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    - UROLOGY, NEPHROLOGY AND ANDROLOGY (151 journals)

UROLOGY, NEPHROLOGY AND ANDROLOGY (151 journals)                     

Showing 1 - 144 of 144 Journals sorted alphabetically
Actas Urológicas Españolas     Full-text available via subscription   (Followers: 1)
Actas Urológicas Españolas (English Edition)     Full-text available via subscription   (Followers: 1)
Advances in Chronic Kidney Disease     Hybrid Journal   (Followers: 15)
Advances in Urology     Open Access   (Followers: 13)
African Journal of Nephrology     Open Access   (Followers: 1)
African Journal of Urology     Open Access   (Followers: 7)
AJP Renal Physiology     Hybrid Journal   (Followers: 8)
Aktuelle Urologie     Hybrid Journal   (Followers: 4)
American Journal of Kidney Diseases     Hybrid Journal   (Followers: 53)
American Journal of Men's Health     Open Access   (Followers: 9)
American Journal of Nephrology     Full-text available via subscription   (Followers: 31)
Andrologia     Hybrid Journal   (Followers: 3)
Andrology     Hybrid Journal   (Followers: 5)
Andrology & Gynecology : Current Research     Hybrid Journal   (Followers: 4)
Andrology and Genital Surgery     Open Access   (Followers: 8)
Arab Journal of Nephrology and Transplantation     Open Access   (Followers: 2)
Arab Journal of Urology     Open Access   (Followers: 7)
Archives of Clinical Nephrology     Open Access   (Followers: 2)
Archivio Italiano di Urologia e Andrologia     Open Access   (Followers: 1)
Archivos Españoles de Urología     Open Access   (Followers: 1)
Asian Journal of Andrology     Open Access   (Followers: 1)
Asian Journal of Urology     Open Access   (Followers: 3)
Asian Pediatric Nephrology Association     Open Access   (Followers: 3)
Bangladesh Journal of Urology     Open Access   (Followers: 5)
Basic and Clinical Andrology     Open Access  
BJU International     Hybrid Journal   (Followers: 19)
BJUI Compass     Open Access   (Followers: 1)
BMC Nephrology     Open Access   (Followers: 9)
BMC Urology     Open Access   (Followers: 13)
Canadian Journal of Kidney Health and Disease     Open Access   (Followers: 7)
Canadian Urological Association Journal     Open Access   (Followers: 1)
Cancer Urology     Open Access   (Followers: 1)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Case Reports in Nephrology     Open Access   (Followers: 6)
Case Reports in Nephrology and Dialysis     Open Access   (Followers: 8)
Case Reports in Urology     Open Access   (Followers: 11)
Clinical and Experimental Nephrology     Hybrid Journal   (Followers: 5)
Clinical Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 24)
Clinical Kidney Journal     Open Access   (Followers: 5)
Clinical Medicine Insights : Urology     Open Access   (Followers: 3)
Clinical Nephrology     Full-text available via subscription   (Followers: 8)
Cuadernos de Cirugía     Open Access  
Current Opinion in Nephrology & Hypertension     Hybrid Journal   (Followers: 12)
Current Opinion in Urology     Hybrid Journal   (Followers: 11)
Current Urology     Open Access   (Followers: 10)
Current Urology Reports     Hybrid Journal   (Followers: 5)
Der Nephrologe     Hybrid Journal  
Der Urologe     Hybrid Journal   (Followers: 1)
Diabetic Nephropathy     Open Access  
EMC - Urología     Full-text available via subscription  
Enfermería Nefrológica     Open Access   (Followers: 1)
European Urology     Hybrid Journal   (Followers: 23)
European Urology Focus     Hybrid Journal   (Followers: 4)
European Urology Oncology     Hybrid Journal  
European Urology Open Science     Open Access   (Followers: 8)
Forum Nefrologiczne     Full-text available via subscription  
Geriatric Nephrology and Urology     Hybrid Journal   (Followers: 7)
Giornale di Clinica Nefrologica e Dialisi     Open Access  
Hellenic Urology     Open Access   (Followers: 3)
IJU Case Reports     Open Access  
Indian Journal of Nephrology     Open Access   (Followers: 2)
Indian Journal of Urology     Open Access   (Followers: 5)
International Brazilian Journal of Urology     Open Access   (Followers: 5)
International Journal of Nephrology     Open Access   (Followers: 2)
International Journal of Nephrology and Renovascular Disease     Open Access   (Followers: 2)
International Journal of Urology     Hybrid Journal   (Followers: 10)
International Urology and Nephrology     Hybrid Journal   (Followers: 6)
Journal für Urologie und Urogynäkologie/Österreich     Hybrid Journal  
Journal of Clinical Nephrology     Open Access   (Followers: 1)
Journal of Clinical Urology     Hybrid Journal   (Followers: 12)
Journal of Endoluminal Endourology     Open Access  
Journal of Endourology     Hybrid Journal   (Followers: 2)
Journal of Endourology Case Reports     Hybrid Journal  
Journal of Genital System & Disorders     Hybrid Journal   (Followers: 1)
Journal of Integrative Nephrology and Andrology     Open Access   (Followers: 2)
Journal of Kidney Cancer and VHL     Open Access  
Journal of Lower Genital Tract Disease     Hybrid Journal  
Journal of Nephrology     Hybrid Journal   (Followers: 5)
Journal of Nephrology Research     Open Access   (Followers: 2)
Journal of Pediatric Nephrology     Open Access   (Followers: 3)
Journal of Renal Care     Hybrid Journal   (Followers: 8)
Journal of Renal Nursing     Full-text available via subscription   (Followers: 8)
Journal of Renal Nutrition     Hybrid Journal   (Followers: 28)
Journal of Renal Nutrition and Metabolism     Open Access   (Followers: 2)
Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 38)
Journal of The Egyptian Society of Nephrology and Transplantation     Open Access  
Journal of Urology & Nephrology     Open Access  
Kidney Diseases     Open Access   (Followers: 3)
Kidney International     Hybrid Journal   (Followers: 52)
Kidney International Reports     Open Access   (Followers: 6)
Kidney Medicine     Open Access   (Followers: 1)
Kidney Research Journal     Open Access   (Followers: 6)
Kidneys (Počki)     Open Access  
Nature Reviews Nephrology     Full-text available via subscription   (Followers: 29)
Nature Reviews Urology     Full-text available via subscription   (Followers: 9)
Nefrología     Open Access  
Nefrología (English Edition)     Open Access  
Nephro-Urology Monthly     Open Access   (Followers: 1)
Nephrology     Hybrid Journal   (Followers: 13)
Nephrology Dialysis Transplantation     Hybrid Journal   (Followers: 26)
Nephron     Hybrid Journal   (Followers: 3)
Nephron Clinical Practice     Full-text available via subscription   (Followers: 3)
Nephron Experimental Nephrology     Full-text available via subscription   (Followers: 4)
Nephron Extra     Open Access   (Followers: 1)
Nephron Physiology     Full-text available via subscription   (Followers: 4)
Neurourology and Urodynamics     Hybrid Journal   (Followers: 1)
OA Nephrology     Open Access   (Followers: 2)
Open Access Journal of Urology     Open Access   (Followers: 6)
Open Journal of Nephrology     Open Access   (Followers: 4)
Open Journal of Urology     Open Access   (Followers: 6)
Open Urology & Nephrology Journal     Open Access  
Paediatric Nephrology Journal of Bangladesh     Open Access   (Followers: 4)
Portuguese Journal of Nephrology & Hypertension     Open Access   (Followers: 1)
Progrès en Urologie     Full-text available via subscription  
Progrès en Urologie - FMC     Full-text available via subscription  
Prostate Cancer and Prostatic Diseases     Hybrid Journal   (Followers: 4)
Renal Failure     Open Access   (Followers: 11)
Renal Replacement Therapy     Open Access   (Followers: 3)
Research and Reports in Urology     Open Access   (Followers: 4)
Revista de Nefrología, Diálisis y Trasplante     Open Access   (Followers: 1)
Revista Mexicana de Urología     Open Access  
Revista Urologia Colombiana     Open Access  
Scandinavian Journal of Urology     Hybrid Journal   (Followers: 6)
Seminars in Nephrology     Hybrid Journal   (Followers: 11)
The Prostate     Hybrid Journal   (Followers: 6)
Therapeutic Advances in Urology     Open Access   (Followers: 3)
Translational Research in Urology     Open Access   (Followers: 1)
Trends in Urology & Men's Health     Partially Free   (Followers: 1)
Urine     Open Access  
Uro-News     Hybrid Journal  
Urolithiasis     Hybrid Journal   (Followers: 1)
Urologia Internationalis     Full-text available via subscription   (Followers: 1)
Urologia Journal     Hybrid Journal  
Urologic Clinics of North America     Full-text available via subscription   (Followers: 3)
Urologic Nursing     Full-text available via subscription   (Followers: 3)
Urological Science     Open Access  
Urologicheskie Vedomosti     Open Access  
Urologie in der Praxis     Hybrid Journal  
Urology     Hybrid Journal   (Followers: 26)
Urology Case Reports     Open Access   (Followers: 3)
Urology Times     Free   (Followers: 3)
Urology Video Journal     Open Access  
World Journal of Nephrology and Urology     Open Access   (Followers: 5)
World Journal of Urology     Hybrid Journal   (Followers: 10)

           

Similar Journals
Journal Cover
Journal of the American Society of Nephrology
Journal Prestige (SJR): 4.819
Citation Impact (citeScore): 7
Number of Followers: 38  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 1046-6673 - ISSN (Online) 1533-3450
Published by American Society of Nephrology Homepage  [2 journals]
  • This Months Highlights

    • Free pre-print version: Loading...

      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022060694
      Issue No: Vol. 33, No. 8 (2022)
       
  • Polycystin-2 in the Endoplasmic Reticulum: Bending Ideas about the Role of
           the Cilium

    • Free pre-print version: Loading...

      Authors: Caplan; M. J.
      Pages: 1433 - 1434
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022050557
      Issue No: Vol. 33, No. 8 (2022)
       
  • Identifying Antigen-Specific T Cells in ANCA-Associated Vasculitis: A
           Glimpse of the Future'

    • Free pre-print version: Loading...

      Authors: Shochet, L; Kitching, A. R.
      Pages: 1435 - 1437
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022060668
      Issue No: Vol. 33, No. 8 (2022)
       
  • Unfulfilled Expectations Open New Horizons: What Have We Learned about
           Volume-Regulated Anion Channels in the Kidney'

    • Free pre-print version: Loading...

      Authors: Pochynyuk, O; Palygin, O.
      Pages: 1437 - 1439
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022050588
      Issue No: Vol. 33, No. 8 (2022)
       
  • Collaboration between Dialysis Providers

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      Authors: Silberzweig, J; Bhat, J. G, Dittrich, M. O, Durvasula, R, Giullian, J, Hymes, J. L, Johnson, D, Schiller, B, Spech, R, Spry, L, Walker, G. S, Watnick, S, Yee, J, Freedman, B. I.
      Pages: 1440 - 1444
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021111475
      Issue No: Vol. 33, No. 8 (2022)
       
  • Vaccination, Transplantation, and a Social Contract

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      Authors: Kates, O. S; Limaye, A. P, Kaplan, B.
      Pages: 1445 - 1447
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021111501
      Issue No: Vol. 33, No. 8 (2022)
       
  • High-Resolution Mass Spectrometry for the Measurement of PTH and PTH
           Fragments: Insights into PTH Physiology and Bioactivity

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      Authors: Ulmer, C. Z; Kritmetapak, K, Singh, R. J, Vesper, H. W, Kumar, R.
      Pages: 1448 - 1458
      Abstract: Full-length parathyroid hormone (PTH 1–84) is crucial for the regulation of calcium and phosphate homeostasis and bone remodeling. PTH 1–84 is metabolized into various PTH fragments, which are measured with varying levels of efficiency by PTH immunoassays. These PTH fragments, which increase in serum as CKD progresses, could potentially modulate the effects of PTH 1–84 and contribute to CKD-associated bone disorders. To obtain a true biologic representation of total PTH bioactivity, it is necessary to measure not only PTH 1–84 but also PTH fragments that are present in circulation. Traditional second-generation PTH immunoassays collectively measure PTH 1–84, PTH fragments, and post-translationally modified PTH 1–84, making it difficult to accurately predict the character of underlying renal osteodystrophy. This review highlights current advances in methods available for PTH measurement and the clinical relevance of PTH fragments in CKD. We emphasize the usefulness of mass spectrometry as a potential reference method for PTH measurement.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022010036
      Issue No: Vol. 33, No. 8 (2022)
       
  • Optimizing the Design and Analysis of Future AKI Trials

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      Authors: Legrand, M; Bagshaw, S. M, Koyner, J. L, Schulman, I. H, Mathis, M. R, Bernholz, J, Coca, S, Gallagher, M, Gaudry, S, Liu, K. D, Mehta, R. L, Pirracchio, R, Ryan, A, Steubl, D, Stockbridge, N, Erlandsson, F, Turan, A, Wilson, F. P, Zarbock, A, Bokoch, M. P, Casey, J. D, Rossignol, P, Harhay, M. O.
      Pages: 1459 - 1470
      Abstract: AKI is a complex clinical syndrome associated with an increased risk of morbidity and mortality, particularly in critically ill and perioperative patient populations. Most AKI clinical trials have been inconclusive, failing to detect clinically important treatment effects at predetermined statistical thresholds. Heterogeneity in the pathobiology, etiology, presentation, and clinical course of AKI remains a key challenge in successfully testing new approaches for AKI prevention and treatment. This article, derived from the "AKI" session of the "Kidney Disease Clinical Trialists" virtual workshop held in October 2021, reviews barriers to and strategies for improving the design and implementation of clinical trials in patients with, or at risk of, developing AKI. The novel approaches to trial design included in this review span adaptive trial designs that increase the knowledge gained from each trial participant; pragmatic trial designs that allow for the efficient enrollment of sufficiently large numbers of patients to detect small, but clinically significant, treatment effects; and platform trial designs that use one trial infrastructure to answer multiple clinical questions simultaneously. This review also covers novel approaches to clinical trial analysis, such as Bayesian analysis and assessing heterogeneity in the response to therapies among trial participants. We also propose a road map and actionable recommendations to facilitate the adoption of the reviewed approaches. We hope that the resulting road map will help guide future clinical trial planning, maximize learning from AKI trials, and reduce the risk of missing important signals of benefit (or harm) from trial interventions.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021121605
      Issue No: Vol. 33, No. 8 (2022)
       
  • Housing: A Critical Contributor to Kidney Disease Disparities

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      Authors: Novick; T. K., Baweja, M., on behalf of the American Society of Nephrology Healthcare Justice Committee Advocacy Scholarship Work Group are, Novick, Baweja, Browne, Mahooty, Ng, Rizzolo, Robinson, Sekkarie, Young
      Pages: 1471 - 1473
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022040424
      Issue No: Vol. 33, No. 8 (2022)
       
  • Addressing Inequities in Kidney Care for Indigenous People in Canada

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      Authors: Harasemiw, O; Komenda, P, Tangri, N.
      Pages: 1474 - 1476
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022020215
      Issue No: Vol. 33, No. 8 (2022)
       
  • Targeted Disruption of a Proximal Tubule-Specific TMEM174 Gene in Mice
           Causes Hyperphosphatemia and Vascular Calcification

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      Authors: Miyazaki-Anzai, S; Keenan, A. L, Blaine, J, Miyazaki, M.
      Pages: 1477 - 1486
      Abstract: BackgroundThe proximal tubules play a critical role in phosphate (Pi) homeostasis by reabsorbing Pi via sodium-dependent Pi cotransporters. NPT2A is a major proximal-specific Pi cotransporter, whose expression is regulated by circulating hormones, such as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23). In this study, we aimed to find a novel regulator in Pi homeostasis.MethodsUsing RNA-seq and RT-qPCR analysis, we identified proximal tubule cell–enriched genes. We next used RNAi screening of the identified proximal tubular cell–enriched genes to identify a novel proximal tubule–specific gene that contributes to FGF23- and PTH-mediated inhibition of Pi uptake and NPT2 reduction. We created mice lacking this novel regulator of Pi homeostasis to examine whether the novel regulator contributes to Pi homeostasis in vivo.ResultsWe identified 54 kidney-enriched genes, 19 of which are expressed in renal primary proximal tubule cells. One of the proximal tubule–specific genes, TMEM174, interacted with NPT2A, and its knockdown blocked the reduction of NPT2A protein by FGF23 and PTH treatments in human and opossum proximal tubule cells. TMEM174 KO mice had significantly increased levels of serum Pi, FGF23, and PTH, resulting in vascular calcification.ConclusionsTMEM174 is a novel regulator of Pi homeostasis that interacts with NPT2A.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021121578
      Issue No: Vol. 33, No. 8 (2022)
       
  • Myeloid CCR2 Promotes Atherosclerosis after AKI

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      Authors: Hüsing, A. M; Wulfmeyer, V. C, Gaedcke, S, Fleig, S. V, Rong, S, DeLuca, D, Haller, H, Schmitt, R, von Vietinghoff, S.
      Pages: 1487 - 1500
      Abstract: BackgroundThe risk of cardiovascular events rises after AKI. Leukocytes promote atherosclerotic plaque growth and instability. We established a model of enhanced remote atherosclerosis after renal ischemia-reperfusion (IR) injury and investigated the underlying inflammatory mechanisms.MethodsAtherosclerotic lesions and inflammation were investigated in native and bone marrow–transplanted LDL receptor–deficient (LDLr–/–) mice after unilateral renal IR injury using histology, flow cytometry, and gene expression analysis.ResultsAortic root atherosclerotic lesions were significantly larger after renal IR injury than in controls. A gene expression screen revealed enrichment for chemokines and their cognate receptors in aortas of IR-injured mice in early atherosclerosis, and of T cell–associated genes in advanced disease. Confocal microscopy revealed increased aortic macrophage proximity to T cells. Differential aortic inflammatory gene regulation in IR-injured mice largely paralleled the pattern in the injured kidney. Single-cell analysis identified renal cell types that produced soluble mediators upregulated in the atherosclerotic aorta. The analysis revealed a marked early increase in Ccl2, which CCR2+ myeloid cells mainly expressed. CCR2 mediated myeloid cell homing to the post-ischemic kidney in a cell-individual manner. Reconstitution with Ccr2–/– bone marrow dampened renal post-ischemic inflammation, reduced aortic Ccl2 and inflammatory macrophage marker CD11c, and abrogated excess aortic atherosclerotic plaque formation after renal IR.ConclusionsOur data introduce an experimental model of remote proatherogenic effects of renal IR and delineate myeloid CCR2 signaling as a mechanistic requirement. Monocytes should be considered as mobile mediators when addressing systemic vascular sequelae of kidney injury.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022010048
      Issue No: Vol. 33, No. 8 (2022)
       
  • Channel Function of Polycystin-2 in the Endoplasmic Reticulum Protects
           against Autosomal Dominant Polycystic Kidney Disease

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      Authors: Padhy, B; Xie, J, Wang, R, Lin, F, Huang, C.-L.
      Pages: 1501 - 1516
      Abstract: BackgroundMutations of PKD2, which encodes polycystin-2, cause autosomal dominant polycystic kidney disease (ADPKD). The prevailing view is that defects in polycystin-2–mediated calcium ion influx in the primary cilia play a central role in the pathogenesis of cyst growth. However, polycystin-2 is predominantly expressed in the endoplasmic reticulum (ER) and more permeable to potassium ions than to calcium ions.MethodsThe trimeric intracellular cation (TRIC) channel TRIC-B is an ER-resident potassium channel that mediates potassium–calcium counterion exchange for inositol trisphosphate–mediated calcium ion release. Using TRIC-B as a tool, we examined the function of ER-localized polycystin-2 and its role in ADPKD pathogenesis in cultured cells, zebrafish, and mouse models.ResultsAgonist-induced ER calcium ion release was defective in cells lacking polycystin-2 and reversed by exogenous expression of TRIC-B. Vice versa, exogenous polycystin-2 reversed an ER calcium-release defect in cells lacking TRIC-B. In a zebrafish model, expression of wild-type but not nonfunctional TRIC-B suppressed polycystin-2–deficient phenotypes. Similarly, these phenotypes were suppressed by targeting the ROMK potassium channel (normally expressed on the cell surface) to the ER. In cultured cells and polycystin-2–deficient zebrafish phenotypes, polycystin-2 remained capable of reversing the ER calcium release defect even when it was not present in the cilia. Transgenic expression of Tric-b ameliorated cystogenesis in the kidneys of conditional Pkd2-inactivated mice, whereas Tric-b deletion enhanced cystogenesis in Pkd2-heterozygous kidneys.ConclusionsPolycystin-2 in the ER appears to be critical for anticystogenesis and likely functions as a potassium ion channel to facilitate potassium–calcium counterion exchange for inositol trisphosphate–mediated calcium release. The results advance the understanding of ADPKD pathogenesis and provides proof of principle for pharmacotherapy by TRIC-B activators.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022010053
      Issue No: Vol. 33, No. 8 (2022)
       
  • Immunological Interaction of HLA-DPB1 and Proteinase 3 in ANCA Vasculitis
           is Associated with Clinical Disease Activity

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      Authors: Chen, D. P; McInnis, E. A, Wu, E. Y, Stember, K. G, Hogan, S. L, Hu, Y, Henderson, C. D, Blazek, L. N, Mallal, S, Karosiene, E, Peters, B, Sidney, J, James, E. A, Kwok, W. W, Jennette, J. C, Ciavatta, D. J, Falk, R. J, Free, M. E.
      Pages: 1517 - 1527
      Abstract: BackgroundPR3-ANCA vasculitis has a genetic association with HLA-DPB1. We explored immunologic and clinical features related to the interaction of HLA-DPB1*04:01 with a strongly binding PR3 peptide epitope (PR3225–239).MethodsPatients with ANCA vasculitis with active disease and disease in remission were followed longitudinally. Peripheral blood mononuclear cells from patients and healthy controls with HLA-DPB1*04:01 were tested for HLA-DPB1*04:01 expression and interaction with a PR3 peptide identified via in silico and in vitro assays. Tetramers (HLA/peptide multimers) identified autoreactive T cells in vitro.ResultsThe HLA-DPB1*04:01 genotype was associated with risk of relapse in PR3-ANCA (HR for relapse 2.06; 95% CI, 1.01 to 4.20) but not in myeloperoxidase (MPO)-ANCA or the combined cohort. In silico predictions of HLA and PR3 peptide interactions demonstrated strong affinity between ATRLFPDFFTRVALY (PR3225–239) and HLA-DPB1*04:01 that was confirmed by in vitro competitive binding studies. The interaction was tested in ex vivo flow cytometry studies of labeled peptide and HLA-DPB1*04:01-expressing cells. We demonstrated PR3225–239 specific autoreactive T cells using synthetic HLA multimers (tetramers). Patients in long-term remission off therapy had autoantigenic peptide and HLA interaction comparable to that of healthy volunteers.ConclusionsThe risk allele HLA-DPB1*04:01 has been associated with PR3-ANCA, but its immunopathologic role was unclear. These studies demonstrate that HLA-DPB1*04:01 and PR3225–239 initiate an immune response. Autoreactive T cells specifically recognized PR3225–239 presented by HLA-DPB1*04:01. Although larger studies should validate these findings, the pathobiology may explain the observed increased risk of relapse in our cohort. Moreover, lack of HLA and autoantigen interaction observed during long-term remission signals immunologic nonresponsiveness.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021081142
      Issue No: Vol. 33, No. 8 (2022)
       
  • Renal Deletion of LRRC8/VRAC Channels Induces Proximal Tubulopathy

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      Authors: Lopez-Cayuqueo, K. I; Planells-Cases, R, Pietzke, M, Oliveras, A, Kempa, S, Bachmann, S, Jentsch, T. J.
      Pages: 1528 - 1545
      Abstract: BackgroundVolume-regulated anion channels (VRACs) are heterohexamers of LRRC8A with LRRC8B, -C, -D, or -E in various combinations. Depending on the subunit composition, these swelling-activated channels conduct chloride, amino acids, organic osmolytes, and drugs. Despite VRACs’ role in cell volume regulation, and large osmolarity changes in the kidney, neither the localization nor the function of VRACs in the kidney is known.MethodsMice expressing epitope-tagged LRRC8 subunits were used to determine the renal localization of all VRAC subunits. Mice carrying constitutive deletions of Lrrc8b–e, or with inducible or cell-specific ablation of Lrrc8a, were analyzed to assess renal functions of VRACs. Analysis included histology, urine and serum parameters in different diuresis states, and metabolomics.ResultsThe kidney expresses all five VRAC subunits with strikingly distinct localization. Whereas LRRC8C is exclusively found in vascular endothelium, all other subunits are found in the nephron. LRRC8E is specific for intercalated cells, whereas LRRC8A, LRRC8B, and LRRC8D are prominent in basolateral membranes of proximal tubules. Conditional deletion of LRRC8A in proximal but not distal tubules and constitutive deletion of LRRC8D cause proximal tubular injury, increased diuresis, and mild Fanconi-like symptoms.ConclusionsVRAC/LRRC8 channels are crucial for the function and integrity of proximal tubules, but not for more distal nephron segments despite their larger need for volume regulation. LRRC8A/D channels may be required for the basolateral exit of many organic compounds, including cellular metabolites, in proximal tubules. Proximal tubular injury likely results from combined accumulation of several transported molecules in the absence of VRAC channels.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021111458
      Issue No: Vol. 33, No. 8 (2022)
       
  • Complementary Nck1/2 Signaling in Podocytes Controls {alpha}
           Actinin-4-Mediated Actin Organization, Adhesion, and Basement Membrane
           Composition

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      Authors: Martin, C. E; Phippen, N. J, Keyvani Chahi, A, Tilak, M, Banerjee, S. L, Lu, P, New, L. A, Williamson, C. R, Platt, M. J, Simpson, J. A, Krendel, M, Bisson, N, Gingras, A.-C, Jones, N.
      Pages: 1546 - 1567
      Abstract: BackgroundMaintenance of the kidney filtration barrier requires coordinated interactions between podocytes and the underlying glomerular basement membrane (GBM). GBM ligands bind podocyte integrins, which triggers actin-based signaling events critical for adhesion. Nck1/2 adaptors have emerged as essential regulators of podocyte cytoskeletal dynamics. However, the precise signaling mechanisms mediated by Nck1/2 adaptors in podocytes remain to be fully elucidated.MethodsWe generated podocytes deficient in Nck1 and Nck2 and used transcriptomic approaches to profile expression differences. Proteomic techniques identified specific binding partners for Nck1 and Nck2 in podocytes. We used cultured podocytes and mice deficient in Nck1 and/or Nck2, along with podocyte injury models, to comprehensively verify our findings.ResultsCompound loss of Nck1/2 altered expression of genes involved in actin binding, cell adhesion, and extracellular matrix composition. Accordingly, Nck1/2-deficient podocytes showed defects in actin organization and cell adhesion in vitro, with podocyte detachment and altered GBM morphology present in vivo. We identified distinct interactomes for Nck1 and Nck2 and uncovered a mechanism by which Nck1 and Nck2 cooperate to regulate actin bundling at focal adhesions via α actinin-4. Furthermore, loss of Nck1 or Nck2 resulted in increased matrix deposition in vivo, with more prominent defects in Nck2-deficient mice, consistent with enhanced susceptibility to podocyte injury.ConclusionThese findings reveal distinct, yet complementary, roles for Nck proteins in regulating podocyte adhesion, controlling GBM composition, and sustaining filtration barrier integrity.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021101343
      Issue No: Vol. 33, No. 8 (2022)
       
  • Albuminuria-Lowering Effect of Dapagliflozin, Eplerenone, and Their
           Combination in Patients with Chronic Kidney Disease: A Randomized
           Crossover Clinical Trial

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      Authors: Provenzano, M; Puchades, M. J, Garofalo, C, Jongs, N, DMarco, L, Andreucci, M, De Nicola, L, Gorriz, J. L, Heerspink, H. J. L, on behalf of the ROTATE-3 study group, ROTATE-3 study group members, Pennino, De Gregorio, Polese, Caturano, Minutolo, Sasso, Gagliardi, Zicarelli, Crugliano, Civera, Panizo, Sen, Xie
      Pages: 1569 - 1580
      Abstract: BackgroundSodium glucose cotransporter 2 (SGLT2) inhibitors and mineralocorticoid receptor antagonists (MRAs) reduce the urinary albumin-to-creatinine ratio (UACR) and confer kidney and cardiovascular protection in patients with CKD. We assessed efficacy and safety of the SGLT2 inhibitor dapagliflozin and MRA eplerenone alone and in combination in patients with CKD.MethodsWe conducted a randomized open-label crossover trial in patients with urinary albumin excretion ≥100 mg/24 hr, eGFR 30–90 ml/min per 1.73 m2, who had been receiving maximum tolerated stable doses of an ACE inhibitor (ACEi) or angiotensin receptor blocker (ARB). Patients were assigned to 4-week treatment periods with dapagliflozin 10 mg/day, eplerenone 50 mg/day, or their combination in random order, separated by 4-week washout periods. Primary outcome was the correlation in UACR changes between treatments. Secondary outcome was the percent change in 24-hour UACR from baseline.ResultsOf 57 patients screened, 46 were randomly assigned (mean eGFR, 58.1 ml/min per 1.73 m2; median UACR, 401 mg/g) to the three groups. Mean percentage change from baseline in UACR after 4 weeks of treatment with dapagliflozin, eplerenone, and dapagliflozin-eplerenone was –19.6% (95% confidence interval [CI], –34.3 to –1.5), –33.7% (95% CI, –46.1 to –18.5), and –53% (95% CI, –61.7 to –42.4; P
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022020207
      Issue No: Vol. 33, No. 8 (2022)
       
  • A Deep Learning Approach for Automated Segmentation of Kidneys and
           Exophytic Cysts in Individuals with Autosomal Dominant Polycystic Kidney
           Disease

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      Authors: Kim, Y; Tao, C, Kim, H, Oh, G.-Y, Ko, J, Bae, K. T.
      Pages: 1581 - 1589
      Abstract: BackgroundTotal kidney volume (TKV) is an important imaging biomarker in autosomal dominant polycystic kidney disease (ADPKD). Manual computation of TKV, particularly with the exclusion of exophytic cysts, is laborious and time consuming.MethodsWe developed a fully automated segmentation method for TKV using a deep learning network to selectively segment kidney regions while excluding exophytic cysts. We used abdominal T2-weighted magnetic resonance images from 210 individuals with ADPKD who were divided into two groups: one group of 157 to train the network and a second group of 53 to test it. With a 3D U-Net architecture using dataset fingerprints, the network was trained by K-fold cross-validation, in that 80% of 157 cases were for training and the remaining 20% were for validation. We used Dice similarity coefficient, intraclass correlation coefficient, and Bland–Altman analysis to assess the performance of the automated segmentation method compared with the manual method.ResultsThe automated and manual reference methods exhibited excellent geometric concordance (Dice similarity coefficient: mean±SD, 0.962±0.018) on the test datasets, with kidney volumes ranging from 178.9 to 2776.0 ml (mean±SD, 1058.5±706.8 ml) and exophytic cysts ranging from 113.4 to 2497.6 ml (mean±SD, 549.0±559.1 ml). The intraclass correlation coefficient was 0.9994 (95% confidence interval, 0.9991 to 0.9996; P
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021111400
      Issue No: Vol. 33, No. 8 (2022)
       
  • Coronary Artery Calcification Score and the Progression of Chronic Kidney
           Disease

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      Authors: Yun, H.-R; Joo, Y. S, Kim, H. W, Park, J. T, Chang, T. I, Son, N.-H, Yoo, T.-H, Kang, S.-W, Sung, S, Lee, K.-B, Lee, J, Oh, K.-H, Han, S. H, on behalf of the KoreaN Cohort Study for Outcomes in Patients With Chronic Kidney Disease (KNOW-CKD) investigators, The KoreaN Cohort Study for Outcomes in Patients With Chronic Kidney Disease (KNOW-CKD), Ahn, Oh, Han, Lee, Koh, So, Ko, Lee, Chae, Jeong, Cho, Oh, Lee, Yoo, Choi, Han, Park, Hong, You, Lee, Hyun, Kim, Kim, Kim, Kim, Chung, Jung, Jin, Sung, Min, Ku, Kim, Kwon, Bae, Kim, Kim, Oh, Choi, Kim, Myeong, Lee, Lee, Kim, Kang, Kim, Kim, Oh, Koo, Seo, Baek, Kim, Chang, Park, Choi, Oh, Lee, Lee, Park, Seong, Heon, Rhee, Kim, Woon, Ji, Kim, Na, Choi, Ham, Lee, Cha
      Pages: 1590 - 1601
      Abstract: BackgroundAn elevated coronary artery calcification score (CACS) is associated with increased cardiovascular disease risk in patients with CKD. However, the relationship between CACS and CKD progression has not been elucidated.MethodsWe studied 1936 participants with CKD (stages G1–G5 without kidney replacement therapy) enrolled in the KoreaN Cohort Study for Outcome in Patients With CKD. The main predictor was Agatston CACS categories at baseline (0 AU, 1–100 AU, and>100 AU). The primary outcome was CKD progression, defined as a ≥50% decline in eGFR or the onset of kidney failure with replacement therapy.ResultsDuring 8130 person-years of follow-up, the primary outcome occurred in 584 (30.2%) patients. In the adjusted cause-specific hazard model, CACS of 1–100 AU (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.04 to 1.61) and CACS>100 AU (HR, 1.42; 95% CI, 1.10 to 1.82) were associated with a significantly higher risk of the primary outcome. The HR associated with per 1-SD log of CACS was 1.13 (95% CI, 1.03 to 1.24). When nonfatal cardiovascular events were treated as a time-varying covariate, CACS of 1–100 AU (HR, 1.31; 95% CI, 1.07 to 1.60) and CACS>100 AU (HR, 1.46; 95% CI, 1.16 to 1.85) were also associated with a higher risk of CKD progression. The association was stronger in older patients, in those with type 2 diabetes, and in those not using antiplatelet drugs. Furthermore, patients with higher CACS had a significantly larger eGFR decline rate.ConclusionOur findings suggest that a high CACS is associated with significantly increased risk of adverse kidney outcomes and CKD progression.
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022010080
      Issue No: Vol. 33, No. 8 (2022)
       
  • The Relationship between Cerebrovascular Reactivity and Cerebral
           Oxygenation during Hemodialysis

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      Authors: Richerson, W. T; Schmit, B. D, Wolfgram, D. F.
      Pages: 1602 - 1612
      Abstract: BackgroundPatients with kidney failure treated with hemodialysis (HD) may be at risk for cerebral hypoperfusion due to HD-induced BP decline in the setting of impaired cerebral autoregulation. Cerebrovascular reactivity (CVR), the cerebrovascular response to vasoactive stimuli, may be a useful indicator of cerebral autoregulation in the HD population and identify those at risk for cerebral hypoperfusion. We hypothesize that CVR combined with intradialytic BP changes will be associated with declines in cerebral oxygenation saturation (ScO2) during HD.MethodsParticipants completed the MRI scans on a non-HD day and cerebral oximetry during HD. We measured CVR with resting-state fMRI (rs-fMRI) without a gas challenge and ScO2 saturation with near-infrared spectroscopy. Regression analysis was used to examine the relationship between intradialytic cerebral oxygen desaturation, intradialytic BP, and CVR in different gray matter regions.ResultsTwenty-six patients on HD had complete data for analysis. Sixteen patients were men, 18 had diabetes, and 20 had hypertension. Mean±SD age was 65.3±7.2 years, and mean±SD duration on HD was 11.5±9.4 months. CVR in the anterior cingulate gyrus (ACG; P=0.03, r2=0.19) and insular cortex (IC; P=0.03, r2=0.19) regions negatively correlated with decline in intradialytic ScO2. Model prediction of intradialytic ScO2 improved when including intradialytic BP change and ultrafiltration rate to the ACG rsCVR (P
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2021101353
      Issue No: Vol. 33, No. 8 (2022)
       
  • A Composite End Point of Graft Status and eGFR at 1 Year to Improve the
           Scientific Registry of Transplant Recipients Five-Tier Rating System

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      Authors: Wang, K; Deng, Y, Stewart, D, Formica, R. N.
      Pages: 1613 - 1624
      Abstract: BackgroundPerformance of kidney transplant programs in the United States is monitored and publicly reported by the Scientific Registry of Transplant Recipients (SRTR). With relatively few allograft failure events per program and increasing homogeneity in program performance, quantifying meaningful differences in program competency based only on 1-year survival rates is challenging.MethodsWe explored whether the traditional end point of allograft failure at 1 year can be improved by incorporating a measure of allograft function (i.e., eGFR) into a composite end point. We divided SRTR data from 2008 through 2018 into a training and validation set and recreated SRTR tiers, using the traditional and composite end points. The conditional 5-year deceased donor allograft survival and 5-year eGFR were then assessed using each approach.ResultsCompared with the traditional end point, the composite end point of graft failure or eGFR
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022010078
      Issue No: Vol. 33, No. 8 (2022)
       
  • On the Importance of Considering Glycosylation When Evaluating Biologic
           Therapies

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      Authors: Lemaire; M.
      Pages: 1625 - 1625
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022040461
      Issue No: Vol. 33, No. 8 (2022)
       
  • Authors Reply: "On the Importance of Considering Glycosylation when
           Evaluating Biologic Therapies"

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      Authors: Angeletti, A; Ravani, P, Bruschi, M, Ghiggeri, G. M.
      Pages: 1626 - 1626
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022050534
      Issue No: Vol. 33, No. 8 (2022)
       
  • Serum Protein-Induced Tubular Injury

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      Authors: ONeill; W. C.
      Pages: 1627 - 1627
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022050568
      Issue No: Vol. 33, No. 8 (2022)
       
  • Authors Reply: Serum Protein-induced Tubular Injury

    • Free pre-print version: Loading...

      Authors: Lidberg, K; Himmelfarb, J, Kelly, E, Akilesh, S.
      Pages: 1627 - 1628
      PubDate: 2022-07-29T10:00:25-07:00
      DOI: 10.1681/ASN.2022060657
      Issue No: Vol. 33, No. 8 (2022)
       
 
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