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American Journal of Physiology. Renal Physiology

Aleksandra Novikov, Yiling Fu, Winnie Huang, Brent Freeman, Rohit Patel, Charlotte van Ginkel, Hermann Koepsell, Meinrad Busslinger, Akira Onishi, Josselin Nespoux, Volker Vallon
Inhibitors of the sodium-glucose cotransporter SGLT2 enhance urinary glucose and urate excretion and lower plasma urate levels. The mechanisms remain unclear, but a role for enhanced glucose in the tubular fluid has been proposed, which may interact with tubular urate transporters like GLUT9 or URAT1. Studies were performed in non-diabetic mice using the SGLT2 inhibitor canagliflozin and gene targeted mice lacking the urate transporter GLUT9 in the tubule or mice with whole body knockout of SGLT2, SGLT1, or URAT1...
November 14, 2018: American Journal of Physiology. Renal Physiology
Ryosuke Fujii, Jun Ueyama, Takuya Kanno, Koji Suzuki, Nobuyuki Hamajima, Kenji Wakai, Yukiharu Hasegawa, Takaaki Kondo
The redox state of human serum albumin (HSA) has attracted interest as a possible biomarker for oxidative stress (OS) in humans. Although previous studies on this topic have taken only clinical settings into consideration, evidence of its efficacy in nonclinical settings remains to be established. The present study aimed to examine and validate the relationship between HSA redox state and renal function in a rural Japanese population. We analyzed two independent datasets from health check-up programs conducted in 2013 and 2016: one for discovery (n = 267) and the other for replication (n = 367)...
November 14, 2018: American Journal of Physiology. Renal Physiology
Felix Knauf, Heino Velazquez, Victoria Pfann, Zhirong Jiang, Peter S Aronson
The apical membrane chloride-oxalate exchanger SLC26A6 has been demonstrated to play a role in proximal tubule NaCl transport based on studies in microperfused tubules. The present study is directed at characterizing the role of SLC26A6 in NaCl homeostasis in vivo under physiological conditions. Free-flow micropuncture studies revealed that volume and chloride absorption were similar in surface proximal tubules of wild-type and Slc26a6-/- mice. Moreover, the increments in urine flow rate and sodium excretion following thiazide and furosemide infusion were identical in wild-type and Slc26a6-/- mice, indicating no difference in NaCl delivery out of the proximal tubule...
November 14, 2018: American Journal of Physiology. Renal Physiology
Josephine Liwang, Joseph A Ruiz, Lauren M LaRocque, Fitra Rianto, Fuying Ma, Yanhua Wang
Hypertonicity increases water permeability, independently of vasopressin, in the inner medullary collecting duct (IMCD) by increasing aquaporin-2 (AQP2) membrane accumulation. We investigated whether protein kinase C (PKC) and adenosine monophosphate kinase (AMPK) are involved in hypertonicity-regulated water permeability. Increasing perfusate osmolality from 150-290 mosM and bath osmolality from 290-430 mosM significantly stimulated osmotic water permeability. The PKC inhibitors, chelerythrine (10 µM) and rottlerin (50 µM) significantly reversed the increase in osmotic water permeability stimulated by hypertonicity in perfused rat terminal IMCDs...
November 14, 2018: American Journal of Physiology. Renal Physiology
Stephan Kemmner, Quirin Bachmann, Stefanie Steiger, Georg Lorenz, Mohsen Honarpisheh, Orestes Foresto-Neto, Shijun Wang, Javier Carbajo-Lozoya, Verena Alt, Christian Schulte, Stefan Chmielewski, Hans A R Bluyssen, Uwe Heemann, Marcus Baumann, Maciej Lech, Christoph Schmaderer
Renal ischemia/reperfusion injury (IRI) leads to acute kidney injury or delayed allograft function which predisposes to fibrosis in the native kidney or kidney transplant. Here we investigated the role of the signal transducer and activator of transcription 1 (STAT1) in inflammatory responses following renal IRI. Our study showed that a subsequent stimulation of Janus Kinase 2/STAT1 and toll-like receptor 4 pathways led to greater STAT1 activation followed by increased cytokine transcription compared to single-pathway stimulation in murine renal tubular cells...
November 7, 2018: American Journal of Physiology. Renal Physiology
Cesar A Romero, Nitin Kumar, Pablo Nakagawa, Morel E Worou, Tang-Dong Liao, Edward L Peterson, Oscar A Carretero
The anti-fibrotic peptide Ac-SDKP is released from Thymosin β4 (Tβ4) by meprin-α and prolyl oligopeptidase (POP) enzymes and is hydrolyzed by angiotensin-converting enzyme (ACE). Ac-SDKP is present in urine however it is not clear if de novo tubular release exists or the glomerular filtration is the main source. We hypothesized that Ac-SDKP is released in the lumen of the nephron and that it has an anti-fibrotic effect. We determined the presence of Tβ4, meprin-α, and POP in the kidneys of Sprague-Dawley rats...
November 7, 2018: American Journal of Physiology. Renal Physiology
Annegien Kenter, Sari E Van Rossum-Fikkert, Mahdi Salih, Paul C M S Verhagen, Geert J L H Van Leenders, Jeroen A A Demmers, Gert Jansen, Joost H Gribnau, Robert Zietse, Ewout J Hoorn
In autosomal dominant polycystic kidney disease (ADPKD) paracrine signaling molecules in cyst fluid can induce proliferation and cystogenesis of neighboring renal epithelial cells. However, the identity of this "cyst inducing factor" is still unknown. The aim of this study was to identify paracrine signaling proteins in cyst fluid using an 3D in vitro cystogenesis assay. We collected cyst fluid from 15 ADPKD patients who underwent kidney or liver resection (55 cysts from 13 nephrectomies, 5 cysts from 2 liver resections)...
November 7, 2018: American Journal of Physiology. Renal Physiology
Josephine Koch, Nienke M A Idzerda, Wendy Dam, Solmaz Assa, Casper Fm Franssen, Jacob van den Born
Syndecan-1, a transmembrane heparan sulfate proteoglycan, associates with renal and cardiovascular functioning. We earlier reported syndecan-1 to be involved in renal tubular regeneration. We now examined plasma values of syndecan-1 in a hemodialysis cohort and its association with volume, inflammatory and endothelial markers in addition to outcome. Predialysis syndecan-1 levels were two-fold higher in males compared to females (P=0.0003). Patients in the highest predialysis plasma syndecan-1 tertile had a significantly higher ultrafiltration rate (P=0...
October 31, 2018: American Journal of Physiology. Renal Physiology
Scott Culver Thomson
Tubuloglomerular feedback (TGF) responses become anomalous in rats fed high NaCl diet after subtotal nephrectomy (STN) such that stimulating TGF causes single nephron GFR (SNGFR) to increase rather than decrease. Micropuncture experiments were performed to determine whether this anomaly results from heightened nitric oxide response to distal delivery, which is a known mechanism for resetting TGF, or from connecting tubule TGF (cTGF), which is a novel amiloride-inhibitable system for offsetting TGF responses...
October 31, 2018: American Journal of Physiology. Renal Physiology
Jose Luis Izquierdo-Garcia, Nicolás Nin, Pablo Cardinal-Fernandez, Yeny Rojas, Marta de Paula, Rosario Granados, Leticia Martínez-Caro, Jesus Ruiz-Cabello, José Ángel Lorente
The aim of this study is the identification of metabolomic biomarkers of sepsis and sepsis-induced acute kidney injury (AKI) in an experimental model. Pigs were anesthetized and monitored to measure mean arterial pressure (MAP), systemic blood flow (QT), mean pulmonary arterial pressure (MPAP), renal artery blood flow (QRA), renal cortical blood flow (QRC), and urine output (UO). Sepsis was induced at t=0 min by the administration of live Escherichia coli (n=6) or saline (n=8). At t=300 min, animals were sacrificed...
October 31, 2018: American Journal of Physiology. Renal Physiology
Masahiro Okabe, Masaru Motojima, Yoichi Miyazaki, Ira Pastan, Takashi Yokoo, Taiji Matsusaka
Podocyte injury is a key event for progressive renal failure. We have previously established a mouse model of inducible podocyte injury (NEP25) that progressively develops glomerulosclerosis after immunotoxin injection. We performed polysome analysis of intact and injured podocytes utilizing the NEP25 and RiboTag transgenic mice, in which a hemagglutinin-tag is attached to ribosomal protein L22 selectively in podocytes. Podocyte-specific polysomes were successfully obtained by immunoprecipitation with an anti-hemagglutinin antibody from glomerular homogenate and analyzed using a microarray...
October 31, 2018: American Journal of Physiology. Renal Physiology
Ziwei Fu, Jiajia Hu, Li Zhou, Yanting Chen, Mokan Deng, Xiyang Liu, Jiahui Su, Aihua Lu, Tianxin Yang
(Pro)renin receptor (PRR) is a new component of the renin-angiotensin-aldosterone system (RAAS) and regulates renin activity. The objective of the present study was to test potential roles of renal PRR and intrarenal RAAS in physiological status of late pregnancy. Late pregnant Sprague-Dawley rats were studied either 19-21 days after sperm was observed in vaginal smears. Experiments were performed on age-matched virgin rats, and late pregnant rats treated with specific PRR inhibitor PRO20 (700μg/kg/day sc for 14 days, 3 times a day for every 8 h) or vehicle...
October 31, 2018: American Journal of Physiology. Renal Physiology
Alice Doreille, Mélanie Dieudé, Heloise Cardinal
Independent of the initial cause of kidney disease, microvascular injury to the peritubular capillary network appears to play a central role in the development of interstitial fibrosis in both native and transplanted kidney disease. This association is explained by mechanisms such as the upregulation of pro-fibrotic genes and epigenetic changes induced by hypoxia, capillary leakage, endothelial and pericyte transition to interstitial fibroblasts as well modifications in the secretome of endothelial cells. Alloimmune injury due to antibody-mediated rejection and ischemia-reperfusion injury are the two main etiologies of microvascular damage in kidney transplant recipients...
October 31, 2018: American Journal of Physiology. Renal Physiology
Siwei Wei, Youguang Gao, Xingui Dai, Weijun Fu, Shumin Cai, Haihong Fang, Zhenhua Zeng, Zhongqing Chen
Sepsis is the leading cause of death in the intensive care unit and continues to lack effective treatment. It is widely accepted that HMGB1 is a key inflammatory mediator in the pathogenesis of sepsis. Moreover, some studies indicate that the functions of HMGB1 depend on its molecular localization and post-translational modifications. Our previous study confirms that SIRT1, a type III deacetylase, can ameliorate sepsis-associated acute kidney injury (SA-AKI). We explored the effect and mechanism of SIRT1 on HMGB1 using a mouse model of cecal ligation and puncture (CLP)-induced sepsis and LPS-treated human kidney (HK-2) cell line...
October 31, 2018: American Journal of Physiology. Renal Physiology
Lennart Tonneijck, Marcel H A Muskiet, Charles J Blijdorp, Mark M Smits, Jos W Twisk, Mark H H Kramer, A H Jan Danser, Michaela Diamant, Jaap A Joles, Ewout J Hoorn, Daniel Henri van Raalte
Glucagon-like peptide-1 (GLP-1) receptor agonists (RA's) are well-established glucose-lowering drugs for type 2 diabetes mellitus (T2DM)-management. Acute GLP-1RA-administration increases urinary excretion of sodium and other electrolytes. The renal tubular effects of prolonged GLP-1RA-treatment are, however, largely unknown. In this secondary analysis of a randomized trial, we determined the renal tubular effects of 8-week treatment with lixisenatide 20 μg, a short-acting (prandial) GLP-1RA, versus titrated once-daily insulin glulisine in 35 overweight T2DM-patients on stable insulin glargine background therapy (age 62±7years, HbA1c 8...
October 24, 2018: American Journal of Physiology. Renal Physiology
Francis Monty Hughes, Stephanie J Sexton, Patrick D Ledig, Chloe E Yun, Huixia Jin, J Todd Purves
Bladder outlet obstruction (BOO) leads to progressive voiding dysfunction. Acutely, obstruction triggers inflammation that drives bladder dysfunction. Over time, inflammation leads to decreased bladder nerve density and increased fibrosis that is responsible for eventual decompensation and irreversibility. We have previously shown that BOO triggers inflammation, reduced bladder nerve density and increased fibrosis via activation of the NLRP3 inflammasome in an acutely obstructed (12 day) rat model. However, as BOO progresses the bladder may become decompensated with an increase in post-void residual volume (PVR) and decreased voiding efficiency...
October 24, 2018: American Journal of Physiology. Renal Physiology
Michael Fähling, Alexander Paliege, Sofia Jönsson, Mediha Becirovic-Agic, Jacqueline M Melville, Trude Skogstrand, Michael Hultström
The aim was to identify new targets that regulate gene expression at the post-transcriptional level in Angiotensin II (ANGII)-mediated hypertension. Heparin affinity chromatography was used to enrich nucleic acid-binding proteins from kidneys of two-kidney, one-clip (2K1C) hypertensive Wistar rats. The experiment was repeated with 14 days ANGII infusion using Alzet osmotic mini pumps, with or without ANGII receptor AT1a inhibition using Losartan in the drinking water. Mean arterial pressure increased after 2K1C or ANGII infusion and was inhibited with Losartan...
October 17, 2018: American Journal of Physiology. Renal Physiology
Ida Aringer, Katharina Artinger, Alexander H Kirsch, Corinna Schabhüttl, Katharina Jandl, Thomas Bärnthaler, Agnes Mooslechner, Sereina A Herzog, Moritz Uhlig, Andrijana Kirsch, Sasa Frank, Miriam Banas, Marion Pollheimer, Philipp Eller, Alexander R Rosenkranz, Akos Heinemann, Kathrin Eller
Prostaglandin E2 (PGE2 ) signaling is known to modulate inflammation and vascular resistance. Receptors of PGE2 (E-type prostanoid receptors, EP) might be an attractive pharmacological target in immune-mediated diseases such as glomerulonephritis. We hypothesized that selective EP4 antagonism improves nephrotoxic serum nephritis (NTS) by its anti-inflammatory properties. Mice were subjected to NTS and treated with the EP4 antagonist ONO AE3-208 [10 mg/kg bw/day] or vehicle starting from disease initiation. In one set of experiments treatment was started 4 days after NTS induction...
October 17, 2018: American Journal of Physiology. Renal Physiology
Leslie A Bruggeman, John Francis O'Toole, John Sedor
The mechanism that explains the association of APOL1 variants with non-diabetic kidney diseases in African Americans remains unclear. Kidney disease risk is inherited as a recessive trait and many studies investigating the intracellular function of APOL1 have indicated the APOL1 variants G1 and G2 are associated with cytotoxicity. Whether cytotoxicity results from the absence of a protective effect conferred by the G0 allele or induced by a deleterious effect of variant allele expression has not be conclusively established...
October 17, 2018: American Journal of Physiology. Renal Physiology
Pauline Erpicum, Pascal Rowart, Jean-Olivier Defraigne, Jean-Marie Krzesinski, François Jouret
Renal segmental metabolism is reflected by the complex distribution of the main energy pathways along the nephron, with fatty acid oxidation preferentially used in the cortex area. Ischemia/reperfusion injury (IRI) is due to the restriction of renal blood flow, rapidly leading to a metabolic switch towards anaerobic conditions. Subsequent unbalance between energy demand and oxygen/nutrient delivery compromises kidney cell functions, resulting to a complex inflammatory cascade including the production of reactive oxygen species (ROS)...
October 17, 2018: American Journal of Physiology. Renal Physiology
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