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  • 1.
    Chen, Yun
    et al.
    Department of Physiology, University of Gothenburg, Gothenburg, Sweden, Department of Physiology, University of Gothenburg, Box 432, SE 405 30 Gothenburg, Sweden.
    Lasaitiene, Daina
    Department of Physiology, University of Gothenburg, Gothenburg, Sweden.
    Gabrielsson, Britt G.
    RCEM, Department of Internal Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Carlsson, Lena M. S.
    RCEM, Department of Internal Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Billig, Håkan
    Department of Physiology, University of Gothenburg, Gothenburg, Sweden.
    Carlsson, Björn
    RCEM, Department of Internal Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Marcussen, Niels
    Institute of Pathology, Aarhus Kommunehospital, Aarhus, Denmark.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, KC - Kirurgi- och onkologicentrum, Onkologiska kliniken.
    Friberg, Peter
    Department of Physiology, University of Gothenburg, Gothenburg, Sweden.
    Neonatal Losartan Treatment Suppresses Renal Expression of Molecules Involved in Cell-Cell and Cell-Matrix Interactions2004Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 15, nr 5, s. 1232-1243Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Lack of neonatal angiotensin II type I receptor (AT1) stimulation produces renal abnormalities characterized by papillary atrophy and impaired urinary concentrating ability, but the mechanisms involved are still unclear. DNA microarray was used to identify genes that are differentially expressed in renal medulla in response to neonatal treatment with AT 1 receptor antagonist losartan (30 mg/kg per d), which commenced within 24 h after birth. The data showed that losartan treatment for 48 h downregulated 68 genes, ~30% of which encode various components of cytoskeleton and cytoskeleton-associated proteins, extracellular matrix, and enzymes involved in extracellular matrix maturation or turnover. With the use of immunohistochemistry and Western immunoblot, the microarray data were confirmed and it was demonstrated that losartan suppressed renal expression of syndecan 2, a-smooth muscle actin, MHC class II, and leukocyte type 12-lipoxygenase by day 4. In addition, losartan inhibited medullary expression of integrin a6 and caused relocalization of integrins a6 and a3. Moreover, losartan inhibited cell proliferation in medullary tubules by day 9, as detected by Ki-67 immunostaining. This study provides new data supporting the contention that a lack of AT1 receptor stimulation results in abnormal matrix assembly, disturbed cell-cell and cell-matrix interactions, and subsequent abnormal tubular maturation. Moreover, regulation of the expression of leukocyte type 12-lipoxygenase and a-smooth muscle actin by the renin-angiotensin system in the immature kidney adds new knowledge toward the understanding of renal vascular development.

  • 2.
    Grams, Morgan E
    et al.
    Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
    Sang, Yingying
    Departments of Epidemiology, Baltimore, Maryland, USA.
    Coresh, Josef
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
    Ballew, Shoshana H
    Departments of Epidemiology, Baltimore, Maryland, USA.
    Matsushita, Kunihiro
    Departments of Epidemiology, Baltimore, Maryland, USA.
    Levey, Andrew S
    Departments of Epidemiology, Baltimore, Maryland, USA.
    Greene, Tom H
    5Division of Clinical Epidemiology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
    Molnar, Miklos Z
    6Division of Nephrology, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
    Szabó, Zoltán
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Kalantar-Zadeh, Kamyar
    University of California Irvine Medical Center, Irvine, California, USA.
    Kovesdy, Csaba P
    University of Tennessee Health Science Center, Memphis, Tennessee, USA.
    Candidate Surrogate End Points for ESRD after AKI2016Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 27, nr 9, s. 2851-2859Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AKI, a frequently transient condition, is not accepted by the US Food and Drug Association as an end point for drug registration trials. We assessed whether an intermediate-term change in eGFR after AKI has a sufficiently strong relationship with subsequent ESRD to serve as an alternative end point in trials of AKI prevention and/or treatment. Among 161,185 United States veterans undergoing major surgery between 2004 and 2011, we characterized in-hospital AKI by Kidney Disease Improving Global Outcomes creatinine criteria and decline in eGFR from prehospitalization to postdischarge time points and quantified associations of these values with ESRD and mortality over a median of 3.8 years. An eGFR decline of ≥30% at 30, 60, and 90 days after discharge occurred in 3.1%, 2.5%, and 2.6%, of survivors without AKI and 15.9%, 12.2%, and 11.7%, of survivors with AKI. For patients with in-hospital AKI compared with those with no AKI and stable eGFR, a 30% decline in eGFR at 30, 60, and 90 days after discharge demonstrated adjusted hazard ratios (95% confidence intervals) of ESRD of 5.60 (4.06 to 7.71), 6.42 (4.76 to 8.65), and 7.27 (5.14 to 10.27), with corresponding estimates for 40% decline in eGFR of 6.98 (5.21 to 9.35), 8.03 (6.11 to 10.56), and 10.95 (8.10 to 14.82). Risks for mortality were smaller but consistent in direction. A 30%-40% decline in eGFR after AKI could be a surrogate end point for ESRD in trials of AKI prevention and/or treatment, but additional trial evidence is needed.

  • 3.
    Hermsen, Meyke
    et al.
    Radboud Univ Nijmegen, Netherlands.
    de Bel, Thomas
    Radboud Univ Nijmegen, Netherlands.
    den Boer, Marjolijn
    Radboud Univ Nijmegen, Netherlands.
    Steenbergen, Eric J.
    Radboud Univ Nijmegen, Netherlands.
    Kers, Jesper
    Univ Amsterdam, Netherlands; Univ Amsterdam, Netherlands; Ragon Inst Massachusetts Gen Hosp Massachusetts I, MA USA.
    Florquin, Sandrine
    Univ Amsterdam, Netherlands.
    Roelofs, Joris J. T. H.
    Univ Amsterdam, Netherlands.
    Stegall, Mark D.
    Mayo Clin, MN USA; Mayo Clin, MN USA.
    Alexander, Mariam P.
    Mayo Clin, MN USA; Mayo Clin, MN USA.
    Smith, Byron H.
    Mayo Clin, MN USA; Mayo Clin, MN USA.
    Smeets, Bart
    Radboud Univ Nijmegen, Netherlands.
    Hilbrands, Luuk B.
    Radboud Univ Nijmegen, Netherlands.
    van der Laak, Jeroen
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Radboud Univ Nijmegen, Netherlands.
    Deep Learning-Based Histopathologic Assessment of Kidney Tissue2019Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 30, nr 10, s. 1968-1979Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The development of deep neural networks is facilitating more advanced digital analysis of histopathologic images. We trained a convolutional neural network for multiclass segmentation of digitized kidney tissue sections stained with periodic acid-Schiff (PAS). Methods We trained the network using multiclass annotations from 40 whole-slide images of stained kidney transplant biopsies and applied it to four independent data sets. We assessed multiclass segmentation performance by calculating Dice coefficients for ten tissue classes on ten transplant biopsies from the Radboud University Medical Center in Nijmegen, The Netherlands, and on ten transplant biopsies from an external center for validation. We also fully segmented 15 nephrectomy samples and calculated the networks glomerular detection rates and compared network-based measures with visually scored histologic components (Banff classification) in 82 kidney transplant biopsies. Results The weighted mean Dice coefficients of all classes were 0.80 and 0.84 in ten kidney transplant biopsies from the Radboud center and the external center, respectively. The best segmented class was "glomeruli" in both data sets (Dice coefficients, 0.95 and 0.94, respectively), followed by "tubuli combined" and "interstitium." The network detected 92.7% of all glomeruli in nephrectomy samples, with 10.4% false positives. In whole transplant biopsies, the mean intraclass correlation coefficient for glomerular counting performed by pathologists versus the network was 0.94. We found significant correlations between visually scored histologic components and network-based measures. Conclusions This study presents the first convolutional neural network for multiclass segmentation of PAS-stained nephrectomy samples and transplant biopsies. Our network may have utility for quantitative studies involving kidney histopathology across centers and provide opportunities for deep learning applications in routine diagnostics.

  • 4.
    Jayne, David R. W.
    et al.
    Addenbrookes Hospital, England.
    Bruchfeld, Annette N.
    Karolinska University Hospital, Sweden.
    Harper, Lorraine
    University of Birmingham, England.
    Schaier, Matthias
    Heidelberg University, Germany.
    Venning, Michael C.
    Manchester Royal Infirm, England.
    Hamilton, Patrick
    Manchester Royal Infirm, England.
    Burst, Volker
    Uniklin Cologne, Germany.
    Grundmann, Franziska
    Uniklin Cologne, Germany.
    Jadoul, Michel
    Clin University of St Luc, Belgium.
    Szombati, Istvan
    Budai Irgalmasrendi Korhaz, Hungary.
    Tesar, Vladimir
    Charles University of Prague, Czech Republic.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Potarca, Antonia
    ChemoCentryx Inc, CA USA.
    Schall, Thomas J.
    ChemoCentryx Inc, CA USA.
    Bekker, Pirow
    ChemoCentryx Inc, CA USA.
    Randomized Trial of C5a Receptor Inhibitor Avacopan in ANCA-Associated Vasculitis2017Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 28, nr 9, s. 2756-2767Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Alternative C activation is involved in the pathogenesis of ANCA-associated vasculitis. However, glucocorticoids used as treatment contribute to the morbidity and mortality of vasculitis. We determined whether avacopan (CCX168), an orally administered, selective C5a receptor inhibitor, could replace oral glucocorticoids without compromising efficacy. In this randomized, placebo-controlled trial, adults with newly diagnosed or relapsing vasculitis received placebo plus prednisone starting at 60 mg daily (control group), avacopan (30 mg, twice daily) plus reduced-dose prednisone (20 mg daily), or avacopan (30 mg, twice daily) without prednisone. All patients received cyclophosphamide or rituximab. The primary efficacy measure was the proportion of patients achieving a amp;gt;= 50% reduction in Birmingham Vasculitis Activity Score by week 12 and no worsening in any body system. We enrolled 67 patients, 23 in the control and 22 in each of the avacopan groups. Clinical response at week 12 was achieved in 14 of 20 (70.0%) control patients, 19 of 22 (86.4%) patients in the avacopan plus reduced-dose prednisone group (difference from control 16.4%; two-sided 90% confidence limit, -4.3% to 37.1%; P=0.002 for noninferiority), and 17 of 21 (81.0%) patients in the avacopan without prednisone group (difference from control 11.0%; two-sided 90% confidence limit, -11.0% to 32.9%; P=0.01 for noninferiority). Adverse events occurred in 21 of 23 (91%) control patients, 19 of 22 (86%) patients in the avacopan plus reduced-dose prednisone group, and 21 of 22 (96%) patients in the avacopan without prednisone group. In conclusion, C5a receptor inhibition with avacopan was effective in replacing high-dose glucocorticoids in treating vasculitis.

  • 5.
    Mossberg, Maria
    et al.
    Lund University, Sweden.
    Stahl, Anne-lie
    Lund University, Sweden.
    Kahn, Robin
    Lund University, Sweden.
    Kristoffersson, Ann-Charlotte
    Lund University, Sweden.
    Tati, Ramesh
    Lund University, Sweden.
    Heijl, Caroline
    Lund University, Sweden.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Leeb-Lundberg, L. M. Fredrik
    Lund University, Sweden.
    Karpman, Diana
    Lund University, Sweden.
    Cl-Inhibitor Decreases the Release of Vasculitis-Like Chemotactic Endothelial Microvesicles2017Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 28, nr 8, s. 2472-2481Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The kinin system is activated during vasculitis and may contribute to chronic inflammation. C1-inhibitor is the main inhibitor of the kinin system. In this study, we investigated the presence of the kinin B1 receptor on endothelial microvesicles and its contribution to the inflammatory process. Compared with controls (n=15), patients with acute vasculitis (n=12) had markedly higher levels of circulating endothelial micro vesicles, identified by flow cytometry analysis, and significantly more microvesicles that were positive for the kinin B1 receptor (Pamp;lt;0.001). Compared with microvesicles from wild-type cells, B1 receptor-positive microvesicles derived from transfected human embryonic kidney cells induced a significant neutrophil chemotactic effect, and a B1 receptor antagonist blocked this effect. Likewise, patient plasma induced neutrophil chemotaxis, an effect decreased by reduction of microvesicle levels and by blocking the B1 receptor. We used a perfusion system to study the effect of patient plasma (n=6) and control plasma (n=6) on the release of microvesicles from glomerular endothelial cells. Patient samples induced the release of significantly more B1 receptor-positive endothelial microvesicles than control samples, an effect abrogated by reduction of the microvesicles in the perfused samples. Perfusion of C1-inhibitor depleted plasma over glomerular endothelial cells promoted excessive release of B1 receptor-positive endothelial microvesicles compared with normal plasma, an effect significantly decreased by addition of C1-inhibitor or B1 receptor-antagonist. Thus, B1 receptor-positive endothelial microvesicles may contribute to chronic inflammation by inducing neutrophil chemotaxis, and the reduction of these microvesicles by C1-inhibitor should be explored as a potential treatment for neutrophil-induced inflammation.

  • 6.
    Nordquist, Lina
    et al.
    Uppsala University, Sweden.
    Friederich-Persson, Malou
    Uppsala University, Sweden.
    Fasching, Angelica
    Uppsala University, Sweden.
    Liss, Per
    Uppsala University, Sweden.
    Shoji, Kumi
    University of Tokyo, Japan.
    Nangaku, Masaomi
    University of Tokyo, Japan.
    Hansell, Peter
    Uppsala University, Sweden.
    Palm, Fredrik
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Uppsala University, Sweden.
    Activation of Hypoxia-Inducible Factors Prevents Diabetic Nephropathy2015Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 26, nr 2, s. 328-338Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Hyperglycemia results in increased oxygen consumption and decreased oxygen tension in the kidney. We tested the hypothesis that activation of hypoxia-inducible factors (HIFs) protects against diabetes-induced alterations in oxygen metabolism and kidney function. Experimental groups consisted of control and streptozotocin-induced diabetic rats treated with or without chronic cobalt chloride to activate HIFs. We elucidated the involvement of oxidative stress by studying the effects of acute administration of the superoxide dismutase mimetic tempol. Compared with controls, diabetic rats displayed tissue hypoxia throughout the kidney, glonnerular hyperfiltration, increased oxygen consumption, increased total mitochondrial leak respiration, and decreased tubular sodium transport efficiency. Diabetic kidneys showed proteinuria and tubulointerstitial damage. Cobalt chloride activated HIFs, prevented the diabetes-induced alterations in oxygen metabolism, mitochondrial leak respiration, and kidney function, and reduced proteinuria and tubulointerstitial damage. The beneficial effects of tempol were less pronounced after activation of HIFs, indicating improved oxidative stress status. In conclusion, activation of HIFs prevents diabetes-induced alteration in kidney oxygen metabolism by normalizing glomerular filtration, which reduces tubular electrolyte load, preventing mitochondrial leak respiration and improving tubular transport efficiency. These improvements could be related to reduced oxidative stress and account for the reduced proteinuria and tubulointerstitial damage. Thus, pharnnacologic activation of the HIF system may prevent development of diabetic nephropathy.

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