is a group of hereditary disorders that affect the quality and/or quantity of dental enamel. This paper describes the clinicopathological features of a patient who was born of consanguineous parents and who presented with oral alterations, including yellow and misshapen teeth, intrapulpal calcifications, delayed tooth eruption, and gum enlargement. Scanning electron microscopy of the teeth revealed hypoplastic enamel, and a renal ultrasound detected bilateral nephrocalcinosis, leading to a diagnosis of AI and nephrocalcinosis syndrome. Read More

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https://www.karger.com/Article/FullText/322828
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http://dx.doi.org/10.1159/000322828DOI Listing
January 2012
7 Reads

Identification of a novel WNK4 mutation in Chinese patients with pseudohypoaldosteronism type II.

Nephron Physiol 2011 24;118(3):p53-61. Epub 2010 Dec 24.

Department of Nephrology, School of Medicine, Shanghai Jiao Tong University, China.

Background: It has been reported that mutations in WNK1 and WNK4 cause pseudohypoaldosteronism type II (PHA2), an autosomal dominant renal disease. WNK kinase proteins are expressed in the kidney and regulate ion transport including the thiazide-sensitive sodium chloride cotransporter (NCC). In this report, we screened 4 Chinese PHA2 pedigrees for WNK4 mutations, identified a novel mutation, and studied its effects on NCC protein trafficking in vitro. Read More

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http://dx.doi.org/10.1159/000321879DOI Listing
January 2012
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Hyponatremia and inflammation: the emerging role of interleukin-6 in osmoregulation.

Nephron Physiol 2011 22;118(2):45-51. Epub 2010 Dec 22.

Department of Internal Medicine - Nephrology, Erasmus Medical Center, Rotterdam, The Netherlands.

Although hyponatremia is a recognized complication of several inflammatory diseases, its pathophysiology in this setting has remained elusive until recently. A growing body of evidence now points to an important role for interleukin-6 in the non-osmotic release of vasopressin. Here, we review this evidence by exploring the immuno-neuroendocrine pathways connecting interleukin-6 with vasopressin. Read More

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https://www.karger.com/Article/FullText/322238
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http://dx.doi.org/10.1159/000322238DOI Listing
September 2011
3 Reads

Fluid shear stress induces renal epithelial gene expression through polycystin-2-dependent trafficking of extracellular regulated kinase.

Nephron Physiol 2011 23;117(4):p27-36. Epub 2010 Nov 23.

Department of Medicine, The Mount Sinai School of Medicine, New York, NY 10000209, USA.

Background: The cilium and cilial proteins have emerged as principal mechanosensors of renal epithelial cells responsible for translating mechanical forces into intracellular signals. Polycystin-2 (PC-2), a cilial protein, regulates flow/shear-induced changes in intracellular Ca(2+) ([Ca(2+)](i)) and recently has been implicated in the regulation of mitogen-activated protein (MAP) kinases. We hypothesize that fluid shear stress (FSS) activates PC-2 which regulates MAP kinase and, in turn, induces MAP kinase-dependent gene expression, specifically, monocyte chemoattractant protein-1 (MCP-1). Read More

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http://dx.doi.org/10.1159/000321640DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997441PMC
July 2011
2 Reads

Loop disorders: insights derived from defined genotypes.

Nephron Physiol 2011 11;118(1):p7-14. Epub 2010 Nov 11.

Zentrum für Kinder- und Jugendmedizin, Philipps-Universität, Marburg, Deutschland.

Great progress has been made in the last 15 years in the characterization and the pathophysiological understanding of renal salt and water wasting associated with inherited disorders of the thick ascending limb (TAL) of Henle's loop, the loop disorders. Besides careful clinical observations and innovative physiological concepts, molecular genetics have made this progress possible. So far, mutations in five different genes may be responsible for the loop disorders. Read More

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http://dx.doi.org/10.1159/000320882DOI Listing
March 2011
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Renal stone disease.

Authors:
John A Sayer

Nephron Physiol 2011 11;118(1):p35-44. Epub 2010 Nov 11.

Institute of Human Genetics, International Centre for Life, Newcastle University, Newcastle upon Tyne, UK.

Background/aims: Renal stone disease may be seen as a clinical symptom of an underlying pathological process predisposing to crystallization within the renal tract. Renal stones may be comprised of calcium salts, uric acid, cystine and various other insoluble complexes. Nephrolithiasis may be the manifestation of rare single gene disorders or part of more common idiopathic renal stone-forming diseases. Read More

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http://dx.doi.org/10.1159/000320902DOI Listing
March 2011
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Disorders of water and acid-base homeostasis.

Authors:
Fiona E Karet

Nephron Physiol 2011 11;118(1):p28-34. Epub 2010 Nov 11.

Department of Medical Genetics and Division of Renal Medicine, University of Cambridge, Cambridge, UK.

Disorders of water balance lead either to dehydration or overhydration. Because there is an intimate relationship between water and sodium concentration (water generally following salt), one can distinguish hypotonic, isotonic and hypertonic dehydration and the same for overhydration. The vast majority of water balance disorders are acquired. Read More

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http://dx.doi.org/10.1159/000320885DOI Listing
March 2011
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Disorders of calcium metabolism.

Authors:
John F O'Toole

Nephron Physiol 2011 11;118(1):p22-7. Epub 2010 Nov 11.

Division of Nephrology, Department of Internal Medicine, MetroHealth Medical Center, and Case Western Reserve University School of Medicine, Cleveland, Ohio 44109-1998, USA.

The genetic contribution to calcium metabolism is well recognized. Many of the proteins that contribute to calcium homeostasis through intestinal absorption, bone deposition and resorption, renal reabsorption and the molecules regulating these processes have been identified. Mutations in many of the genes coding for these proteins have been identified and often have clear clinical phenotypes. Read More

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http://dx.doi.org/10.1159/000320884DOI Listing
March 2011
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Genetic disorders of NaCl transport in the distal convoluted tubule.

Authors:
R Tyler Miller

Nephron Physiol 2011 11;118(1):p15-21. Epub 2010 Nov 11.

Case-Western Reserve University, Louis Stokes VAMC, Ramelkamp Center for Research and Education, MetroHealth Medical Center, Cleveland, Ohio, USA.

The distal convoluted tubule (DCT) reabsorbs 5-10% of filtered Na, and is an important site for regulation of Na balance. Additionally, the amount and composition of the tubular fluid that leaves the DCT affects H and K secretion in more distal nephrin segments. Mutations in five genes whose products are expressed in the DCT demonstrate these points and help to define the mechanisms by which the DCT contributes to control of electrolyte balance and volume. Read More

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http://dx.doi.org/10.1159/000320883DOI Listing
March 2011
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Disorders of the renal proximal tubule.

Nephron Physiol 2011 11;118(1):p1-6. Epub 2010 Nov 11.

Department of Pediatrics, VU University Medical Center, Amsterdam, The Netherlands.

Following glomerular filtration, the bulk of solutes are reabsorbed in the proximal tubule to prevent excessive losses of vital metabolites. In this nephron segment, reabsorption is largely active via dedicated transporters. Hereditary defects in proximal tubular function are characterized by malabsorption affecting amino acids, glucose, potassium, phosphate, bicarbonate, low-molecular-weight proteins and other solutes handled by this nephron segment. Read More

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http://dx.doi.org/10.1159/000320880DOI Listing
March 2011
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Selective blockade of oxytocin and vasopressin V(1a) receptors in anaesthetised rats: evidence that activation of oxytocin receptors rather than V(1a) receptors increases sodium excretion.

Nephron Physiol 2011 11;117(3):p21-6. Epub 2010 Nov 11.

Centre for Nephrology, University College London Medical School, London, UK.

Background: Although it is known that moderate-to-high doses of the neurohypophysial hormones oxytocin and vasopressin are natriuretic, doubts remain over the identity of the receptors responsible. To address this issue, we have used highly selective antagonists of oxytocin and vasopressin receptors in animals with elevated endogenous circulating levels of the 2 hormones.

Methods: Rats were anaesthetised and prepared surgically for clearance studies, thereby raising plasma oxytocin and vasopressin concentrations. Read More

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http://dx.doi.org/10.1159/000320290DOI Listing
July 2011
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Transient receptor potential melastatin 6 knockout mice are lethal whereas heterozygous deletion results in mild hypomagnesemia.

Nephron Physiol 2011 1;117(2):p11-9. Epub 2010 Sep 1.

Department of Physiology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Background: Hypomagnesemia with secondary hypocalcemia is due to disturbed renal and intestinal magnesium (Mg(2+)) (re)absorption. The underlying defect is a mutation in the transient receptor potential melastatin type 6 (TRPM6), a Mg(2+)-permeable ion channel expressed in the kidney and intestine. Our aim was to characterize homozygous (-/-) and heterozygous (+/-) TRPM6 knockout mice with respect to Mg(2+) homeostasis. Read More

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http://dx.doi.org/10.1159/000320580DOI Listing
May 2011
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Computation of Na and water deficit of iso-osmolar dehydration.

Nephron Physiol 2011 26;117(1):p1-10. Epub 2010 Aug 26.

Internal Medicine, Dipartimento di Medicina Clinica e Sperimentale, Università del Piemonte Orientale A. Avogadro, Novara, Italy. sainaghi @ med.unipmn.it

Background And Aims: The presence of altered plasma Na concentration (PNa) allows calculations of changes in water and electrolyte contents, which are not feasible during normonatremic derangements. We have developed a computational algorithm whereby the changes in solute (ΔNa and ΔCl) and solvent (ΔV) contents can be computed exactly when Na is lost entirely as NaCl (or NaHCO(3)) and nearly exactly in all other circumstances, except when the losses of Na and Cl occur in the same proportions as those of the normal plasma concentration of these ions.

Methods: In computer experiments, we simulated different fluid depletions containing 140 mEq/l of Na (which is to say, ΔNa/ΔV ≈ 140), coupled with variable ratios in Na to Cl losses (variable ΔNa/ΔCl). Read More

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http://dx.doi.org/10.1159/000320371DOI Listing
April 2011
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