6,125 results match your criteria American journal of physiology. Renal physiology[Journal]


Brown adipocytes and β3 stimulant-induced brown-like adipocytes contribute to prevention of renal crystal formation.

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Department of Nephro-Urology, Nagoya, Japan.

According to recent studies, kidney stones are associated with metabolic syndrome. We focused on brown adipocytes and β3 stimulant-induced brown-like adipocytes to investigate how these adipocytes influence kidney stone disease. For the interscapular brown adipose tissue (iBAT) removal experiment, mice were subjected to either iBAT removal or sham operation (X-BAT group or Sham group), and after 3 weeks, renal crystal deposition was induced by intra-abdominal injection of glyoxylate (GOX) for 6 days. Read More

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http://dx.doi.org/10.1152/ajprenal.00523.2018DOI Listing

AMPK-mediated activation of Akt protects renal tubular cells from stress-induced apoptosis and ameliorates ischemic AKI .

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Medicine / Nephroloy, University of Illinois, Chicago, United States.

We have reported that preconditioning renal tubular cells (RTCs) with A-769662 (a pharmacologic activator of AMPK) reduces apoptosis of RTCs induced by subsequent stress, and ameliorates the severity of ischemic AKI in mice. In this study we examined the role of the PI3K/Akt pathway in mediating these effects. To confirm that any observed novel effects of A-769662 are mediated specifically by AMPK, we developed knockdown ("KD") RTCs using shRNA. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00553.2018
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http://dx.doi.org/10.1152/ajprenal.00553.2018DOI Listing
April 2019
1 Read

Quantitative proteomic analysis of a genetically induced prostate inflammation mouse model via custom 4-plex DiLeu isobaric labeling.

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Department of Urology, Carbone Cancer Center, George M. O'Brien Center of Benign Urology, University of Wisconsin Madison, United States.

Inflammation is involved in many prostate pathologies including infection, benign prostatic hyperplasia (BPH), and prostate cancer (CaP). Preclinical models are critical to our understanding of disease mechanisms, yet few models are genetically tractable. Here we present a comparative quantitative proteomic analysis of urine from mice with and without prostate-specific inflammation induced by conditional prostate epithelial interleukin-1 beta (IL-1 beta) expression. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00387.2018
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http://dx.doi.org/10.1152/ajprenal.00387.2018DOI Listing
April 2019
1 Read

Functional effects of blocking VEGF/VEGFR2 signaling in the rat urinary bladder in acute and chronic CYP-induced cystitis.

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Neurological Sciences, University of Vermont, United States.

High expression of vascular endothelial growth factor (VEGF) is associated with immature angiogenesis within the urinary bladder wall and bladder afferent nerve sensitization leading to visceral hyperalgesia and pelvic pain. Research suggests a shift in VEGF alternative splice variant (VEGF-Aa, VEGF-Ab) expression with several pathologies (e.g. Read More

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http://dx.doi.org/10.1152/ajprenal.00083.2019DOI Listing

Gene Deletion of the Na-Glucose Cotransporter SGLT1Ameliorates Kidney Recovery in a Murine Model of Acute Kidney InjuryInduced by Ischemia-Reperfusion.

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Departments of Medicine and Pharmacology, University of California San Diego and the Veterans Administration San Diego Healthcare System, United States.

The renal Na-glucose cotransporter SGLT1 mediates glucose reabsorption in the late proximal tubule, a hypoxia-sensitive tubular segment that enters the outer medulla. Gene-deletion in mice () was used to determine the role of the cotransporter in acute kidney injury (AKI) induced by ischemia-reperfusion (IR), including the initial injury and the subsequent recovery phase. On day 1 and 16 after IR, absolute and fractional urinary glucose excretion remained greater in versus wild-type littermates (WT), consistent with a sustained contribution of SGLT1 to tubular glucose reabsorption in WT. Read More

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http://dx.doi.org/10.1152/ajprenal.00111.2019DOI Listing

Adenosine kinase inhibition protects against cisplatin-induced nephrotoxicity.

Am J Physiol Renal Physiol 2019 Apr 17. Epub 2019 Apr 17.

Department Of Nephrology, The First Affiliated Hospital of Nanjing Medical University.

Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage and inflammatory responses, are closely linked to cisplatin-induced nephrotoxicity. Adenosine, emerging as a key regulatory molecule, is mostly protective in the pathophysiology of inflammatory diseases. Previous study showed that some of the adenosine receptors led to renal protection against ischemia-reperfusion injury. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00385.2018
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http://dx.doi.org/10.1152/ajprenal.00385.2018DOI Listing
April 2019
1 Read

The Relationship between Maternal Global Nutrient Restriction during Pregnancy and Offspring Kidney Structure and Function:A Systematic Review of Animal studies.

Am J Physiol Renal Physiol 2019 Apr 10. Epub 2019 Apr 10.

School of Biomedical Sciences and Pharmacy, University of Newcastle, Australia.

Background: Maternal under-nutrition during pregnancy is prevalent across the globe, and the origins of many chronic diseases can be traced back to in utero conditions. This systematic review considers the current evidence in animal models regarding the relationship between maternal global nutrient restriction during pregnancy and offspring kidney structure and function.

Methods: CINAHL, Cochrane, EMBASE, MEDLINE and Scopus were searched to November 2017. Read More

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http://dx.doi.org/10.1152/ajprenal.00082.2019DOI Listing
April 2019
2 Reads

Apparently normal kidney development in mice with conditional disruption of ANGII-AT1 receptor genes in FoxD1 positive stroma cell precursors.

Am J Physiol Renal Physiol 2019 Apr 10. Epub 2019 Apr 10.

Institute of Physiology, University of Regensburg.

An intact renin-angiotensin-system involving ANGII-AT1 receptors is crucial for normal kidney development. It is still unclear in which cell types AT1 receptor signaling is required for normal kidney development, maturation and function. Since all kidney cells deriving from stroma progenitor cells express AT1 receptors and since stromal cells fundamentally influence nephrogenesis and tubular maturation, we investigated the relevance of AT1 receptors in stromal progenitors and their descendants for renal development and function. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00305.2018
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http://dx.doi.org/10.1152/ajprenal.00305.2018DOI Listing
April 2019
1 Read

Glycolysis inhibitors suppress renal interstitial fibrosis via divergent effects on fibroblasts and tubular cells.

Am J Physiol Renal Physiol 2019 Apr 10. Epub 2019 Apr 10.

Department of Nephrology, The Key Laboratory of Kidney Disease and Blood Purification of Hunan Province, Second Xiangya Hospital at Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, GA, USA.

Renal interstitial fibrosis is a common pathological feature of chronic kidney disease that may involve changes of metabolism in kidney cells. In this study, we first showed that blockade of glycolysis with either Dichloroacetate (DCA) or shikonin to target different glycolytic enzymes reduced renal fibrosis in the mouse model of unilateral ureteral obstruction (UUO). Both inhibitors evidently suppressed the induction of fibronectin and collagen I in obstructed kidneys with DCA also showed inhibitory effects on collagen IV and a-smooth muscle actin (a-SMA). Read More

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http://dx.doi.org/10.1152/ajprenal.00422.2018DOI Listing

MST3 (Mammalian Ste20 Kinase 3) is involved in ENaC-mediated hypertension.

Am J Physiol Renal Physiol 2019 Apr 10. Epub 2019 Apr 10.

school of pharmacy, China medical university, Taichung, Taiwan, Taiwan.

Liddle syndrome is an inherited form of human hypertension caused by increasing ENaC (epithelial sodium channel) expression. Increased Na retention through ENaC with subsequent volume expansion causes hypertension. In addition to ENaC, NKCC (Na-K-Cl cotransporter) and NCC (Na-Cl symporter) are responsible for Na reabsorption in the kidneys. Read More

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http://dx.doi.org/10.1152/ajprenal.00455.2018DOI Listing
April 2019
4 Reads

Cre/lox System: Cre-ating Unintended Damage.

Authors:
Leslie Gewin

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

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

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http://dx.doi.org/10.1152/ajprenal.00428.2018DOI Listing

The Role of GM-CSF in a Mouse Model of Experimental Autoimmune prostatitis.

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

Urology, Qilu Hospital of Shandong University, China.

The etiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is still unknown. Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to play an important role in the development of autoimmune and inflammatory diseases. Here, we investigated the expression and function of GM-CSF in CP/CPPS patients and in a mouse model of Experimental Autoimmune prostatitis (EAP). Read More

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http://dx.doi.org/10.1152/ajprenal.00013.2018DOI Listing
April 2019
2 Reads

Targeting STAT3 Signaling in Kidney Disease.

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

Medicine/Nephrology, Stony Brook University School of Medicine, United States.

The Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway is a multifaceted transduction system which regulates cellular responses to incoming signaling ligands. Signal transducer and activator of transcription 3 (STAT3) is a central member of the JAK/STAT signaling cascade and has long been recognized for its increased transcriptional activity in cancers and autoimmune disorders, but has only recently been in the spotlight for its role in the progression of kidney disease. While genetic knockout and manipulation studies have demonstrated the salutary benefits of inhibiting STAT3 activity in several kidney disease models, pharmacological inhibition has yet to make it to the clinical forefront. Read More

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http://dx.doi.org/10.1152/ajprenal.00034.2019DOI Listing

Loss of reticulocalbin 2 lowers blood pressure and restrains angiotensin II-induced hypertension in vivo.

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

Radiology, University of Virginia, United States.

Hypertension affects over one billion people worldwide and increases risk for heart failure, stroke and chronic kidney disease. Despite high prevalence and devastating impact, its etiology still remains poorly understood for most hypertensive cases. encoding reticulocalbin 2, is a candidate gene for atherosclerosis we previously demonstrated in mice. Read More

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http://dx.doi.org/10.1152/ajprenal.00567.2018DOI Listing
April 2019
3 Reads

Genetic Disruption of Npr1 Depletes T Regulatory Cells and Provokes High Levels of Proinflammatory Cytokines and Fibrosis in the Kidneys of Female Mutant Mice.

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

Department of Physiology SL39, Tulane University Health Sciences Center, United States.

The present study was designed to determine the effects of gene-knockout of guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) on immunogenic responses affecting kidney function and blood pressure (BP) in Npr1 (coding for GC-A/NPRA) null mutant mice. We used female Npr1 gene-disrupted ( Npr1, 0-copy), heterozygous ( Npr1, 1-copy), wild-type ( Npr1, 2-copy) and gene-duplicated ( Npr1, 4-copy) mice. Expression levels of Toll-like receptor 2/4 (TLR2/TLR4) mRNA were increased 4- to 5-fold in 1-copy mice and 6- to 10-fold in 0-copy mice; protein levels were increased 2. Read More

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http://dx.doi.org/10.1152/ajprenal.00621.2018DOI Listing

Peptidyl arginine deiminase-4 exacerbates ischemic AKI by finding NEMO (NFκB Essential Modulator).

Am J Physiol Renal Physiol 2019 Apr 3. Epub 2019 Apr 3.

Anesthesiology, Columbia University, United States.

Peptidyl arginine deiminase-4 (PAD4) catalyzes the conversion of peptidylarginine residues to peptidylcitrulline. We previously showed that kidney ischemia and reperfusion (IR) injury increases renal proximal tubular PAD4 expression and activity. Furthermore, kidney PAD4 plays a critical role in ischemic acute kidney injury (AKI) injury by promoting renal tubular inflammation, neutrophil infiltration and NFκB activation. Read More

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http://dx.doi.org/10.1152/ajprenal.00089.2019DOI Listing
April 2019
1 Read

Heritability and individuality of the plasma sodium concentration: a twin study in the US Veteran population.

Am J Physiol Renal Physiol 2019 Mar 25. Epub 2019 Mar 25.

Division of Nephrology & Hypertension, Department of Medicine, Oregon Health & Science University and the VA Portland Health Care System, United States.

Little is known about the population genetics of water balance. A recent meta-GWAS on plasma sodium concentration identified novel loci of high biological plausibility, yet heritability was never convincingly shown in European ancestry. The present analysis linked the Vietnam Era Twin Registry with the Department of Veterans Affairs VistA database. Read More

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http://dx.doi.org/10.1152/ajprenal.00581.2018DOI Listing
March 2019
1 Read

Functional changes in low and high threshold afferents in obstruction-induced bladder overactivity.

Am J Physiol Renal Physiol 2019 Mar 25. Epub 2019 Mar 25.

Departmente of Human Physiology and Centre for Neuroscience, Flinders University.

Neural mechanisms of lower urinary tract symptoms in obstruction-induced bladder overactivity remain unclear. We made the first single unit recordings from the different type of spinal afferents to determine the effects of bladder outlet obstruction in guinea pigs. A model of gradual bladder outlet obstruction in male guinea pigs was used to produce overactive bladder. Read More

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http://dx.doi.org/10.1152/ajprenal.00058.2019DOI Listing
March 2019
1 Read

Elevated Serum Anion Gap in Adults with Moderate Chronic Kidney Disease Increases Risk for Progression to End Stage Renal Disease.

Am J Physiol Renal Physiol 2019 Mar 25. Epub 2019 Mar 25.

Medicine, University of California, San Francisco, United States.

Background: Acid retention associated with reduced GFR exacerbates nephropathy progression in partial nephrectomy models of CKD and might be reflected in CKD patients with reduced eGFR by increased anion gap (AG).

Methods: We explored the presence of AG and its association with CKD in 14,924 adults, aged ≥20 years and eGFR≥15ml/min/1.73m, enrolled in the National Health and Nutrition Examination Survey III, 1988-1994 using multivariable regression analysis. Read More

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http://dx.doi.org/10.1152/ajprenal.00496.2018DOI Listing
March 2019
1 Read

Expansion of regulatory T cells using low-dose interleukin-2 attenuates hypertension in an experimental model of systemic lupus erythematos.

Am J Physiol Renal Physiol 2019 Mar 20. Epub 2019 Mar 20.

Physiology & Biophysics, University of Mississippi Medical Center, United States.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder that is characterized by prevalent hypertension, renal injury, and cardiovascular disease. Numerous studies report a low prevalence and/or impaired function of regulatory T cells (T) in both patients with SLE and murine models of the disease. Evidence suggests that T dysfunction in SLE results from a deficiency in interleukin (IL)-2. Read More

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http://dx.doi.org/10.1152/ajprenal.00616.2018DOI Listing
March 2019
1 Read

BIOPOLYMER-DELIVERED VASCULAR ENDOTHELIAL GROWTH FACTOR IMPROVES RENAL OUTCOMES FOLLOWING REVASCULARIZATION.

Am J Physiol Renal Physiol 2019 Mar 20. Epub 2019 Mar 20.

Physiology and Biophysics, Medicine, and Radiology, University of Mississippi Medical Center, United States.

Renal angioplasty and stenting (PTRAs) resolves renal artery stenosis, but inconsistently improves renal function, possibly due to persistent parenchymal damage. We developed a bioengineered fusion of a drug delivery vector (elastin-like polypeptide, ELP) with vascular endothelial growth factor (VEGF), and showed its therapeutic efficacy. We tested the hypothesis that combined ELP-VEGF therapy with PTRAs improves renal recovery more efficiently than PTRAs alone by protecting the stenotic renal parenchyma. Read More

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http://dx.doi.org/10.1152/ajprenal.00607.2018DOI Listing
March 2019
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Plasma MicroRNA Profile is a Biomarker Associated with Urothelial Carcinoma in Chronic Hemodialysis Patients.

Am J Physiol Renal Physiol 2019 Mar 20. Epub 2019 Mar 20.

Department of Biomedical Sciences and Engineering, National Central University, Taiwan.

The incidence of UC is higher in chronic dialysis patients than in the general population. This study is to investigate the plasma miRNA profiling as the ancillary diagnosis biomarker associated with urothelial carcinoma in chronic hemodialysis patients. We have successfully screened out and detected miRNAs expressions from plasma in eight dialysis patients through quantitative real-time PCR array analysis and identified eight candidate miRNAs. Read More

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http://dx.doi.org/10.1152/ajprenal.00014.2019DOI Listing

The potential role of myosin motor proteins in mediating the subcellular distribution of NHE3 in the renal proximal tubule.

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

Heart Institute (InCor), University of São Paulo Medical School, Brazil.

Isoform 3 of the Na/H exchanger (NHE3) is responsible for the majority of the reabsorption of NaCl, NaHCO and, consequently, water in the renal proximal tubule. As such, this transporter plays an essential role in acid-base balance, extracellular fluid volume homeostasis and determining systemic arterial blood pressure levels. NHE3 activity is modulated by a number of mechanisms, including the redistribution of the transporter between the body of the microvilli (where NHE3 is active) and the base of the microvilli (where NHE3 is less active). Read More

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http://dx.doi.org/10.1152/ajprenal.00577.2018DOI Listing

Sustained, delayed and small increments in glomerular permeability to macromolecules during systemic endothelin-1 infusion mediated via the ET receptor.

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

Department of Nephrology, Lund University, Sweden.

Emerging evidence indicates that endogenous production of endothelin 1 (ET-1), a 21-amino-acid peptide vasoconstrictor, plays an important role in proteinuric kidney disease. Previous studies in rats have shown that chronic administration of ET-1 leads to increased glomerular albumin leakage. The underlying mechanisms are however currently not known. Read More

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http://dx.doi.org/10.1152/ajprenal.00040.2019DOI Listing
March 2019
1 Read

Vitamin D receptor activation protects against lipopolysaccharide-induced acute kidney injury through suppression of tubular cell apoptosis.

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

Medicine, The University of Chicago, United States.

Acute kidney injury (AKI) is a common complication of sepsis characterized by a rapid degradation of renal function. The effect of vitamin D on AKI remains poorly understood. Here we showed that vitamin D receptor (VDR) activation protects against lipopolysaccharide (LPS)-induced AKI by blocking renal tubular epithelial cell apoptosis. Read More

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http://dx.doi.org/10.1152/ajprenal.00332.2018DOI Listing
March 2019
2 Reads

Chronic Kidney Disease and the Gut Microbiome.

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

Internal Medicine, University of Arkansas for Medical Sciences, United States.

The gut microbiome is composed of a diverse population of bacteria which have beneficial and adverse effects on human health. The microbiome has recently gained attention and is increasingly noted to play a significant role in health and a number of disease states. Increasing urea concentration during chronic kidney disease (CKD) leads to alterations in the intestinal flora that can increase production of gut-derived toxins and alter the intestinal epithelial barrier. Read More

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http://dx.doi.org/10.1152/ajprenal.00298.2018DOI Listing
March 2019
1 Read

Urine Podoplanin Heralds the Onset of Ischemia-Reperfusion Injury of the Kidney.

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

Medicine, Brigham and Women's Hospital, United States.

Ischemia-reperfusion injury represents one of the most common causes of acute kidney injury, a serious and often deadly condition that affects up to 20% of all hospitalized patients in the United States. However, the current standard assay used universally for the diagnosis of acute kidney injury-serum creatinine-does not detect renal damage early in its course. Serendipitously, we found that the immunofluorescent signal of the constitutive podocyte marker podoplanin fades in the glomerulus and intensifies in the tubulointerstitial compartment of the kidney, shortly following ischemia-reperfusion injury in 8-10 week-old male C57Bl/6j mice. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00538.2018
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http://dx.doi.org/10.1152/ajprenal.00538.2018DOI Listing
March 2019
5 Reads

Prompt apoptotic response to high glucose in SGLT expressing renal cells.

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

Department of Women´s and Children´s Health, Karolinska Institutet, Sweden.

It is generally believed that cells that are unable to downregulate glucose transport are particularly vulnerable to hyperglycemia. Yet little is known about the relation between expression of glucose transporters and acute toxic effects of high glucose exposure.Here we have, in an ex vivo study on rat renal cells, compared the apoptotic response to a moderate increase in glucose concentration. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00615.2018
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http://dx.doi.org/10.1152/ajprenal.00615.2018DOI Listing
March 2019
6 Reads

Targeting a fibrotic bottleneck may provide an OPENING in the treatment of LUTS.

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

Urology, University of Wisconsin-Madison, United States.

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http://dx.doi.org/10.1152/ajprenal.00102.2019DOI Listing

Transcriptome-proteome integration of archival human renal cell carcinoma biopsies enable identification of molecular mechanisms.

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

Clinical Medicine, University of Bergen, Norway.

Renal cell cancer is among the most common forms of cancer in humans, with around 35,000 deaths attributed to kidney carcinoma in the European Union (EU) in 2012 alone. Clear cell renal cell carcinoma (ccRCC) represents the most common form of kidney cancer and the most lethal of all genitourinary cancers. Here we apply omics technologies to archival core biopsies to investigate the biology underlying ccRCC. Read More

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http://dx.doi.org/10.1152/ajprenal.00424.2018DOI Listing

Heart-kidney interactions: mechanistic insights from animal models.

Authors:
Shan Liu

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

School of Medicine, South China University of Technology, China.

Pathological changes in heart or kidney can instigate the release of a cascade of cardiorenal mediators that promote injury in the other organ. Combined dysfunction of heart and kidney is referred to as cardiorenal syndrome and gained considerable attention. Cardiorenal syndrome has been classified into 5 distinct entities, each with different major pathophysiological changes. Read More

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http://dx.doi.org/10.1152/ajprenal.00624.2017DOI Listing

Paracellular calcium transport in the proximal tubule and the formation of kidney stones.

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

Division of Nephrology and Hypertension and the Kidney Institute, University of Kansas Medical Center, United States.

The proximal tubule (PT) is responsible for the majority of calcium reabsorption by the kidney. Most PT calcium transport appears to be passive, although the molecular facilitators have not been well-established. Emerging evidence supports a major role for PT calcium transport in idiopathic hypercalciuria and the development of kidney stones. Read More

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http://dx.doi.org/10.1152/ajprenal.00519.2018DOI Listing
March 2019
2 Reads

TRPV4 deletion protects against hypokalemia during systemic K deficiency.

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

Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, United States.

Tight regulation of K balance is fundamental for normal physiology. Reduced dietary K intake, which is common in Western diets, often leads to hypokalemia and associated cardiovascular- and kidney-related pathologies. Distal nephron and specifically the collecting duct (CD) is the major site of controlled K reabsorption via H-K-ATPase in the state of dietary K deficiency. Read More

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http://dx.doi.org/10.1152/ajprenal.00043.2019DOI Listing
March 2019
2 Reads

Tubule-vascular feedback in renal autoregulation.

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

Hypertension and Vascular Research, Henry Ford Hospital, United States.

Afferent arteriole (Af-Art) diameter regulates pressure and flow into the glomerulus, which are the main determinants of the glomerular filtration rate (GFR). Thus, Af-Art resistance is crucial for sodium filtration. Af-Arts play a role as integrative centers, where systemic and local systems interact to determine the final degree of resistance. Read More

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http://dx.doi.org/10.1152/ajprenal.00381.2018DOI Listing

Loss of miR-17~92 results in dysregulation of Cftr in nephron progenitors.

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

Pediatrics, University of Pittsburgh, United States.

We have previously demonstrated that loss of miR-17~92 in nephron progenitors in a mouse modelresults in renal hypodysplasia and chronic kidney disease. Clinically, decreased congenital nephron endowment due to renal hypodysplasia is associated with an increased risk of hypertension and chronic kidney disease, and this is at least partly dependent on the self-renewal of nephron progenitors. Here, we present evidence for a novel molecular mechanism regulating the self-renewal of nephron progenitors and congenital nephron endowment by the highly conserved miR-17~92cluster. Read More

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http://dx.doi.org/10.1152/ajprenal.00450.2018DOI Listing
March 2019
2 Reads

Potassium Sparing Effects of Furosemide in Mice on High Potassium Diets.

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

Dept of Cellular and Integrative Physiology, University of Nebraska Medical Center, United States.

On a regular "Western" diet, furosemide induces a kaliuresis and reduction in plasma [K] by inhibiting Na reabsorption in the thick ascending limb of Henle's loop (TAL), enhancing the delivery of Na to the aldosterone sensitive distal nephron. In the aldosterone-sensitive distal nephron, the increased Na delivery stimulates K wasting and due to an exaggerated exchange of epithelial Na channel (ENaC)-mediated Na reabsorption for secreted K. The effects of furosemide are different in mice given a high K, alkaline diet (HK). Read More

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http://dx.doi.org/10.1152/ajprenal.00614.2018DOI Listing
March 2019
4 Reads

Calcium-sensing receptor activation attenuates collagen expression in renal proximal tubular epithelial cells.

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

Department of nephrology, Southeast University School of Medicine, China.

Experimental studies showed that pharmacological activation of calcium-sensing receptor (CaSR) attenuated renal fibrosis in some animal models beyond modification of bone and mineral homeostasis; however, its underlying mechanisms remain largely unknown. Since excessive collagen deposition is the key feature of fibrosis, the present study aimed to examine whether CaSR was involved in the regulation of collagen expression in rats with adenine diet (AD)-induced renal fibrosis and in profibrotic TGF-β1-treated renal proximal tubular epithelial cells (PTECs). The results showed that the CaSR agonist cinacalcet significantly attenuated renal collagen accumulation and tubular injury in AD rats. Read More

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http://dx.doi.org/10.1152/ajprenal.00413.2018DOI Listing
March 2019
1 Read

cGMP induces degradation of NKCC2 in the thick ascending limb via the ubiquitin-proteasomal system.

Authors:
Gustavo R Ares

Am J Physiol Renal Physiol 2019 May 27;316(5):F838-F846. Epub 2019 Feb 27.

Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital , Detroit, Michigan.

The thick ascending limb of Henle's loop (TAL) reabsorbs NaCl via the apical Na-K-2Cl cotransporter (NKCC2). NKCC2 activity is regulated by surface NKCC2 levels. The second messenger cGMP decreases NKCC2 activity by decreasing surface NKCC2 levels. Read More

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http://dx.doi.org/10.1152/ajprenal.00287.2018DOI Listing

Comparison of diabetic nephropathy between male and female eNOS db/db mice.

Am J Physiol Renal Physiol 2019 Feb 27. Epub 2019 Feb 27.

Department of Physiology and Anatomy, UNTHSC, United States.

Sex is an important biological variable that impacts diverse physiological and pathological processes, including progression of diabetic nephropathy. Diabetic nephropathy is one of the most common complications of diabetes mellitus and is the leading cause of end stage renal disease. eNOS db/db mouse is an appropriate and valuable model to study mechanisms in the development of diabetic nephropathy due to similarities of the features of diabetic kidney disease in this model to those in humans. Read More

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http://dx.doi.org/10.1152/ajprenal.00023.2019DOI Listing
February 2019
1 Read

A Dual Blocker of Endothelin A/B Receptors Mitigates Hypertension but not Renal Dysfunction in a Rat Model of Chronic Kidney Disease and Sleep Apnea.

Am J Physiol Renal Physiol 2019 Feb 27. Epub 2019 Feb 27.

Vascular Physiology Group, Cell Biology and Physiology, University of New Mexico School of Medicine, United States.

Obstructive sleep apnea (OSA) is characterized by recurrent episodes of pharyngeal collapse during sleep resulting in intermittent hypoxia (IH), and is associated with high incidence of hypertension and accelerated renal failure. In rodents, endothelin-1 (ET-1) contributes to IH-induced hypertension, and ET-1 levels inversely correlate with glomerular filtration rate (GFR) in end-stage chronic kidney disease (CKD) patients. Therefore, we hypothesized that a dual ET receptor antagonist, macitentan (Actelion Pharmaceuticals) will attenuate and reverse hypertension and renal dysfunction in a rat model of combined IH and CKD. Read More

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http://dx.doi.org/10.1152/ajprenal.00018.2019DOI Listing
February 2019
2 Reads

Podocyte-specific Expression of Cre Recombinase Promotes Glomerular Basement Membrane Thickening.

Am J Physiol Renal Physiol 2019 Feb 27. Epub 2019 Feb 27.

Medicine-Nephrology, University of Alabama at Birmingham, United States.

Conditional gene targeting using Cre recombinase has offered a powerful tool to modify gene function precisely in defined cells/tissues and at specific times. However, in mammalian cells, Cre recombinase can be genotoxic. The importance of including Cre-expressing control mice to avoid misinterpretation and to maximize the validity of the experimental results has been increasingly recognized. Read More

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http://dx.doi.org/10.1152/ajprenal.00359.2018DOI Listing
February 2019
2 Reads

Dynamic changes in histone deacetylases following kidney ischemia reperfusion injury are critical for promoting proximal tubule proliferation.

Am J Physiol Renal Physiol 2019 Feb 27. Epub 2019 Feb 27.

Medicine, University of Alabama at Birmingham, United States.

Deranged histone deacetylase (HDAC) activity causes uncontrolled proliferation, fibrosis, and organ damage. It is unclear whether deranged HDAC activity results in acute kidney injury in the renal hypoperfusion model of bilateral ischemia-reperfusion-injury (IRI) and if in vivo inhibition is an appropriate therapeutic approach to limit injury. Mice were implanted with i. Read More

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http://dx.doi.org/10.1152/ajprenal.00499.2018DOI Listing
February 2019
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The Effects of Aerobic Exercise on Vascular Function in Non-Dialysis Chronic Kidney Disease: A Randomized Controlled Trial.

Am J Physiol Renal Physiol 2019 Feb 27. Epub 2019 Feb 27.

Kinesiology & Applied Physiology, University of Delaware, United States.

Background: Endothelial dysfunction and arterial stiffness are non-traditional risk factors of chronic kidney disease (CKD) related cardiovascular disease (CVD) that could be targeted with exercise. This study investigated the effect of moderate-to-vigorous aerobic exercise on vascular function in non-dialysis CKD.

Methods: In this randomized, controlled trial 36 non-dialysis CKD patients (Mean±SEM; Age, 58±2years; eGFR, 44±2ml/min/1. Read More

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https://www.physiology.org/doi/10.1152/ajprenal.00539.2018
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http://dx.doi.org/10.1152/ajprenal.00539.2018DOI Listing
February 2019
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IPSE, a parasite-derived host immunomodulatory protein, is a potential therapeutic for hemorrhagic cystitis.

Am J Physiol Renal Physiol 2019 Feb 20. Epub 2019 Feb 20.

Children's National Medical Center, United States.

Chemotherapy-induced hemorrhagic cystitis is characterized by bladder pain and voiding dysfunction caused by hemorrhage and inflammation. Novel therapeutic options to treat hemorrhagic cystitis are needed. We previously reported that systemic administration of the Schistosomiasis haematobium-derived protein H-IPSE (IL-4-inducing principle from Schistosoma mansoni eggs), is superior to 3 doses of MESNA in alleviating hemorrhagic cystitis. Read More

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http://dx.doi.org/10.1152/ajprenal.00468.2018DOI Listing
February 2019
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Time dependent p53 inhibition determines senescence attenuation and long term outcome after renal ischemia/reperfusion.

Am J Physiol Renal Physiol 2019 Feb 20. Epub 2019 Feb 20.

Children's Hospital, Medical School Hannover, Germany.

Inhibition of p53 has been shown to be an efficient strategy for ameliorating kidney ischemia/reperfusion (I/R) injury in experimental models. The therapeutic value of p53 siRNA based inhibition for I/R in renal transplantation is currently evaluated in clinical studies. While the major rationale for these studies is the suppression of pro-apoptotic properties, there are more, equally important injury response pathways regulated by p53. Read More

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http://dx.doi.org/10.1152/ajprenal.00333.2018DOI Listing
February 2019

Physiological effects of altering oxygenation during kidney normothermic machine perfusion.

Am J Physiol Renal Physiol 2019 May 20;316(5):F823-F829. Epub 2019 Feb 20.

Department of Surgery, University of Cambridge, Addenbrooke's Hospital , Cambridge , United Kingdom.

Kidney normothermic machine perfusion (NMP) has historically used a 95% O-5% CO gas mixture. Using a porcine model of organ retrieval, NMP, and reperfusion, we tested the hypothesis that reducing perfusate oxygenation ( ) would be detrimental to renal function and cause injury. In the minimal ischemic injury experiment, kidneys sustained 10 min of warm ischemia and 2 h of static cold storage before 1 h of NMP with either 95%, 25%, or 12% O with 5% CO and N balance. Read More

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http://dx.doi.org/10.1152/ajprenal.00178.2018DOI Listing
May 2019
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Angiotensin II and salt-induced decompensation in Balb/CJ mice is aggravated by fluid retention related to low oxidative stress.

Am J Physiol Renal Physiol 2019 Feb 20. Epub 2019 Feb 20.

Department of medical cellbiology, Uppsala Universitet, Sweden.

Aim: Balb/CJ mice are more sensitive to treatment with Angiotensin II (AngII) and high salt (Salt) diet compared to C57BL/6J. Together with higher mortality, they develop edema, signs of heart failure and acute kidney injury. The aim of the present study was to identify differences in renal gene regulation that may affect kidney function and fluid balance, which could contribute to decompensation in Balb/CJ after AngII+Salt treatment. Read More

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http://dx.doi.org/10.1152/ajprenal.00483.2018DOI Listing
February 2019
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A Model of Uric Acid Transport in the Rat Proximal Tubule.

Am J Physiol Renal Physiol 2019 Feb 20. Epub 2019 Feb 20.

Dpt of Pharmacology and Toxicology, University of Lausanne, Switzerland.

The objective of this study was to investigate theoretically the mechanisms underlying uric acid transport in the proximal tubule (PT) of rat kidneys, and their modulation by factors including Na, parathyroid hormone (PTH), Angiotensin II, and SGLT2 inhibitors. To that end, we incorporated the transport of uric acid and its conjugate anion urate in our mathematical model of water and solute transport in the rat PT. The model accounts for parallel urate reabsorption and secretion pathways on apical and basolateral membranes, and their coupling to lactate and alpha-ketoglutarate transport. Read More

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http://dx.doi.org/10.1152/ajprenal.00603.2018DOI Listing
February 2019
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Arteriovenous conduits for hemodialysis: how to better modulate the pathophysiological vascular response to optimize vascular access durability.

Am J Physiol Renal Physiol 2019 May 20;316(5):F794-F806. Epub 2019 Feb 20.

Department of Medicine and Division of Nephrology, University of Alabama at Birmingham , Birmingham, Alabama.

Vascular access is the lifeline for patients on hemodialysis. Arteriovenous fistulas (AVFs) are the preferred vascular access, but AVF maturation failure remains a significant clinical problem. Currently, there are no effective therapies available to prevent or treat AVF maturation failure. Read More

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http://dx.doi.org/10.1152/ajprenal.00440.2018DOI Listing

Direct and indirect inhibition of the circadian clock protein Per1: effects on ENaC and blood pressure.

Am J Physiol Renal Physiol 2019 May 13;316(5):F807-F813. Epub 2019 Feb 13.

Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida , Gainesville, Florida.

Circadian rhythms govern physiological functions and are important for overall health. The molecular circadian clock comprises 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
May 2019
1 Read