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  • 51.
    Peng, Xiang
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Jinan University, Guangdong, China.
    Ramström, Sofia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Hälsouniversitetet.
    Kurz, Tino
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet.
    Grenegård, Magnus
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. University of Örebro, Sweden.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    The neutrophil serine protease PR3 induces shape change of platelets via the Rho/Rho kinase and Ca2+ signaling pathways2014Inngår i: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 134, nr 2, s. 418-425Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: Proteinase 3 (PR3) is released from neutrophil azurophilic granules and exerts complex effects on the inflammatory process. PR3 catalyzes the degradation of a number of macromolecules, but the consequences on blood cells are less well defined. In the present study, the effect of PR3 on human platelets was thoroughly investigated. Methods: The experiments were performed on washed platelets freshly isolated from blood donated by healthy human volunteers. Platelets shape change and aggregation was measured on a Chrono-Log aggregometer. The phosphorylated form of MYPT1 was visualized by immunostaining. Platelet activation was further evaluated by flow cytometry. Results: PR3 induced platelet shape change but not aggregation. Flow cytometry analysis showed that PR3 induced no P-selectin expression or binding of fibrinogen to the platelets, and it did not change the activation in response to PAR1- or PAR4-activating peptides or to thrombin. Furthermore, Fura-2 measurement and immuno-blotting analysis, respectively, revealed that PR3 stimulated small intracellular Ca2+ mobilization and Thr696-specific phosphorylation of the myosin phosphatase target subunit 1 (MYPT1). Separate treatment of platelets with the Rho/Rho kinase inhibitor Y-27632 and the intracellular Ca2+ chelator BAPTA/AM reduced the shape change induced by PR3 whereas concurrent treatment completely inhibited it. Conclusion: The data shows that the neutrophil protease PR3 is a direct modulator of human platelets and causes shape change through activation of the Rho/Rho kinase and Ca2+ signaling pathways. This finding highlights an additional mechanism in the complex interplay between neutrophils and platelets.

  • 52.
    Persson, Ulf
    et al.
    Lund University, Sweden Lundby Hospital, Sweden .
    Gullstrand, Birgitta
    Lund University, Sweden .
    Pettersson, Asa
    Lund University, Sweden .
    Sturfelt, Gunnar
    Lund University, Sweden .
    Truedsson, Lennart
    Lund University, Sweden .
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    A Candidate Gene Approach to ANCA-Associated Vasculitis Reveals Links to the C3 and CTLA-4 Genes but not to the IL1-Ra And Fc gamma-RIIa Genes2013Inngår i: Kidney and Blood Pressure Research, ISSN 1420-4096, E-ISSN 1423-0143, Vol. 37, nr 6, s. 641-648Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background/Aims: The aim of the study is to search for associations between Antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) and polymorphisms in the genes of four key molecules possibly involved in different pathogenic pathways; complement C3, CTLA-4, Fc gamma-RIIa and IL1-Ra. Patients and Methods: Patients with AAV (n=105) subgrouped as microscopic polyangiitis or granulomatosis with polyangiitis (Wegeners granulomatosis) and myeloperoxidase (MPO) or proteinase 3 (PR3) ANCA positive were compared to a control group of 200 blood donors. Polymorphisms in the genes were analysed with PCR amplification of DNA. Results: The diagnosis of AAV was confirmed in the 105 cases. The gene frequency of C3F was 0.27 in the PR3-ANCA subgroup (p=0.041) compared to 0,19 in the control group. The number of patients homozygous for the shortest 86 bp allele of CTLA-4 was significantly decreased in the whole group of patients (p=0.049). No differences were evident in the Fc gamma-RIIa and IL1-Ra polymorphisms when compared to controls, neither in the whole group of patients, nor in any of the sub-groups. Conclusion: The aberrant gene frequency of the C3F allele among PR3-ANCA positive patients and the findings with the CTLA-4 polymorphism indicates that complement may be involved in pathogenesis and that T-cell activation also is of importance in these diseases.

  • 53.
    Pippias, Maria
    et al.
    University of Amsterdam, Netherlands.
    Stel, Vianda S.
    University of Amsterdam, Netherlands.
    Areste-Fosalba, Nuria
    University Hospital Virgen Macarena, Spain.
    Couchoud, Cecile
    Agence Biomed, France.
    Fernandez-Fresnedo, Gema
    University Hospital Marques de Valdecilla, Spain.
    Finne, Patrik
    University of Helsinki, Finland; Finnish Registry Kidney Disease, Finland.
    Heaf, James G.
    University of Copenhagen, Denmark.
    Hoitsma, Andries
    Radboud University of Nijmegen, Netherlands.
    De Meester, Johan
    Dutch Speaking Belgian Renal Registry NBVN, Belgium.
    Palsson, Runolfur
    Landspitali, Iceland; Fac Med, Iceland; University of Iceland, Iceland.
    Ravani, Pietro
    University of Calgary, Canada; University of Calgary, Canada.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Traynor, Jamie P.
    Meridian Court, Scotland.
    Reisaeter, Anna V.
    National Hospital Norway, Norway.
    Caskey, Fergus J.
    Southmead Hospital, England; University of Bristol, England.
    Jager, Kitty J.
    University of Amsterdam, Netherlands.
    Long-term Kidney Transplant Outcomes in Primary Glomerulonephritis: Analysis From the ERA-EDTA Registry2016Inngår i: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 100, nr 9, s. 1955-1962Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background We evaluated the 15-year kidney allograft survival in patients with primary glomerulonephritis and determined if the risk of graft loss varied with donor source within each glomerulonephritis group. Methods Using data from the European Renal Association-European Dialysis and Transplant Association Registry, Kaplan-Meier, competing risk, and Cox regression analyses were performed on adult, first kidney transplant recipients during 1991 to 2010 (n = 14 383). Follow-up was set to December 31, 2011. Adjustments for pretransplant dialysis duration, sex, country, and transplant era were made. Death-adjusted graft survival was assessed in patients with glomerulonephritis and compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native kidney disease cannot recur. Additionally, death-adjusted graft survival was compared between living and deceased donor transplants within each glomerulonephritis group. Results All glomerulonephritides had a 15-year death-adjusted graft survival probability above 55%. The 15-year risk of death-adjusted graft failure compared to ADPKD ranged from 1.17 (95% confidence interval [95% CI], 1.05-1.31) for immunoglobulin A nephropathy to 2.09 (95% CI, 1.56-2.78) for membranoproliferative glomerulonephritis type II. The expected survival benefits of living over deceased donor transplants were not present in membranoproliferative glomerulonephritis type I (adjusted hazard ratios [HRa], 1.08; 95% CI, 0.73-1.60) or type II (HRa, 0.90; 95% CI, 0.32-2.52) but present in immunoglobulin A nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0.45-1.06). Conclusions This large European study shows favorable long-term kidney graft survival in all primary glomerulonephritides, although this remains lower than graft survival in ADPKD, and confirms that the reluctance to use living donors in some primary glomerulonephritides remains unfounded. These data will further inform prospective renal transplant recipients and donors during pretransplant counselling.

  • 54.
    Rydell, Helena
    et al.
    Lund University, Sweden.
    Clyne, Naomi
    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.
    Home- or Institutional Hemodialysis? - a Matched Pair-Cohort Study Comparing Survival and Some Modifiable Factors Related to Survival2016Inngår i: Kidney and Blood Pressure Research, ISSN 1420-4096, E-ISSN 1423-0143, Vol. 41, nr 4, s. 392-401Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background/Aims: Survival for dialysis patients is poor. Earlier studies have shown better survival in home-hemodialysis (HHD). The aims of this study are to compare survival for matched patients with HHD and institutional hemodialysis (IHD) and to elucidate the effect on factors related to survival such as hyperphosphatemia, fluid overload and anemia. Methods: In this retrospective, observational study, incident patients starting HHD and IHD were matched according to sex, age, comorbidity and date of start. Survival analysis was performed both as "intention to treat" including renal transplantation and "on treatment" with censoring at the date of transplantation. Dialysis doses, laboratory parameters and prescriptions of medications were compared. Results: After matching, 41 pairs of patients, with HHD and IHD, were included. Survival among HHD patients was longer compared with IHD, median survival being 17.3 and 13.0 years (p=0.016), respectively. The "on treatment" analysis, also favoured HHD (p=0.015). HHD patients had lower phosphate, 1.5 mmol/L compared with 2.1 mmol/L (pamp;lt;0.001) and no antihypertensives and diuretics compared with 2 for IHD patients at 6 (p=0.001) and 18 months (p=0.014). There were no differences in hemoglobin or albumin. Conclusion: HHD shows better survival compared with IHD, also after controlling for patient selection. This could be caused by better phosphate and/or fluid balance associated with higher dialysis doses. (C) 2016 The Author(s) Published by S. Karger AG, Basel

  • 55.
    Rydell, Helena
    et al.
    Lund Univ, Sweden.
    Ivarsson, Kerstin
    Lund Univ, Sweden.
    Almquist, Martin
    Lund Univ, Sweden.
    Clyne, Naomi
    Lund Univ, 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. Lund Univ, Sweden.
    Fewer hospitalizations and prolonged technique survival with home hemodialysis: a matched cohort study from the Swedish Renal Registry2019Inngår i: BMC Nephrology, ISSN 1471-2369, E-ISSN 1471-2369, BMC NEPHROLOGY, Vol. 20, artikkel-id 480Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Patients on home hemodialysis (HHD) exhibit superior survival compared with patients on institutional hemodialysis (IHD) and peritoneal dialysis (PD). There is a sparsity of reports comparing morbidity between HHD and IHD or PD and none in a European population. The aim of this study is to compare morbidity between modalities in a Swedish population. Methods: The Swedish Renal Registry was used to retrieve patients starting on HHD, IHD or PD. Patients were matched according to sex, age, comorbidity and start date. The Swedish Inpatient Registry was used to determine comorbidity before starting renal replacement therapy (RRT) and hospital admissions during RRT. Dialysis technique survival was compared between HHD and PD. Results: RRT was initiated with HHD for 152 patients; these were matched with 608 patients with IHD and 456 with PD. Patients with HHD had significantly lower annual admission rate and number of days in hospital. (median 1.7 admissions; 12 days) compared with IHD (2.2; 14) and PD (2.8; 20). The annual admission rate was significantly lower for patients with HHD compared with IHD for cardiovascular diagnoses and compared with PD for infectious disease diagnoses. Dialysis technique survival was significantly longer with HHD compared with PD. Conclusions: Patients choosing HHD as initial RRT spend less time in hospital compared with patients on IHD and PD and they were more likely than PD patients, to remain on their initial modality. These advantages, in combination with better survival and higher likelihood of renal transplantation, are important incentives for promoting the use of HHD.

  • 56.
    Rydell, Helena
    et al.
    Skåne University Hospital, Sweden .
    Krutzen, Lena
    Skåne University Hospital, Sweden .
    Simonsen, Ole
    Skåne University Hospital, Sweden .
    Clyne, Naomi
    Skåne University Hospital, Sweden .
    Segelmark, Marten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Njurmedicinska kliniken US. Skåne University Hospital, Sweden .
    Excellent long time survival for Swedish patients starting home-hemodialysis with and without subsequent renal transplantations2013Inngår i: Hemodialysis International, ISSN 1492-7535, E-ISSN 1542-4758, Vol. 17, nr 4, s. 523-531Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Survival for patients on dialysis is poor. Earlier reports have indicated that home-hemodialysis is associated with improved survival but most of the studies are old and report only short-time survival. The characteristics of patient populations are often incompletely described. In this study, we report long-term survival for patients starting home-hemodialysis as first treatment and estimate the impact on survival of age, comorbidity, decade of start of home-hemodialysis, sex, primary renal disease and subsequent renal transplantation. One hundred twenty-eight patients starting home-hemodialysis as first renal replacement therapy 1971-1998 in Lund were included. Data were collected from patient files, the Swedish Renal Registry and Swedish census. Survival analysis was made as intention-to-treat analysis (including survival after transplantation) and on-dialysis-treatment analysis with patients censored at the day of transplantation. Ten-, twenty- and thirty-year survival were 68%, 36% and 18%. Survival was significantly affected by comorbidity, age and what decade the patients started home-hemodialysis. For patients younger than 60 years and with no comorbidities, the corresponding figures were 75%, 47% and 23% and a subsequent renal transplantation did not significantly influence survival. Long-term survival for patients starting home-hemodialysis is good, and improves decade by decade. Survival is significantly affected by patient age and comorbidity, but the contribution of subsequent renal transplantation was not significant for younger patients without comorbidities.

  • 57.
    Sandin, Charlotta
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland. Linköpings universitet, Medicinska fakulteten.
    Eriksson, Per
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland. Linköpings universitet, Medicinska fakulteten.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US. Linköpings universitet, Medicinska fakulteten.
    Skogh, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland. Linköpings universitet, Medicinska fakulteten.
    Kastbom, Alf
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland. Linköpings universitet, Medicinska fakulteten.
    IgA- and SIgA anti-PR3 antibodies in serum versus organ involvement and disease activity in PR3-ANCA associated vasculitis.2016Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 184, nr 2, s. 208-215Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Circulating IgA class anti-neutrophil cytoplasm antibodies (ANCA) directed against proteinase 3 (PR3) have been reported in ANCA-associated vasculitis (AAV) with mucosal involvement. However, secretory IgA (SIgA) PR3-ANCA has not been reported previously. In this study we compared serum levels of SIgA PR3-ANCA and IgA PR3-ANCA with IgG PR3-ANCA in relation to disease characteristics. Among 73 patients with AAV and PR3-ANCA at diagnosis, 84% tested positive for IgG PR3-ANCA, 47% for IgA-ANCA and 36% for SIgA PR3-ANCA at the time of sampling for the present study. IgA and IgG PR3-ANCA were similarly represented among patients with different organ manifestations, i.e. upper airway, lung or kidney at time of sampling. However, SIgA PR3-ANCA was significantly less represented among patients with upper airway involvement. During active disease, the proportions of IgA PR3-ANCA and SIgA PR3-ANCA positive patients were significantly higher as compared to inactive disease. Eight patients were prospectively sampled during 24 months from onset of active disease. In these patients, IgA PR3-ANCA and SIgA PR3-ANCA more often turned negative after remission induction as compared to IgG PR3-ANCA. Our findings suggest that serum IgA PR3-ANCA and SIgA PR3-ANCA are more closely related to disease activity in AAV as compared to IgG PR3-ANCA. Further studies are required to reveal if this has implications for disease activity monitoring. The mean number of PR3-ANCA isotypes increased along with disease activity, suggesting a global B-cell activation during active disease. This article is protected by copyright. All rights reserved.

  • 58.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Alport syndrome caused by inversion of a 21 Mb fragment of the long arm of the X-chromosome comprising exon 9 through 51 of the COL4A5 gene2005Inngår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, nr 118, s. 23-28Artikkel i tidsskrift (Fagfellevurdert)
  • 59.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Alports syndrome in Southern Sweden2005Inngår i: Clinical Nephrology, ISSN 0301-0430, Vol. Aug, nr 64(2), s. 85-90Artikkel i tidsskrift (Fagfellevurdert)
  • 60.
    Segelmark, Mårten
    Lunds Universitet.
    ANCA and IgG subclasses. In: Gross WL, ed. ANCA Associated Vasculitides1993Inngår i: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, nr 336, s. 71-75Artikkel i tidsskrift (Fagfellevurdert)
  • 61.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    ANCA antigens, proteinase 3 and myeloperoxidase, are not expressed in endothelial cells.2000Inngår i: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, nr 57, s. 1981-1990Artikkel i tidsskrift (Fagfellevurdert)
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    Segelmark, Mårten
    USiL.
    Anti-GBM antibodies inGoodpasture Syndrome: Anatomy of an epitope1997Inngår i: Nephrology, Dialysis and Transplantation, ISSN 0931-0509, E-ISSN 1460-2385, nr 12, s. 646-648Artikkel i tidsskrift (Fagfellevurdert)
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    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Antigen and epitope specificity of anti-glomerular basement membrane antiodies in patients with Goodpasture´s disease with or without anti-neutrophil cytoplasmic antibodies.2007Inngår i: J Am Soc Nephrol, Vol. Apr, nr 18(4), s. 1338-43Artikkel i tidsskrift (Fagfellevurdert)
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    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Antigen restriction and IgG subclasses among anti-GBM autoantibodies.1990Inngår i: Nephrology Dial Transplant, ISSN 1460-2385, nr 5, s. 991-996Artikkel i tidsskrift (Fagfellevurdert)
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    USiL.
    Autoantibodies againstcomponents of renal basement membranes.1997Inngår i: Neckars seminars in nephrologyArtikkel i tidsskrift (Fagfellevurdert)
  • 66.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Autoantibody response to BPI predict disease severity and outcome in cystic fibrosis2007Inngår i: J Cyst Fibros, Vol. May, nr 6(3), s. 228-33Artikkel i tidsskrift (Fagfellevurdert)
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    Segelmark, Mårten
    USiL.
    Auto-anticorps dirigéscontre les composants des membranes basales rénales1996Inngår i: Flammarion Médecine-Sciences - Actulaités Néphrologiques, s. 303-314Artikkel i tidsskrift (Fagfellevurdert)
  • 68.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Binding and inhibition of myeloperoxidase (MPO) - A major function of ceruloplasmin?1997Inngår i: Clin Exp Immunol, ISSN 0009-9104, nr 108, s. 167-174Artikkel i tidsskrift (Fagfellevurdert)
  • 69.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Circulating cytokine profile in ANCA-associated vasculitis-prediction of outcome?2004Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, Vol. Aug, nr 13(4), s. 275-83Artikkel i tidsskrift (Fagfellevurdert)
  • 70.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Clinical evaluation of a capture ELISA for detection of Proteinase 3 antineutrophil cytoplasmtic antibodies (PR3-ANCA)1998Inngår i: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, nr 53, s. 1230-1236Artikkel i tidsskrift (Fagfellevurdert)
  • 71.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Complement C3 and C4 genotypes in systemic vasculits1999Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, nr 116(2), s. 379-82Artikkel i tidsskrift (Fagfellevurdert)
  • 72.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Deficiency of the mannan-binding ledtin pathway of complement and poor outcome in cystic fibrosis: bacterial colonization may be decisive for a relationship2005Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. Feb, nr 139(2), s. 306-13Artikkel i tidsskrift (Fagfellevurdert)
  • 73.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Development and validation of a consensus methodology for the classification of the Primary Systemic Vasculitides for epidemiological studies2007Inngår i: Ann Rheum Dis, Vol. Feb, nr 66(2), s. 222-7Artikkel i tidsskrift (Fagfellevurdert)
  • 74.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Epitope mapping of anti-PR3 antibodies usin chimeric human PR3/mouse PR3 recombinant proteins.2004Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. Jan, nr 135(1), s. 164-72Artikkel i tidsskrift (Fagfellevurdert)
  • 75.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Expression of p300-truncated fragments results in the modulation of apoptosis in rat mesangial cells2000Inngår i: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, nr 57, s. 1873-1881Artikkel i tidsskrift (Fagfellevurdert)
  • 76.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Genes that link nephritis to autoantibodies and innate immunity.2011Inngår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 364, nr 7, s. 679-680Artikkel i tidsskrift (Annet vitenskapelig)
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    Segelmark, Mårten
    USiL.
    Glomerular basement membraneantibodies.1996Bok (Fagfellevurdert)
  • 78.
    Segelmark, Mårten
    Lunds Universitet.
    Glomerulonefriter. In: Njursjukdomar2008Bok (Fagfellevurdert)
  • 79.
    Segelmark, Mårten
    Lunds Universitet.
    Glomerulonefriter vid systemsjukdomar ochinfektioner.2008Bok (Fagfellevurdert)
  • 80.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Goodpasture’s diseaseIn: Schoenfeld Y, Cervera R, Gershwin ME, eds. Diagnostic Criteria for the Autoimmune Diseases2008 (oppl. 23)Bok (Fagfellevurdert)
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    Incidence and Survival rates in Wegener´s granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and Polyarteritis nodosa2009Inngår i: Rheumatology (Oxford), Vol. Dec, nr 48(12), s. 1560-5Artikkel i tidsskrift (Fagfellevurdert)
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    Increased circulating levels of proteinase 3 in patients with anti-neutrophilic cytoplasmic autoantibodies-associated systemic vasculitis in remission2003Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. Mar, nr 131(3), s. 528-35Artikkel i tidsskrift (Fagfellevurdert)
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    Increased expression of the secretory leukocyte proteinbase inhibitor in Wegener´s granulomatosis2003Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, Vol. Jan, nr 131(1), s. 190-6Artikkel i tidsskrift (Fagfellevurdert)
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    Increased Membrane Expression and Plasma Concentrations of Proteianse 3 (PR3) in Vasculitis is not a Consequence of the -564 A/G Gene Promotor Polymorphism2006Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. Jul, nr 145(1), s. 63-70Artikkel i tidsskrift (Fagfellevurdert)
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    Increased monocyte transcription of the proteianse 3 gene2005Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. Jul, nr 141(1), s. 174-82Artikkel i tidsskrift (Fagfellevurdert)
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    Abstract [en]

    n/a

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    Proteinase 3 and CD177 are expressed on the plasma membrane of the same subset of neutrophils.2007Inngår i: J Leukoc Biol., Vol. Feb, nr 81(2), s. 458-64Artikkel i tidsskrift (Fagfellevurdert)
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    Pseudomonas induced lung damage in systic fibrosis correlate to BPI-autoantibodies.2003Inngår i: Clinical and Experimental Rheumatology, ISSN 0392-856X, E-ISSN 1593-098X, nr 21;6;32, s. S095-S100Artikkel i tidsskrift (Fagfellevurdert)
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