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Kidney International

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https://www.readbyqxmd.com/read/29329643/iga-nephropathy-and-iga-vasculitis-with-nephritis-have-a-shared-feature-involving-galactose-deficient-iga1-oriented-pathogenesis
#1
Hitoshi Suzuki, Junichi Yasutake, Yuko Makita, Yuki Tanbo, Kohei Yamasaki, Tadashi Sofue, Toshiki Kano, Yusuke Suzuki
Galactose-deficient IgA1 has been proposed as an important effector molecule in IgA nephropathy (IgAN). We previously showed that the galactose-deficient IgA1-specific monoclonal antibody KM55 can detect circulating galactose-deficient IgA1 in patients with IgAN, enabling us to study the molecular roles of galactose-deficient IgA1. Herein, we further examined the pathophysiological significance of galactose-deficient IgA1 in glomerular deposits of patients with IgAN by immunohistochemistry using KM55. Immunostaining of galactose-deficient IgA1 with KM55 was performed in paraffin-embedded sections of renal biopsy specimens from 48 patients with IgAN and 49 patients with other renal diseases such as lupus nephritis, HCV-related nephropathy, IgA vasculitis with nephritis (IgA-VN), and membranous nephropathy...
January 9, 2018: Kidney International
https://www.readbyqxmd.com/read/29325997/reduced-cortical-oxygenation-predicts-a-progressive-decline-of-renal-function-in-patients-with-chronic-kidney-disease
#2
Menno Pruijm, Bastien Milani, Edward Pivin, Agata Podhajska, Bruno Vogt, Matthias Stuber, Michel Burnier
Renal tissue hypoxia is a final pathway in the development and progression of chronic kidney disease (CKD), but whether renal oxygenation predicts renal function decline in humans has not been proven. Therefore, we performed a prospective study and measured renal tissue oxygenation by blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI) in 112 patients with CKD, 47 with hypertension without CKD, and 24 healthy control individuals. Images were analyzed with the twelve-layer concentric objects method that divided the renal parenchyma in 12 layers of equal thickness and reports the mean R2* value of each layer (a high R2* corresponds to low oxygenation), along with the change in R2* between layers called the R2* slope...
January 9, 2018: Kidney International
https://www.readbyqxmd.com/read/29325996/direct-acting-antiviral-therapy-for-hepatitis-c-virus-infection-in-the-kidney-transplant-recipient
#3
REVIEW
Donald F Chute, Raymond T Chung, Meghan E Sise
Hepatitis C virus infection (HCV) is a common comorbidity in patients who have undergone kidney transplantation and is associated with increased morbidity and mortality compared with recipients who do not have chronic HCV infection. Because interferon-α-based therapies can precipitate acute rejection, they are relatively contraindicated after kidney transplantation. Thus, the majority of kidney transplant recipients with HCV remain untreated. There are now all-oral, interferon-free direct-acting antiviral therapies for HCV infection that are extremely effective and well tolerated in the general population...
January 9, 2018: Kidney International
https://www.readbyqxmd.com/read/29310826/changes-in-v-atpase-subunits-of-human-urinary-exosomes-reflect-the-renal-response-to-acute-acid-alkali-loading-and-the-defects-in-distal-renal-tubular%C3%A2-acidosis
#4
Ganesh Pathare, Nasser A Dhayat, Nilufar Mohebbi, Carsten A Wagner, Ion A Bobulescu, Orson W Moe, Daniel G Fuster
In the kidney, final urinary acidification is achieved by V-ATPases expressed in type A intercalated cells. The B1 subunit of the V-ATPase is required for maximal urinary acidification, while the role of the homologous B2 subunit is less clear. Here we examined the effect of acute acid/alkali loading in humans on B1 and B2 subunit abundance in urinary exosomes in normal individuals and of acid loading in patients with distal renal tubular acidosis (dRTA). Specificities of B1 and B2 subunit antibodies were verified by yeast heterologously expressing human B1 and B2 subunits, and murine wild-type and B1-deleted kidney lysates...
January 6, 2018: Kidney International
https://www.readbyqxmd.com/read/29310825/potassium-intake-modulates-the-thiazide-sensitive-sodium-chloride-cotransporter-ncc-activity-via-the-kir4-1-potassium-channel
#5
Ming-Xiao Wang, Catherina A Cuevas, Xiao-Tong Su, Peng Wu, Zhong-Xiuzi Gao, Dao-Hong Lin, James A McCormick, Chao-Ling Yang, Wen-Hui Wang, David H Ellison
Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we tested whether dietary potassium intake modulates Kir4.1 and whether this is essential for mediating the effect of potassium diet on NCC. High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice...
January 6, 2018: Kidney International
https://www.readbyqxmd.com/read/29310824/c3-glomerulonephritis-and-dense-deposit-disease-share-a-similar-disease-course-in-a-large-united-states-cohort-of-patients-with-c3-glomerulopathy
#6
Andrew S Bomback, Dominick Santoriello, Rupali S Avasare, Renu Regunathan-Shenk, Pietro A Canetta, Wooin Ahn, Jai Radhakrishnan, Maddalena Marasa, Paul E Rosenstiel, Leal C Herlitz, Glen S Markowitz, Vivette D D'Agati, Gerald B Appel
C3 glomerulonephritis (C3GN) and dense deposit disease comprise the two classes of C3 glomerulopathy. Studies from Europe and Asia have aided our understanding of this recently defined disorder, but whether these data apply to a diverse United States patient population remains unclear. We, therefore, reviewed clinical and histopathological data, including generation of a C3 Glomerulopathy Histologic Index to score biopsy activity and chronicity, to determine predictors of progression to end-stage renal disease (ESRD) and advanced chronic kidney disease (CKD) in 111 patients (approximately 35% non-white) with C3 glomerulopathy: 87 with C3GN and 24 with dense deposit disease...
January 6, 2018: Kidney International
https://www.readbyqxmd.com/read/29290310/baseline-total-kidney-volume-and-the-rate-of-kidney-growth-are-associated-with-chronic-kidney-disease-progression-in-autosomal-dominant-polycystic-kidney-disease
#7
Alan S L Yu, Chengli Shen, Douglas P Landsittel, Peter C Harris, Vicente E Torres, Michal Mrug, Kyongtae T Bae, Jared J Grantham, Frederic F Rahbari-Oskoui, Michael F Flessner, William M Bennett, Arlene B Chapman
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive enlargement of kidney cysts leading to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Identification of an early biomarker that can predict progression of CKD is urgently needed. In an earlier Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP) study (a prospective, multicenter, observational analysis of 241 patients with ADPKD initiated in 2000), baseline height-adjusted total kidney volume (htTKV) was shown to be associated with development of CKD stage 3 after eight years of follow-up...
December 28, 2017: Kidney International
https://www.readbyqxmd.com/read/29276101/cd44-is-required-for-the-pathogenesis-of-experimental-crescentic-glomerulonephritis-and-collapsing-focal-segmental-glomerulosclerosis
#8
Jennifer Eymael, Shagun Sharma, Markus A Loeven, Jack F Wetzels, Fieke Mooren, Sandrine Florquin, Jeroen K Deegens, Brigith K Willemsen, Vikram Sharma, Toin H van Kuppevelt, Marinka A Bakker, Tammo Ostendorf, Marcus J Moeller, Henry B Dijkman, Bart Smeets, Johan van der Vlag
A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in glomerular disease. However, it remains unknown whether CD44-positive parietal epithelial cells contribute to the pathogenesis of scarring glomerular diseases. Here, we evaluated this in experimental crescentic glomerulonephritis and the transgenic anti-Thy1...
December 21, 2017: Kidney International
https://www.readbyqxmd.com/read/29276100/revisiting-raas-blockade-in-ckd-with-newer-potassium-binding-drugs
#9
Panagiotis I Georgianos, Rajiv Agarwal
Among patients with proteinuric chronic kidney disease (CKD), current guideline recommendations mandate the use of agents blocking the renin angiotensin aldosterone system (RAAS) as first-line antihypertensive therapy based on randomized trials demonstrating that RAAS inhibitors are superior to other antihypertensive drug classes in slowing nephropathy progression to end-stage renal disease. However, the opportunities for adequate RAAS blockade in CKD are often limited, and an important impediment is the risk of hyperkalemia, especially when RAAS inhibitors are used in maximal doses or are combined...
December 21, 2017: Kidney International
https://www.readbyqxmd.com/read/29276099/lethal-3-malignant-brain-tumor-like-2-l3mbtl2-protein-protects-against-kidney-injury-by-inhibiting-the-dna-damage-p53-apoptosis-pathway-in-renal-tubular-cells
#10
Huihui Huang, Chunhua Xu, Yang Wang, Chenling Meng, Wenjing Liu, Yueshui Zhao, Xiao-Ru Huang, Wenxing You, Bo Feng, Zhi-Hua Zheng, Yu Huang, Hui-Yao Lan, Jinzhong Qin, Yin Xia
DNA damage contributes to renal tubular cell death during kidney injury, but how DNA damage in tubular cells is regulated is not fully understood. Lethal (3) malignant brain tumor like 2 (L3MBTL2), a novel polycomb group protein, has been implicated in regulating chromatin architecture. However, the biological functions of L3MBTL2 are largely undefined. Here we found that L3MBTL2 was expressed in the nuclei of renal tubular epithelial cells in mice. Ablation of L3mbtl2 in renal tubular cells resulted in increases in nuclear DNA damage, p53 activation, apoptosis, tubular injury and kidney dysfunction after cisplatin treatment or unilateral ureteral obstruction...
December 21, 2017: Kidney International
https://www.readbyqxmd.com/read/29273332/global-glomerulosclerosis-with-nephrotic-syndrome-the-clinical-importance-of-age%C3%A2-adjustment
#11
Musab S Hommos, Caihong Zeng, Zhihong Liu, Jonathan P Troost, Avi Z Rosenberg, Matthew Palmer, Walter K Kremers, Lynn D Cornell, Fernando C Fervenza, Laura Barisoni, Andrew D Rule
Globally sclerotic glomeruli (GSG) occur with both normal aging and kidney disease. However, it is unknown whether any GSG or only GSG exceeding that expected for age is clinically important. To evaluate this, we identified patients with a glomerulopathy that often presents with nephrotic syndrome (focal segmental glomerulosclerosis, membranous nephropathy, or minimal change disease) in the setting of the Nephrotic Syndrome Study Network (NEPTUNE), China-Digital Kidney Pathology (DiKiP), and the Southeast Minnesota cohorts...
December 19, 2017: Kidney International
https://www.readbyqxmd.com/read/29273331/systemic-biopolymer-delivered-vascular-endothelial-growth-factor-promotes-therapeutic-angiogenesis-in-experimental-renovascular-disease
#12
Alejandro R Chade, Maxx L Williams, Erika Guise, Luke J Vincent, Taylor W Harvey, Marija Kuna, Fakhri Mahdi, Gene L Bidwell
We recently developed a therapeutic biopolymer composed of an elastin-like polypeptide (ELP) fused to vascular endothelial growth factor (VEGF) and showed long-term renoprotective effects in experimental renovascular disease after a single intra-renal administration. Here, we sought to determine the specificity, safety, efficacy, and mechanisms of renoprotection of ELP-VEGF after systemic therapy in renovascular disease. We tested whether kidney selectivity of the ELP carrier would reduce off-target binding of VEGF in other organs...
December 19, 2017: Kidney International
https://www.readbyqxmd.com/read/29241626/c5a-receptor-1-promotes-autoimmunity-neutrophil-dysfunction-and-injury-in-experimental-anti-myeloperoxidase-glomerulonephritis
#13
Jonathan Dick, Poh-Yi Gan, Sharon L Ford, Dragana Odobasic, Maliha A Alikhan, Sven H Loosen, Pam Hall, Clare L Westhorpe, Anqi Li, Joshua D Ooi, Trent M Woodruff, Charles R Mackay, A Richard Kitching, Michael J Hickey, Stephen R Holdsworth
The prospects for complement-targeted therapy in ANCA-associated vasculitis have been enhanced by a recent clinical trial in which C5a receptor 1 (C5aR1) inhibition safely replaced glucocorticoids in induction treatment. C5aR1 primes neutrophils for activation by anti-neutrophil cytoplasmic antibody (ANCA) and is therefore required in models of glomerulonephritis induced by anti-myeloperoxidase antibody. Although humoral and cellular autoimmunity play essential roles in ANCA-associated vasculitis, a role for C5aR1 in these responses has not been described...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29241625/vinculin-is-required-to-maintain-glomerular-barrier-integrity
#14
Franziska Lausecker, Xuefei Tian, Kazunori Inoue, Zhen Wang, Christopher E Pedigo, Hossam Hassan, Chang Liu, Margaret Zimmer, Stephanie Jinno, Abby L Huckle, Hellyeh Hamidi, Robert S Ross, Roy Zent, Christoph Ballestrem, Rachel Lennon, Shuta Ishibe
Cell-matrix interactions and podocyte intercellular junctions are key for maintaining the glomerular filtration barrier. Vinculin, a cytoplasmic protein, couples actin filaments to integrin-mediated cell-matrix adhesions and to cadherin-based intercellular junctions. Here, we examined the role of vinculin in podocytes by the generation of a podocyte-specific knockout mouse. Mice lacking podocyte vinculin had increased albuminuria and foot process effacement following injury in vivo. Analysis of primary podocytes isolated from the mutant mice revealed defects in cell protrusions, altered focal adhesion size and signaling, as well as impaired cell migration...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29241624/the-macrophage-phenotype-and-inflammasome-component-nlrp3-contributes-to-nephrocalcinosis-related-chronic-kidney-disease-independent-from-il-1-mediated-tissue-injury
#15
Hans-Joachim Anders, Beatriz Suarez-Alvarez, Melissa Grigorescu, Orestes Foresto-Neto, Stefanie Steiger, Jyaysi Desai, Julian A Marschner, Mohsen Honarpisheh, Chongxu Shi, Jutta Jordan, Lisa Müller, Nicolai Burzlaff, Tobias Bäuerle, Shrikant R Mulay
Primary/secondary hyperoxalurias involve nephrocalcinosis-related chronic kidney disease (CKD) leading to end-stage kidney disease. Mechanistically, intrarenal calcium oxalate crystal deposition is thought to elicit inflammation, tubular injury and atrophy, involving the NLRP3 inflammasome. Here, we found that mice deficient in NLRP3 and ASC adaptor protein failed to develop nephrocalcinosis, compromising conclusions on nephrocalcinosis-related CKD. In contrast, hyperoxaluric wild-type mice developed profound nephrocalcinosis...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29241623/knockout-of-the-interleukin-36-receptor-protects-against-renal-ischemia-reperfusion-injury-by-reduction-of-proinflammatory-cytokines
#16
Hirofumi Nishikawa, Yoshinori Taniguchi, Tatsuki Matsumoto, Naoki Arima, Mamoru Masaki, Yoshiko Shimamura, Kosuke Inoue, Taro Horino, Shimpei Fujimoto, Kentaro Ohko, Toshihiro Komatsu, Keiko Udaka, Shigetoshi Sano, Yoshio Terada
IL-36, a newly named member of the IL-1 cytokine family, includes 3 isoforms, IL-36α, IL-36β, and IL-36γ, all of which bind to a heterodimer containing the IL-36 receptor (IL-36R). Little is known about the role of the IL-36 axis in acute kidney injury (AKI) pathogenesis. Therefore, we evaluated IL-36 function in the bilateral renal ischemia-reperfusion injury model of AKI using IL-36R knockout and wild-type mice. IL-36R was found to be expressed in the kidney, mainly in proximal tubules. In IL-36R knockout mice, plasma creatinine, blood urea nitrogen, and IL-6 levels after ischemia-reperfusion injury were significantly lower than those in wild-type mice...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29241621/confocal-super-resolution-imaging-of-the-glomerular-filtration-barrier-enabled-by-tissue%C3%A2-expansion
#17
David Unnersjö-Jess, Lena Scott, Sonia Zambrano Sevilla, Jaakko Patrakka, Hans Blom, Hjalmar Brismar
The glomerular filtration barrier, has historically only been spatially resolved using electron microscopy due to the nanometer-scale dimensions of these structures. Recently, it was shown that the nanoscale distribution of proteins in the slit diaphragm can be resolved by fluorescence based stimulated emission depletion microscopy, in combination with optical clearing. Fluorescence microscopy has advantages over electron microscopy in terms of multiplex imaging of different epitopes, and also the amount of volumetric data that can be extracted from thicker samples...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29241622/higher-blood-urea-nitrogen-is-associated-with-increased-risk-of-incident-diabetes-mellitus
#18
Yan Xie, Benjamin Bowe, Tingting Li, Hong Xian, Yan Yan, Ziyad Al-Aly
Experimental evidence suggests that higher levels of urea may increase insulin resistance and suppress insulin secretion. However, whether higher levels of blood urea nitrogen (BUN) are associated with increased risk of incident diabetes mellitus in humans is not known. To study this, we built a national cohort of 1,337,452 United States Veterans without diabetes to characterize the association of BUN and risk of incident diabetes. Over a median follow-up of 4.93 years, there were 172,913 cases of incident diabetes...
December 7, 2017: Kidney International
https://www.readbyqxmd.com/read/29229189/immunoproteasome-inhibition-prevents-chronic-antibody-mediated-allograft-rejection-in-renal%C3%A2-transplantation
#19
Jun Li, Michael Basler, Gerardo Alvarez, Thomas Brunner, Christopher J Kirk, Marcus Groettrup
Chronic antibody-mediated rejection is the major cause of fading allograft function and loss after renal transplantation. Currently, pharmacological agents for the suppression of chronic antibody-mediated rejection are lacking. Non-selective proteasome inhibitors suppress antibody-mediated allograft rejection. However, extensive adverse side effects of these inhibitors severely limit their application. In contrast, immunoproteasome inhibition is effective in preclinical models of autoimmune diseases and was applied over weeks without obvious adverse side effects...
December 4, 2017: Kidney International
https://www.readbyqxmd.com/read/29217079/haploinsufficiency-for-the-six2-gene-increases-nephron-progenitor-proliferation-promoting-branching-and-nephron-number
#20
Alexander N Combes, Sean Wilson, Belinda Phipson, Brandon B Binnie, Adler Ju, Kynan T Lawlor, Cristina Cebrian, Sarah L Walton, Ian M Smyth, Karen M Moritz, Raphael Kopan, Alicia Oshlack, Melissa H Little
The regulation of final nephron number in the kidney is poorly understood. Cessation of nephron formation occurs when the self-renewing nephron progenitor population commits to differentiation. Transcription factors within this progenitor population, such as SIX2, are assumed to control expression of genes promoting self-renewal such that homozygous Six2 deletion results in premature commitment and an early halt to kidney development. In contrast, Six2 heterozygotes were assumed to be unaffected. Using quantitative morphometry, we found a paradoxical 18% increase in ureteric branching and final nephron number in Six2 heterozygotes, despite evidence for reduced levels of SIX2 protein and transcript...
December 4, 2017: Kidney International
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