6,076 results match your criteria American Journal of Physiology - Renal Physiology[Journal]


Direct and Indirect Inhibition of the Circadian Clock Protein PER1: Effects on ENaC and Blood Pressure.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Medicine, Nephrology; Biochemistry and Molecular Biology, University of Florida, United States.

Circadian rhythms govern physiological functions and are important for overall health. The molecular circadian clock is comprised of several transcription factors that mediate circadian control of physiological function in part by regulating gene expression in a tissue-specific manner. These connections are well established but the underlying mechanisms are incompletely understood. Read More

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http://dx.doi.org/10.1152/ajprenal.00408.2018DOI Listing
February 2019

Sex as a Biological Variable in Renal, Metabolic and Cardiovascular Physiology:Eighteen Years of Leadership by the American Physiological Society.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Physiology, Augusta University, United States.

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http://dx.doi.org/10.1152/ajprenal.00019.2019DOI Listing
February 2019

Urinary microRNA in Kidney Disease: Utility and Roles.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Division of Nephrology, Mayo Clinic, United States.

MicroRNAs (miRNAs) are small, noncoding single-stranded RNA oligonucleotides that modulate physiological and pathological processes by modulating target gene expression. Many miRNAs display tissue-specific expression patterns, the dysregulation of which has been associated with various disease states, including kidney disease. Mounting evidence implicates miRNAs in various biological processes, such as cell proliferation, differentiation, and cancer. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00368.2018
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http://dx.doi.org/10.1152/ajprenal.00368.2018DOI Listing
February 2019
1 Read

Exercise Interventions for Improving Objective Physical Function in End-Stage Kidney Disease Patients on Dialysis: A Systematic Review and Meta-Analysis.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Institute for Physical Activity and Nutrition, Deakin University, Australia.

Background: Patients with end stage kidney disease on dialysis have increased mortality and reduced physical activity contributing to impaired physical function. While exercise programmes have demonstrated a positive effect on physiological outcomes such as cardiovascular function and strength, there is a reduced focus on physical function. The aim of this review was to determine whether exercise programmes improve objective measures of physical function indicative of activities of daily living for end stage kidney disease patients on dialysis. Read More

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http://dx.doi.org/10.1152/ajprenal.00317.2018DOI Listing
February 2019

Novel kidney dissociation protocol and image-based flow cytometry facilitate improved analysis of injured proximal tubules.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Medicine/Nephrology, Vanderbilt University Medical Center, United States.

Flow cytometry studies on injured kidney tubules are complicated by a low yield of nucleated single cells. Furthermore, cell-specific responses such as cell cycle dynamics in vivo has conventionally relied on indirect immunohistochemistry and proximal tubule markers that may be downregulated in injury. We report a new tissue dissociation protocol for kidney with an early fixation step that greatly enhances the yield of single cells. Read More

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http://dx.doi.org/10.1152/ajprenal.00354.2018DOI Listing
February 2019

The nephron-arterial network and its interactions.

Am J Physiol Renal Physiol 2019 Feb 13. Epub 2019 Feb 13.

Renal and Vascular Research Section, University of Copenhagen, Biomedicinsk Institut, Denmark.

Tubuloglomerular feedback and the myogenic mechanism form an ensemble in renal afferent arterioles that regulates single nephron blood flow and glomerular filtration. Each mechanism generates a self-sustained oscillation, the mechanisms interact, and the oscillations synchronize. The synchronization generates a bimodal electrical signal in the arteriolar wall that propagates retrograde to a vascular node where it meets similar electrical signals from other nephrons. Read More

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http://dx.doi.org/10.1152/ajprenal.00484.2018DOI Listing
February 2019

Endothelial Cell-Specific Collagen IV α3 Expression Does not Rescue Alport Syndrome in Col4a3-/- Mice.

Am J Physiol Renal Physiol 2019 Feb 6. Epub 2019 Feb 6.

Medince/Division of Nephrology, Washington University School of Medicine, United States.

The glomerular basement membrane (GBM) is a critical component of the kidney's blood filtration barrier. Alport syndrome, a hereditary disease leading to kidney failure, is caused by the loss or dysfunction of the GBM's major type IV collagen (COL4) isoform, α3α4α5. The constituent COL4 achains assemble into heterotrimers in the endoplasmic reticulum prior to secretion into the extracellular space. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00556.2018
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http://dx.doi.org/10.1152/ajprenal.00556.2018DOI Listing
February 2019
2 Reads

Endogenous IL-22 is dispensable for experimental glomerulonephritis.

Am J Physiol Renal Physiol 2019 Feb 6. Epub 2019 Feb 6.

III. Medizinische Klinik und Poliklinik, Universitaetsklinikum Hamburg-Eppendorf, Germany.

In recent years, the cytokine IL-22 attracted considerable attention due to its important immunoregulatory function in barrier tissues, such as the gut, lung and skin. While a regenerative role of IL-22 in renal tubular damage has been demonstrated, the role of IL-22 in the immunopathogenesis of glomerular injury is still unknown. Here, we demonstrate that the IL-22 receptor is expressed in the glomerular compartment of the kidney and that IL-22 expression increases in the renal cortex after induction of glomerular injury in a mouse model for crescentic glomerulonephritis (cGN, nephrotoxic nephritis). Read More

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http://dx.doi.org/10.1152/ajprenal.00303.2018DOI Listing
February 2019
2 Reads

Dietary restriction of iron availability attenuates UPEC pathogenesis in a mouse model of urinary tract infection.

Am J Physiol Renal Physiol 2019 Feb 6. Epub 2019 Feb 6.

Obstetrics and Gynecology, Washington University School of Medicine, United States.

Iron is a critical nutrient required by hosts and pathogens. Uropathogenic Escherichia coli (UPEC), the principal causative agent of urinary tract infections (UTIs), chelate iron for their survival and persistence. Here, we demonstrate that dietary modulation of iron availability limits UPEC burden in a mouse model of UTI. Read More

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http://dx.doi.org/10.1152/ajprenal.00133.2018DOI Listing
February 2019
2 Reads

Renal Sodium Excretion Consequent to Pharmacogenetic Activation of Gq-DREADD in Principal Cells.

Am J Physiol Renal Physiol 2019 Feb 6. Epub 2019 Feb 6.

Physiology, University of Texas Health Science Center at San Antonio, United States.

Stimulation of Gq-coupled metabotropic P2Y receptors decrease the activity of ENaC in renal principal cells of the distal nephron. The physiological consequences of disrupting P2Y receptor signaling in the P2Y receptor knockout mouse are decreased sodium excretion and increased arterial blood pressure. However, because of the global nature of this knockout model, the quantitative contribution of ENaC and the distal nephron versus that of upstream renal vascular and tubular elements to changes in urinary excretion and arterial blood pressure are obscure. Read More

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http://dx.doi.org/10.1152/ajprenal.00612.2018DOI Listing
February 2019

Lipoprotein lipase in mouse kidney: effects of nutritional status and high-fat diet.

Am J Physiol Renal Physiol 2019 Jan 30. Epub 2019 Jan 30.

Medical Biosciences, Umea university, Sweden.

Activity of lipoprotein lipase (LPL) is high in mouse kidney, but the reason is poorly understood. The aim was to characterize localization, regulation and function of LPL in kidney of C57BL/6J mice. We found LPL mainly in proximal tubules, localized inside the tubular epithelial cells, under all conditions studied. Read More

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http://dx.doi.org/10.1152/ajprenal.00474.2018DOI Listing
January 2019

Estrogen-Related Receptor α Mediates Puromycin Aminonucleoside-induced Mesangial Cell apoptosis and Inflammatory Injury.

Am J Physiol Renal Physiol 2019 Jan 30. Epub 2019 Jan 30.

Pediatrics, Nanjing Medical University, China.

Glomerular diseases are the leading causes of chronic kidney disease and mesangial cells (MCs) were demonstrated to be involved in the pathogenesis. Puromycin aminonucleoside (PAN) is a nephrotoxic drug that induced glomerular injury with elusive mechanisms. The present study is undertaken to investigate the role of PAN in MC apoptosis, as well as the underlying mechanism. Read More

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http://dx.doi.org/10.1152/ajprenal.00507.2018DOI Listing
January 2019
1 Read

ACUTE KIDNEY INJURY INDUCES DRAMATIC P21 UP-REGULATION VIA A NOVEL, GLUCOCORTICOID- ACTIVATED, P53 INDEPENDENT, PATHWAY.

Am J Physiol Renal Physiol 2019 Jan 30. Epub 2019 Jan 30.

Clinical division, Fred Hutchinson Cancer Research Center.

P21, a cyclin kinase inhibitor, is acutely up-regulated during AKI and exerts cytoprotective effects. A proposed mechanism is oxidant stress- induced activation of p53, the dominant p21 transcription factor. Glycerol-induced rhabdomyolysis induces profound renal oxidant stress. Read More

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http://dx.doi.org/10.1152/ajprenal.00571.2018DOI Listing
January 2019

LPS REMOVAL REDUCES CD80-MEDIATED ALBUMINURIA IN CRITICALLY ILL PATIENTS WITH GRAM-NEGATIVE SEPSIS.

Am J Physiol Renal Physiol 2019 Jan 23. Epub 2019 Jan 23.

Dept. of Medical and Surgical Sciences, University of Foggia, Italy.

LPS-induced sepsis is a leading cause of acute kidney injury (AKI) in critically ill patients. LPS may induce CD80 expression in podocytes with subsequent onset of proteinuria, a risk factor for progressive chronic kidney disease (CKD) frequently observed after AKI. This study aimed to investigate the therapeutic efficacy of LPS removal in decreasing albuminuria through the reduction of podocyte CD80 expression. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00491.2018
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http://dx.doi.org/10.1152/ajprenal.00491.2018DOI Listing
January 2019
1 Read

Protease-activated receptor 2 exacerbates cisplatin-induced nephrotoxicity.

Am J Physiol Renal Physiol 2019 Jan 23. Epub 2019 Jan 23.

Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of Pharmaceutical Sciences and Faculty of Pharmaceutical Sciences, Japan.

Acute kidney injury (AKI) is associated with hypercoagulability. Tissue factor/factor VIIa complex and factor Xa in the coagulation cascade activate protease-activated receptor 2 (PAR2). Previously, we have shown that PAR2-mediated inflammation aggravates kidney injury in models of diabetic kidney disease and adenine-induced renal fibrosis. Read More

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http://dx.doi.org/10.1152/ajprenal.00489.2018DOI Listing
January 2019

Sympathetic Afferents in the Hypogastric Nerve Facilitate Nociceptive Bladder Activity in Cats.

Am J Physiol Renal Physiol 2019 Jan 23. Epub 2019 Jan 23.

Department of Urology, University of Pittsburgh, United States.

This study in α-chloralose anesthetized cats revealed a role of hypogastric nerve afferent axons in nociceptive bladder activity induced by bladder irritation using 0.25% acetic acid (AA). In cats with intact hypogastric and pelvic nerves, AA irritation significantly (p<0. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00522.2018
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http://dx.doi.org/10.1152/ajprenal.00522.2018DOI Listing
January 2019
5 Reads

Zinc Deficiency Induces Hypertension by Promoting Renal Sodium Reabsorption.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Medicine, Division of Nephrology, Emory University, United States.

Zn deficiency (ZnD) is a common comorbidity of many chronic diseases. In these settings, ZnD exacerbates hypertension. Whether ZnD alone is sufficient to alter blood pressure (BP) is unknown. Read More

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http://dx.doi.org/10.1152/ajprenal.00487.2018DOI Listing
January 2019
1 Read

Inhibition of 5-Lipoxygenase Decreases Renal Fibrosis and Progression of Chronic Kidney Disease.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Medicine, University of Colorado, United States.

In inflammatory diseases, the 5-lipoxygenase (5-LO) pathway contributes to epithelial damage and fibrosis by catalyzing the production of leukotrienes. Antagonists of the 5-LO pathway are currently approved for use in patients and are well tolerated. We found that expression of 5-LO is strongly induced in three models of chronic kidney disease, unilateral ureteral obstruction (UUO), folate nephropathy, and an orthologous mouse model of polycystic kidney disease. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00262.2018
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http://dx.doi.org/10.1152/ajprenal.00262.2018DOI Listing
January 2019
9 Reads

Blockade of ERK1/2 by U0126 alleviates uric acid induced EMT and tubular cell injury in the rats with hyperuricemic nephropathy.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Nephrology, Shanghai East Hospital, Tongji University School of Medicine, China.

Extracellular signal-regulated kinases 1 and 2 (ERK1/2) are serine/threonine kinases and function as regulators of cellular proliferation and differentiation. Recently, we demonstrated that inhibition of ERK1/2 alleviates the development and progression of hyperuricemia nephropathy (HN). However, its potential roles in uric acid-induced tubular epithelial-mesenchymal transition (EMT) and tubular epithelial cell injury are unknown. Read More

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http://dx.doi.org/10.1152/ajprenal.00480.2018DOI Listing
January 2019
2 Reads

The role of regulatory T cells in Experimental Autoimmune Glomerulonephritis.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Institute of Immunology, University Medical Center Hamburg-Eppendorf, Germany.

Anti-glomerular basement membrane (anti-GBM) disease is characterized by antibodies and T cells directed against the Goodpasture antigen α3(IV)NC1 of the GBM. Consequences are the deposition of autoantibodies along the GBM and the development of crescentic glomerulonephritis (GN) with rapid loss of renal function. Foxp3 regulatory T cells (Treg cells) are crucial for the maintenance of peripheral tolerance to self-antigens and the prevention of immunopathology. Read More

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http://dx.doi.org/10.1152/ajprenal.00558.2018DOI Listing
January 2019
2 Reads

Renal Cortical Oxygen Tension is Decreased Following Exposure to Long-term but not Short-term Intermittent Hypoxia in the Rat.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Physiology, University College Cork, Ireland.

Chronic kidney disease (CKD) occurs in more than 50% of patients with obstructive sleep apnea (OSA). However, the impact of intermittent hypoxia (IH) on renal function and oxygen homeostasis is unclear. Male Sprague Dawley rats were exposed to IH (270 secs at 21% O; 90 secs hypoxia, 6. Read More

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http://dx.doi.org/10.1152/ajprenal.00254.2018DOI Listing
January 2019
3 Reads

Multiparametric assessment of renal physiology in healthy volunteers using non-invasive magnetic resonance imaging.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Department of Radiology, Uppsala University, Sweden.

Non-invasive methods of magnetic resonance imaging (MRI) can quantify parameters of kidney function. The main purpose of this study was to determine baseline values of such parameters in healthy volunteers. In 28 healthy volunteers (15 females, 13 males), Arterial Spin Labeling (ASL) to estimate regional renal perfusion, Blood Oxygen Level Dependent (BOLD) transverse relaxation rate (R*) to estimate oxygenation, and Apparent Diffusion Coefficient (ADC), true diffusion (D) and longitudinal relaxation time (T) to estimate tissue properties were determined bilaterally in the cortex, outer and inner medulla. Read More

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http://dx.doi.org/10.1152/ajprenal.00486.2018DOI Listing
January 2019
1 Read

Bladder urothelial BK channel activity is a critical mediator for innate immune response in urinary tract infection pathogenesis.

Am J Physiol Renal Physiol 2019 Jan 16. Epub 2019 Jan 16.

Department of Urology, Yale University, United States.

The open probability of calcium activated voltage gated potassium channel (BK channel) on bladder umbrella urothelial cells is increased by lipopolysaccharide (LPS). It is hypothesized that this channel's activity is important in the urothelial innate immune response during urinary tract infection (UTI). We performed in vivo studies using female C57BL/6 mice whose bladders were inoculated with lipopolysaccharide (150 μl of 1 mg/mL LPS) or uropathogenic E. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00554.2018
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January 2019
6 Reads

CORRIGENDUM.

Authors:

Am J Physiol Renal Physiol 2019 Jan;316(1):F219

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http://dx.doi.org/10.1152/ajprenal.zh2-8690-corr.2018DOI Listing
January 2019
1 Read

Kir4.1/5.1 in the DCT plays a role in the regulation of renal K excretion.

Am J Physiol Renal Physiol 2019 Jan 9. Epub 2019 Jan 9.

Dept of Pharmacology, New York Medical College, United States.

The aim of this mini review is to provide an overview regarding the role of inwardly-rectifying potassium channel 4.1 (Kir4.1)/Kir5. Read More

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http://dx.doi.org/10.1152/ajprenal.00412.2018DOI Listing
January 2019
2 Reads

Uropathogenic Escherichia coli-Induced Fibrosis, leading to Lower Urinary Tract Symptoms, is associated with Type-2 cytokine signaling.

Am J Physiol Renal Physiol 2019 Jan 9. Epub 2019 Jan 9.

Urology, Northwestern University, United States.

Chronic inflammation and prostate fibrosis have been identified as contributors to lower urinary tract symptoms, LUTS, pathophysiology in humans. It has been shown that transurethral infection of an Escherichia coli strain named CP1, which was isolated from a patient with chronic prostatitis, can lead to the develop of differential chronic inflammation and pain in certain mouse strains. Therefore, we hypothesized that differential inflammation would influence fibrotic response in the prostate. Read More

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http://dx.doi.org/10.1152/ajprenal.00222.2018DOI Listing
January 2019
1 Read

Adenine acts in the kidney as a signaling factor and causes salt- and water-losing nephropathy: Early mechanism of adenine-induced renal injury.

Am J Physiol Renal Physiol 2019 Jan 9. Epub 2019 Jan 9.

Internal Medicine, University of Cincinnati, United States.

Chronic adenine feeding is extensively used to develop animal models of chronic renal failure with metabolic features resembling those observed in humans. However, the mechanism by which adenine induces renal failure is poorly understood. In this study, we examined the early effects of adenine on water metabolism and salt balance in rats placed in metabolic cages and fed control or adenine-containing diets for 7 days. Read More

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http://dx.doi.org/10.1152/ajprenal.00142.2018DOI Listing
January 2019
1 Read

TGF-β1 modifies histone acetylation and acetyl-coenzyme A metabolism in renal myofibroblasts.

Am J Physiol Renal Physiol 2019 Jan 9. Epub 2019 Jan 9.

Nephrology, Royal Melbourne Hospital, Australia.

Histone acetylation is an important modulator of gene expression in fibrosis. This study examined the effect of the pre-eminent fibrogenic cytokine TGF-b1 on histone 3 (H3) acetylation and its regulatory kinetics in renal myofibroblasts. Fibroblasts propagated from rat kidneys after ureteric obstruction were treated with recombinant TGF-b1 or vehicle for 48 hours. Read More

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http://dx.doi.org/10.1152/ajprenal.00513.2018DOI Listing
January 2019
1 Read

Identification of NFAT5 as a transcriptional regulator of the EDN1 gene in collecting duct.

Am J Physiol Renal Physiol 2019 Mar 9;316(3):F481-F487. Epub 2019 Jan 9.

Division of Nephrology, University of Utah Health Sciences Center , Salt Lake City, Utah.

The inner medullary collecting duct (IMCD) produces very high levels of endothelin-1 (ET-1) that acts as an autocrine inhibitor of IMCD Na and water reabsorption. Recent studies suggest that IMCD ET-1 production is enhanced by extracellular hypertonicity as can occur during high salt intake. Although NFAT5 has been implicated in the IMCD ET-1 hypertonicity response, no studies in any cell type have identified NFAT5 as a transcriptional regulator of the EDN1 gene; the current study examined this using a mouse IMCD cell line (IMCD3). Read More

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http://dx.doi.org/10.1152/ajprenal.00509.2018DOI Listing
March 2019
1 Read

Iron handling by the human kidney: Glomerular filtration and tubular reabsorption both contribute to urinary iron excretion.

Am J Physiol Renal Physiol 2019 Jan 9. Epub 2019 Jan 9.

laboratory medicine, Radboudumc.

Background: In physiological conditions, circulating iron can be filtered by the glomerulus and is almost completely reabsorbed by the tubular epithelium to prevent urinary iron wasting. Increased urinary iron concentrations have been associated with renal injury. However, it is not clear whether increased urinary iron concentrations in patients are the result of increased glomerular iron filtration and/or insufficient tubular iron reabsorption and if these processes contribute to renal injury. Read More

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http://dx.doi.org/10.1152/ajprenal.00425.2018DOI Listing
January 2019
1 Read

Heterozygous Pkhd1 mice develop cystic liver disease and proximal tubule ectasia that mimics radiographic signs of medullary sponge kidney.

Am J Physiol Renal Physiol 2019 Mar 2;316(3):F463-F472. Epub 2019 Jan 2.

Department of Medicine, The University of Alabama at Birmingham , Birmingham, Alabama.

Heterozygosity for human polycystic kidney and hepatic disease 1 ( PKHD1) mutations was recently associated with cystic liver disease and radiographic findings resembling medullary sponge kidney (MSK). However, the relevance of these associations has been tempered by a lack of cystic liver or renal disease in heterozygous mice carrying Pkhd1 gene trap or exon deletions. To determine whether heterozygosity for a smaller Pkhd1 defect can trigger cystic renal disease in mice, we generated and characterized mice with the predicted truncating Pkhd1 mutation in a region corresponding to the middle of exon 20 cluster of five truncating human mutations (between PKHD1 and PKHD1). Read More

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http://dx.doi.org/10.1152/ajprenal.00181.2018DOI Listing
March 2019
3 Reads

Dietary oxalate and kidney stone formation.

Am J Physiol Renal Physiol 2019 Mar 19;316(3):F409-F413. Epub 2018 Dec 19.

Department of Urology, University of Alabama at Birmingham , Birmingham, Alabama.

Dietary oxalate is plant-derived and may be a component of vegetables, nuts, fruits, and grains. In normal individuals, approximately half of urinary oxalate is derived from the diet and half from endogenous synthesis. The amount of oxalate excreted in urine plays an important role in calcium oxalate stone formation. Read More

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http://dx.doi.org/10.1152/ajprenal.00373.2018DOI Listing
March 2019
2 Reads

G-protein coupled receptor 37L1 regulates renal sodium transport and blood pressure.

Am J Physiol Renal Physiol 2018 Dec 19. Epub 2018 Dec 19.

Medicine, The George Washington University, United States.

GPCRs in the kidney regulate the reabsorption of essential nutrients, ions, and water from the glomerular filtrate. Abnormalities in renal epithelial ion transport play important roles in the pathogenesis of essential hypertension. The orphan G protein-coupled receptor 37L1 (GPR37L1), also known as ETBR-LP2, is expressed in several regions in the brain, but its expression profile and function in peripheral tissues are poorly understood. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00289.2018
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http://dx.doi.org/10.1152/ajprenal.00289.2018DOI Listing
December 2018
3 Reads

Truncating PKHD1 and PKD2 mutations alter energy metabolism.

Am J Physiol Renal Physiol 2019 Mar 19;316(3):F414-F425. Epub 2018 Dec 19.

Department of Medicine, University of Alabama at Birmingham , Birmingham, Alabama.

Deficiency in polycystin 1 triggers specific changes in energy metabolism. To determine whether defects in other human cystoproteins have similar effects, we studied extracellular acidification and glucose metabolism in human embryonic kidney (HEK-293) cell lines with polycystic kidney and hepatic disease 1 ( PKHD1) and polycystic kidney disease (PKD) 2 ( PKD2) truncating defects along multiple sites of truncating mutations found in patients with autosomal recessive and dominant PKDs. While neither the PKHD1 or PKD2 gene mutations nor their position enhanced cell proliferation rate in our cell line models, truncating mutations in these genes progressively increased overall extracellular acidification over time ( P < 0. Read More

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http://dx.doi.org/10.1152/ajprenal.00167.2018DOI Listing
March 2019
3 Reads

Blockade of Enhancer of Zeste Homolog 2 alleviates renal injury associated with hyperuricemia.

Am J Physiol Renal Physiol 2018 Dec 19. Epub 2018 Dec 19.

Nephrology, Shanghai East Hospital, Tongji University School of Medicine, China.

Hyperuricemia has been identified as an independent risk factor for chronic kidney disease (CKD) and is associated with the progression of kidney diseases. It remains unknown whether enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, can regulate metabolism of serum uric acid and progression of renal injury induced by hyperuricemia. In this study, we demonstrated that blockade of EZH2 with 3-DZNeP, a selective EZH2 inhibitor, or silencing of EZH2 with siRNA inhibited uric acid-induced renal fibroblast activation and phosphorylation of Smad3, epidermal growth factor receptor (EGFR) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in cultured renal fibroblasts. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00234.2018
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http://dx.doi.org/10.1152/ajprenal.00234.2018DOI Listing
December 2018
8 Reads

Peroxidasin and eosinophil peroxidase, but not myeloperoxidase, contribute to renal fibrosis in the murine unilateral ureteral obstruction model.

Am J Physiol Renal Physiol 2019 Feb 19;316(2):F360-F371. Epub 2018 Dec 19.

Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.

Renal fibrosis is the pathological hallmark of chronic kidney disease (CKD) and manifests as glomerulosclerosis and tubulointerstitial fibrosis. Reactive oxygen species contribute significantly to renal inflammation and fibrosis, but most research has focused on superoxide and hydrogen peroxide (HO). The animal heme peroxidases myeloperoxidase (MPO), eosinophil peroxidase (EPX), and peroxidasin (PXDN) uniquely metabolize HO into highly reactive and destructive hypohalous acids, such as hypobromous and hypochlorous acid. Read More

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http://dx.doi.org/10.1152/ajprenal.00291.2018DOI Listing
February 2019
3 Reads

Fructose reabsorption by rat proximal tubules: role of Na-linked cotransporters and the effect of dietary fructose.

Am J Physiol Renal Physiol 2019 Mar 19;316(3):F473-F480. Epub 2018 Dec 19.

Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University , Cleveland, Ohio.

Fructose consumption has increased because of widespread use of high-fructose corn syrup by the food industry. Renal proximal tubules are thought to reabsorb fructose. However, fructose reabsorption (J) by proximal tubules has not yet been directly demonstrated, nor the effects of dietary fructose on J. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00247.2018
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http://dx.doi.org/10.1152/ajprenal.00247.2018DOI Listing
March 2019
9 Reads

Recent advances in sex differences in kidney function.

Am J Physiol Renal Physiol 2019 Feb 19;316(2):F328-F331. Epub 2018 Dec 19.

Department of Physiology, Augusta University , Augusta, Georgia.

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http://dx.doi.org/10.1152/ajprenal.00584.2018DOI Listing
February 2019
1 Read

Reply to Wolf: Osmotically inactive sodium and potassium storage.

Am J Physiol Renal Physiol 2018 Dec;315(6):F1881-F1884

David Geffen School of Medicine at UCLA , Los Angeles, California.

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http://dx.doi.org/10.1152/ajprenal.00093.2018DOI Listing
December 2018
1 Read

CORRIGENDUM.

Authors:

Am J Physiol Renal Physiol 2018 Dec;315(6):F1885

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http://dx.doi.org/10.1152/ajprenal.zh2-8688-corr.2018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6336990PMC
December 2018
1 Read

Prohibitin 2-mediated mitophagy attenuates renal tubular epithelial cells injury by regulating mitochondrial dysfunction and NLRP3 inflammasome activation.

Am J Physiol Renal Physiol 2019 Feb 12;316(2):F396-F407. Epub 2018 Dec 12.

Division of Nephrology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University , Shanghai , China.

Accumulating evidence demonstrates that mitochondrial dysfunction and inflammasome activation play a critical role in the pathogenesis of renal tubular injury through the production of reactive oxygen species and cytokines. Prohibitin 2 (PHB2) is a newly identified intracellular receptor of mitophagy (a type of autophagy) that mediates selective removal of damaged mitochondria, and it could possibly play a renoprotective role in kidney disease. In this study, we confirmed that autophagy is activated in tubular epithelial cells treated with angiotensin II and that inhibition of autophagy results in tubular cell injury. Read More

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http://dx.doi.org/10.1152/ajprenal.00420.2018DOI Listing
February 2019
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Lack of urea transporters, UT-A1 and UT-A3, increases nitric oxide accumulation to dampen medullary sodium reabsorption through ENaC.

Am J Physiol Renal Physiol 2018 Dec 12. Epub 2018 Dec 12.

Department of Physiology, Emory University School of Medicine, United States.

While the role of urea in urine concentration is known, the effect of urea handling by the urea transporters, UT-A1 and UT-A3, on sodium balance remains elusive. Serum and urinary sodium concentration is similar between wild-type mice (WT) and UT-A3 null (UT-A3 KO) mice; however, mice lacking both UT-A1 and UT-A3 (UT-A1/A3 KO) have significantly lower serum sodium and higher urinary sodium. Protein expression of renal sodium transporters is unchanged among all three genotypes. Read More

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http://dx.doi.org/10.1152/ajprenal.00166.2018DOI Listing
December 2018
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Periostin induces kidney fibrosis after acute kidney injury via the p38 MAPK pathway.

Am J Physiol Renal Physiol 2019 Mar 12;316(3):F426-F437. Epub 2018 Dec 12.

Department of Internal Medicine, Seoul National University Boramae Medical Center , Seoul , Korea.

Periostin plays a crucial role in fibrosis, and acute kidney injury results in a high risk of progression to chronic kidney disease. Therefore, we hypothesized that periostin was involved in the progression of acute kidney injury to kidney fibrosis. Unilateral ischemia-reperfusion injury (UIRI) was induced in 7- to 8-wk-old male wild-type and periostin-null mice, and the animals were observed for 6 wk. Read More

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http://dx.doi.org/10.1152/ajprenal.00203.2018DOI Listing
March 2019
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Nudel involvement in the high-glucose-induced epithelial-mesenchymal transition of tubular epithelial cells.

Am J Physiol Renal Physiol 2019 Jan 12;316(1):F186-F194. Epub 2018 Dec 12.

Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province , Shijiazhuang, Hebei , China.

Nudel is a newly discovered factor related to cell migration. The tubular epithelial-mesenchymal transition (EMT) includes four steps: the loss of the adhesive properties of epithelial cells, the acquisition of a mesenchymal cell phenotype, the destruction of the tubular basal membrane, and the migration into the renal interstitium. The purpose of this study was to investigate the role of Nudel in the high-glucose-induced EMT of tubular epithelial cells. Read More

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http://dx.doi.org/10.1152/ajprenal.00218.2018DOI Listing
January 2019
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Myo-inositol oxygenase accentuates renal tubular injury initiated by endoplasmic reticulum stress.

Am J Physiol Renal Physiol 2019 Feb 12;316(2):F301-F315. Epub 2018 Dec 12.

Departments of Pathology and Medicine, Northwestern University , Chicago, Illinois.

Besides oxidant stress, endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of various metabolic disorders affecting the kidney. These two forms of stresses are not mutually exclusive to each other and may operate by a feedback loop in worsening the cellular injury. To attest to this contention, studies were performed to assess whether in such a setting, there is worsening of tubulointerstitial injury. Read More

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http://dx.doi.org/10.1152/ajprenal.00534.2018DOI Listing
February 2019
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"I Don't Get No Respect" - The Role of Chloride in Acute Kidney Injury.

Am J Physiol Renal Physiol 2018 Dec 12. Epub 2018 Dec 12.

Department of Medicine, Icahn School of Medicine at Mount Sinai, United States.

Acute kidney injury (AKI) is a major public health problem that complicates 10-40% of hospital admissions. Importantly, AKI is independently associated with increased risk of progression to chronic kidney disease, end stage renal disease, cardiovascular events, and increased risk of in-hospital and long-term mortality. The chloride content of intravenous fluid has garnered much attention over the last decade, and its association with excess use and adverse outcomes including AKI. Read More

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http://dx.doi.org/10.1152/ajprenal.00130.2018DOI Listing
December 2018
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Impact of obesity as an independent risk factor for the development of renal injury: implications from rat models of obesity.

Am J Physiol Renal Physiol 2019 Feb 12;316(2):F316-F327. Epub 2018 Dec 12.

Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi.

Diabetes and hypertension are the major causes of chronic kidney disease (CKD). Epidemiological studies within the last few decades have revealed that obesity-associated renal disease is an emerging epidemic and that the increasing prevalence of obesity parallels the increased rate of CKD. This has led to the inclusion of obesity as an independent risk factor for CKD. Read More

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http://dx.doi.org/10.1152/ajprenal.00162.2018DOI Listing
February 2019
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Unraveling reno-protective effects of SGLT2 inhibition in human proximal tubular cells.

Am J Physiol Renal Physiol 2019 Mar 12;316(3):F449-F462. Epub 2018 Dec 12.

Department of Internal Medicine IV - Nephrology and Hypertension, Medical University Innsbruck , Innsbruck , Austria.

Large clinical trials demonstrated that SGLT2 inhibitors (SGLT2i) slow the progression of kidney function decline in type 2 diabetes. Because the underlying molecular mechanisms are largely unknown, we studied the effects of SGLT2i on gene expression in two human proximal tubular (PT) cell lines under normoglycemic conditions, utilizing two SGLT2i, namely empagliflocin and canagliflocin. Genome-wide expression analysis did not reveal substantial differences between these two SGLT2i. Read More

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http://dx.doi.org/10.1152/ajprenal.00431.2018DOI Listing
March 2019
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Cloning, function, and localization of human, canine, and Drosophila ZIP10 (SLC39A10), a Zn transporter.

Am J Physiol Renal Physiol 2019 Feb 6;316(2):F263-F273. Epub 2018 Dec 6.

Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science , Rochester, Minnesota.

Zinc (Zn) is the second most abundant trace element, but is considered a micronutrient, as it is a cofactor for many enzymes and transcription factors. Whereas Zn deficiency can cause cognitive immune or metabolic dysfunction and infertility, excess Zn is nephrotoxic. As for other ions and solutes, Zn is moved into and out of cells by specific membrane transporters: ZnT, Zip, and NRAMP/DMT proteins. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00573.2017
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http://dx.doi.org/10.1152/ajprenal.00573.2017DOI Listing
February 2019
9 Reads

Dynamic contrast-enhanced MRI promotes early detection of toxin-induced acute kidney injury.

Am J Physiol Renal Physiol 2019 Feb 5;316(2):F351-F359. Epub 2018 Dec 5.

Department of Medicine, Duke University Medical Center , Durham, North Carolina.

Acute kidney injury (AKI) is a common cause of morbidity and mortality in hospitalized patients. Nevertheless, there is limited ability to diagnose AKI in its earliest stages through the collection of structural and functional information. Magnetic resonance imaging (MRI) is increasingly being used to provide structural and functional data that characterize the injured kidney. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00416.2018
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http://dx.doi.org/10.1152/ajprenal.00416.2018DOI Listing
February 2019
5 Reads