Publications
562 results found
Cook HT, 2013, Complement and kidney disease, CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, Vol: 22, Pages: 295-301, ISSN: 1062-4821
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- Citations: 16
Carlin LM, Stamatiades EG, Auffray C, et al., 2013, <i>Nr4a1</i>-Dependent Ly6C<SUP>low</SUP> Monocytes Monitor Endothelial Cells and Orchestrate Their Disposal, CELL, Vol: 153, Pages: 362-375, ISSN: 0092-8674
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- Citations: 521
Willicombe M, Roufosse C, Brookes P, et al., 2013, Potential Importance of 3 Year Surveillance Biopsies in Renal Transplantation, 13th American Transplant Congress (ATC), Publisher: WILEY-BLACKWELL, Pages: 41-42, ISSN: 1600-6135
Mcdaid JP, Tanna A, Bhangal G, et al., 2013, The role of quantitative trait loci (QTL) in the pathogenesis of experimental autoimmune vasculitis (EAV), Publisher: MASSON EDITEUR, Pages: 688-688, ISSN: 0755-4982
McLean A, Chan K, Galliford J, et al., 2013, 1-Year Outcomes of a Prospective, Open Label, Randomized, Controlled Trial of Standard vs Extended-Release Tacrolimus as Maintenance Monotherapy in Kidney Transplantation after Alemtuzumab Induction with Rapid Steroid Withdrawal (TAESR Trial)., 13th American Transplant Congress (ATC), Publisher: WILEY-BLACKWELL, Pages: 358-358, ISSN: 1600-6135
McLean A, Dominy K, De Kort H, et al., 2013, Intra-Graft Expression of Transcripts for Endothelial Activation and NK Cell Markers, Detected by Real-Time qPCR, Is Associated with the Presence of Donor Specific Antibodies, and Identifies Kidney Transplants at Risk of Failure, 13th American Transplant Congress (ATC), Publisher: WILEY-BLACKWELL, Pages: 142-142, ISSN: 1600-6135
Willicombe M, Roufosse C, Brookes P, et al., 2013, CD68 Positive Glomerulitis Predicts the Development of Transplant Glomerulopathy in Patients with Cellular Rejection, 13th American Transplant Congress (ATC), Publisher: WILEY-BLACKWELL, Pages: 43-44, ISSN: 1600-6135
Goekmen MR, Cosyns J-P, Arlt VM, et al., 2013, The Epidemiology, Diagnosis, and Management of Aristolochic Acid Nephropathy A Narrative Review, ANNALS OF INTERNAL MEDICINE, Vol: 158, Pages: 469-477, ISSN: 0003-4819
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- Citations: 112
Lote H, Mannion E, Cook T, et al., 2013, Adenocarcinoma of the seminal vesicles complicated by antineutrophil cytoplasmic antibody vasculitis: a case report and review of the literature., J Med Case Rep, Vol: 7, ISSN: 1752-1947
INTRODUCTION: Adenocarcinoma of the seminal vesicles is a very rare malignancy, with less than 100 cases reported worldwide. It is documented to have a poor prognosis, with the majority of patients developing metastatic disease, most commonly in the prostate, bladder and rectum. Currently there is no standard treatment for metastatic disease and the limited reports of treatment with radiotherapy, chemotherapy and hormonal (anti-androgenic) therapy show that they are generally of modest benefit. The association between malignancy and an increased risk of autoimmune vasculitis has been demonstrated in a number of malignancies, but to date there have been no documented cases of adenocarcinoma of the seminal vesicles associated with anti-neutrophil cytoplasmic antibody vasculitis. CASE PRESENTATION: In this report we describe the case of a 55-year-old Caucasian man with metastatic adenocarcinoma of the seminal vesicles. He previously had received chemotherapy treatment for advanced testicular cancer and later presented with hemospermia. He subsequently developed c-antineutrophil cytoplasmic antibody vasculitis requiring intensive immunosuppression and renal dialysis. CONCLUSION: Adenocarcinoma of the seminal vesicles is a rare diagnosis and our case is more unusual in that our patient previously had chemotherapy treatment for advanced testicular cancer and went on to develop severe antineutrophil cytoplasmic antibody vasculitis when diagnosed with metastatic seminal vesicle cancer. This case illustrates that autoimmune vasculitis can occur in any patient with malignancy and an early referral to the renal team combined with renal biopsy can assist in the earlier diagnosis and more successful management of these rare events. This case should be of interest to oncologists, renal physicians, urologists and general physicians who encounter patients presenting with hemospermia or vasculitis.
Pepper RJ, Hamour S, Chavele KM, et al., 2013, Calprotectin has a pathogenic pro-inflammatory role in anti-neutrophil cytoplasmic antibody associated vasculitis and glomerulonephritis, Spring Meeting for Clinician Scientists in Training, Publisher: ELSEVIER SCIENCE INC, Pages: 86-86, ISSN: 0140-6736
Fossati-Jimack L, Ling GS, Cortini A, et al., 2013, Phagocytosis Is the Main CR3-Mediated Function Affected by the Lupus-Associated Variant of CD11b in Human Myeloid Cells, PLOS ONE, Vol: 8, ISSN: 1932-6203
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- Citations: 50
Pepper RJ, Hamour S, Chavele KM, et al., 2013, Leukocyte and serum S100A8/S100A9 expression reflects disease activity in ANCA-associated vasculitis and glomerulonephritis, Kidney International, Vol: 83, Pages: 1150-1158, ISSN: 1523-1755
Antineutrophil cytoplasm antibody (ANCA)–associatedvasculitis (AAV) commonly results in glomerulonephritis, inwhich neutrophils and monocytes have important roles.The heterodimer calprotectin (S100A8/S100A9, mrp8/14)is a Toll-like receptor-4 ligand found in neutrophils andmonocytes and is elevated in inflammatory conditions. Byimmunohistochemistry of renal biopsies, patients with focalor crescentic glomerular lesions were found to have thehighest expression of calprotectin and those with scleroticthe least. Serum levels of calprotectin as measured by ELISAwere elevated in patients with active AAV and the levelsdecreased but did not normalize during remission,suggesting subclinical inflammation. Calprotectin levels inpatients with limited systemic disease increased followingtreatment withdrawal and were significantly elevated inpatients who relapsed compared with those who did not. Asassessed by flow cytometry, patients with AAV had highermonocyte and neutrophil cell surface calprotectin expressionthan healthy controls, but this was not associated withaugmented mRNA expression in CD14þ monocytes orCD16þ neutrophils. Thus, serum calprotectin is a potentialdisease biomarker in patients with AAV, and may have a rolein disease pathogenesis.
Hull RP, Srivastava PK, D'Souza Z, et al., 2013, Combined ChIP-Seq and transcriptome analysis identifies AP-1/JunD as a primary regulator of oxidative stress and IL-1β synthesis in macrophages, BMC GENOMICS, Vol: 14, ISSN: 1471-2164
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- Citations: 20
Sayed R, Cook HT, Palmer A, 2013, Recognizing isolated IgG4-related nephropathy., CKJ: Clinical Kidney Journal, Vol: 6, Pages: 433-435, ISSN: 2048-8513
IgG4-related tubulointerstitial nephritis is an uncommon cause of renal impairment. It has been associated with dysfunction in a number of other organs giving rise to the term IgG4-related systemic disease; organ involvement can occur metachronously, hence, making it more difficult to identify patients. The exact cause of this condition remains unknown. Here, we present a case of isolated renal involvement which demonstrates how particular biochemical, radiological and histopathological changes should raise the suspicion of IgG4-related nephropathy, especially when there is an absence of clues from any other organ.
de Kort H, Willicombe M, Brookes P, et al., 2013, Microcirculation Inflammation Associates With Outcome in Renal Transplant Patients With De Novo Donor-Specific Antibodies, AMERICAN JOURNAL OF TRANSPLANTATION, Vol: 13, Pages: 485-492, ISSN: 1600-6135
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- Citations: 85
Lawrence C, Willicombe M, Brookes PA, et al., 2013, Preformed Complement-Activating Low-Level Donor-Specific Antibody Predicts Early Antibody-Mediated Rejection in Renal Allografts, TRANSPLANTATION, Vol: 95, Pages: 341-346, ISSN: 0041-1337
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- Citations: 47
Sharp PEH, Martin-Ramirez J, Mangsbo SM, et al., 2013, FcγRIIb on Myeloid Cells and Intrinsic Renal Cells Rather than B Cells Protects from Nephrotoxic Nephritis, JOURNAL OF IMMUNOLOGY, Vol: 190, Pages: 340-348, ISSN: 0022-1767
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- Citations: 15
Ruseva MM, Vernon KA, Lesher AM, et al., 2013, Loss of Properdin Exacerbates C3 Glomerulopathy Resulting from Factor H Deficiency, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 24, Pages: 43-52, ISSN: 1046-6673
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- Citations: 58
Deplano S, Cook HT, Russell R, et al., 2013, P2X7 receptor-mediated Nlrp3-inflammasome activation is a genetic determinant of macrophage-dependent crescentic glomerulonephritis, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 93, Pages: 127-134, ISSN: 0741-5400
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- Citations: 44
Deltas C, Gale D, Cook T, et al., 2013, C3 Glomerulonephritis/CFHR5 Nephropathy Is an Endemic Disease in Cyprus: Clinical and Molecular Findings in 21 Families, COMPLEMENT THERAPEUTICS, Editors: Lambris, Holers, Ricklin, Publisher: SPRINGER-VERLAG BERLIN, Pages: 189-196, ISBN: 978-1-4614-4118-2
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- Citations: 19
Mueller M, Barros P, Witherden AS, et al., 2012, Genomic Pathology of SLE-Associated Copy-Number Variation at the FCGR2C/FCGR3B/FCGR2B Locus, Am J Hum Genet
Reduced FCGR3B copy number is associated with increased risk of systemic lupus erythematosus (SLE). The five FCGR2/FCGR3 genes are arranged across two highly paralogous genomic segments on chromosome 1q23. Previous studies have suggested mechanisms for structural rearrangements at the FCGR2/FCGR3 locus and have proposed mechanisms whereby altered FCGR3B copy number predisposes to autoimmunity, but the high degree of sequence similarity between paralogous segments has prevented precise definition of the molecular events and their functional consequences. To pursue the genomic pathology associated with FCGR3B copy-number variation, we integrated sequencing data from fosmid and bacterial artificial chromosome clones and sequence-captured DNA from FCGR3B-deleted genomes to establish a detailed map of allelic and paralogous sequence variation across the FCGR2/FCGR3 locus. This analysis identified two highly paralogous 24.5 kb blocks within the FCGR2C/FCGR3B/FCGR2B locus that are devoid of nonpolymorphic paralogous sequence variations and that define the limits of the genomic regions in which nonallelic homologous recombination leads to FCGR2C/FCGR3B copy-number variation. Further, the data showed evidence of swapping of haplotype blocks between these highly paralogous blocks that most likely arose from sequential ancestral recombination events across the region. Functionally, we found by flow cytometry, immunoblotting and cDNA sequencing that individuals with FCGR3B-deleted alleles show ectopic presence of FcγRIIb on natural killer (NK) cells. We conclude that FCGR3B deletion juxtaposes the 5'-regulatory sequences of FCGR2C with the coding sequence of FCGR2B, creating a chimeric gene that results in an ectopic accumulation of FcγRIIb on NK cells and provides an explanation for SLE risk associated with reduced FCGR3B gene copy number.
Fragiadaki M, Hill N, Hewitt R, et al., 2012, Hyperglycemia Causes Renal Cell Damage via CCN2-Induced Activation of the TrkA Receptor: Implications for Diabetic Nephropathy, Diabetes, Vol: 61, Pages: 2280-2288, ISSN: 0012-1797
CCN2, a secreted profibrotic protein, is highly expressed in diabetic nephropathy (DN) and implicated in its pathogenesis; however, the actions of CCN2 in DN remain elusive. We previously demonstrated that CCN2 triggers signaling via tropomyosin receptor kinase A (TrkA). Trace expression of TrkA is found in normal kidneys, but its expression is elevated in several nephropathies; yet its role in DN is unexplored. In this study we show de novo expression of TrkA in human and murine DN. We go on to study the molecular mechanisms leading to TrkA activation and show that it involves hypoxia, as demonstrated by ischemia–reperfusion injury and in vitro experiments mimicking hypoxia, implicating hypoxia as a common pathway leading to disease. We also expose renal cells to hyperglycemia, which led to TrkA phosphorylation in mesangial cells, tubular epithelial cells, and podocytes but not in glomerular endothelial cells and renal fibroblasts. In addition, we report that hyperglycemia caused an induction of phosphorylated extracellular signal–related kinase 1/2 and Snail1 that was abrogated by silencing of TrkA or CCN2 using small interfering RNA. In conclusion, we provide novel evidence that TrkA is activated in diabetic kidneys and suggest that anti-TrkA therapy may prove beneficial in DN.
Huang FP, Sattler S, Ling GS, et al., 2012, An essential protective role of IL-10-producing regulatory B cells against IL-33-mediated mucosal inflammation, European Congress of Immunology, Publisher: WILEY-BLACKWELL, Pages: 77-77, ISSN: 0019-2805
Roufosse CA, Shore I, Moss J, et al., 2012, Peritubular Capillary Basement Membrane Multilayering on Electron Microscopy: A Useful Marker of Early Chronic Antibody-Mediated Damage, TRANSPLANTATION, Vol: 94, Pages: 269-274, ISSN: 0041-1337
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- Citations: 20
Lewis MJ, Malik TH, Fossati-Jimack L, et al., 2012, Distinct roles for complement in glomerulonephritis and atherosclerosis revealed in mice with a combination of lupus and hyperlipidemia, ARTHRITIS AND RHEUMATISM, Vol: 64, Pages: 2707-2718, ISSN: 0004-3591
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- Citations: 17
Willicombe M, Brookes P, Sergeant R, et al., 2012, De Novo DQ Donor-Specific Antibodies Are Associated With a Significant Risk of Antibody-Mediated Rejection and Transplant Glomerulopathy, TRANSPLANTATION, Vol: 94, Pages: 172-177, ISSN: 0041-1337
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- Citations: 189
Vernon KA, de Jorge EG, Hall AE, et al., 2012, Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H-Related Protein 5 Deficiency, AMERICAN JOURNAL OF KIDNEY DISEASES, Vol: 60, Pages: 121-125, ISSN: 0272-6386
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- Citations: 70
Lawrence C, Cook HT, Lightstone L, 2012, Seasonal relapsing minimal change disease: a novel strategy for avoiding long-term immunosuppression., Case Rep Nephrol Urol, Vol: 2, Pages: 102-107
BACKGROUND: We describe the case of a young woman with seasonal allergic rhinitis who presented with signs of a lower respiratory tract infection, acute renal impairment and the nephrotic syndrome, demonstrated on biopsy to be due to minimal change disease (MCD) with acute tubular injury. Following initiation of high-dose corticosteroids, her respiratory symptoms and renal impairment improved, and the nephrotic syndrome went rapidly into remission, but relapsed, off treatment, in a seasonal fashion. MANAGEMENT: In view of significant side effects related to corticosteroids, relapses were treated with the calcineurin inhibitor tacrolimus with excellent effect, but the patient was keen to avoid the complications of medium-term immunosuppression and so the drug was weaned early. She relapsed for the second time, whilst off tacrolimus, at the same time of year as at her initial presentation. In subsequent years we have successfully managed this patient with seasonal relapsing MCD with seasonal prophylactic tacrolimus therapy. DISCUSSION: We discuss the natural history of MCD and treatment options and demonstrate the utility of a clear understanding of the natural history of the condition in order to predict disease relapse and tailor therapy to the individual patient.
Bellur SS, Troyanov S, Cook HT, et al., 2012, Immunostaining findings in IgA nephropathy: correlation with histology and clinical outcome in the Oxford Classification patient cohort Reply, NEPHROLOGY DIALYSIS TRANSPLANTATION, Vol: 27, Pages: 2999-3000, ISSN: 0931-0509
Cattran DC, Feehally J, Cook HT, et al., 2012, Kidney disease: Improving global outcomes (KDIGO) glomerulonephritis work group. KDIGO clinical practice guideline for glomerulonephritis, Kidney International Supplements, Vol: 2, Pages: 139-274, ISSN: 2157-1724
The 2011 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Glomerulonephritis (GN) aims to assist practitioners caring for adults and children with GN. Guideline development followed an explicit process of evidence review and appraisal. The guideline contains chapters on various glomerular diseases: steroid-sensitive nephrotic syndrome in children; steroid-resistant nephrotic syndrome in children; minimal-change disease; idiopathic focal segmental glomerulosclerosis; idiopathic membranous nephropathy; membranoproliferative glomerulonephritis; infection-related glomerulonephritis; IgA nephropathy; Henoch-Schönlein purpura nephritis; lupus nephritis; pauci-immune focal and segmental necrotizing glomerulonephritis; and anti-lomerular basement membrane antibody glomerulonephritis. Treatment approaches are addressed in each chapter and guideline recommendations are based on systematic reviews of relevant trials. Appraisal of the quality of the evidence and the strength of recommendations followed the GRADE approach. Limitations of the evidence are discussed and specific suggestions are provided for future research.
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