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2. Klinische immunologie

Author

Berge, R.J.M. ten, Hamann, D., Hack, C.E., Daele, P.L.A. van, Stehouwer, C.D.A., editor, and Koopmans, R.P., editor

Published
2017
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4. List of contributors

Author

Campbell, Jerry L., primary, Cheng, Yi-Hsien, additional, Chou, Wei-Chun, additional, Clewell, H.J., additional, Covington, Tammie R., additional, Efremenko, A.Y., additional, Ellison, Corie A., additional, Fisher, Jeffrey W., additional, Gearhart, Jeffery M., additional, Hack, C.E., additional, Haddad, Sami, additional, Hewitt, N., additional, Housand, Conrad, additional, Kabadi, Shruti V., additional, Li, Miao, additional, Lin, Zhoumeng, additional, Mehta, Darshan, additional, Najjar, A., additional, Nong, Andy, additional, Pendse, S.N., additional, Ruark, Christopher, additional, Schepky, A., additional, Sweeney, Lisa M., additional, Yang, Xiaoxia, additional, and Yoon, Miyoung, additional

Published
2020
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6. The PROCARE consortium: Toward an improved allocation strategy for kidney allografts

Author

Otten, H.G., Joosten, I., Allebes, W.A., van der Meer, A., Hilbrands, L.B., Baas, M., Spierings, E., Hack, C.E., van Reekum, F., van Zuilen, A.D., Verhaar, M.C., Bots, M.L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G., Lambeck, A.J., Bungener, L.B., Roozendaal, C., Tilanus, M.G.J., Vanderlocht, J., Voorter, C.E., Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M., van Ittersum, F., Nurmohamed, A., Lardy, N.M., Swelsen, W.T., van Donselaar-van der Pant, K.A.M.I., van der Weerd, N.C., ten Berge, I.J.M., Bemelman, F.J., Hoitsma, A.J., de Fijter, J.W., Betjes, M.G.H., Roelen, D.L., and Claas, F.H.J.

Published
2014
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13. Clusterin: a protective mediator for ischemic cardiomyocytes?

Author

Krijnen, P.A.J., Cillessen, S.A.G.M., Manoe, R., Muller, A., Visser, C.A., Meijer, C.J.L.M., Musters, R.J.P., Hack, C.E., Aarden, L.A., and Niessen H.W.M.

Subjects
Heart attack -- Research, Heart attack -- Care and treatment, Ischemia -- Research, Biological sciences
Abstract

We examined the relationship between clusterin and activated complement in human heart infarction and evaluated the effect of this protein on ischemic rat neonatal cardiomyoblasts (H9c2) and isolated adult ventricular rat cardiomyocytes as in vitro models of acute myocardial infarction. Clusterin protects cells by inhibiting complement and colocalizes with complement on jeopardized human cardiomyocytes after infarction. The distribution of clusterin and complement factor C3d was evaluated in the infarcted human heart. We also analyzed the protein expression of clusterin in ischemic H9c2 cells. The binding of endogenous and purified human clusterin on H9c2 cells was analyzed by flow cytometry. Furthermore, the effect of clusterin on the viability of ischemically challenged H9c2 cells and isolated adult ventricular rat cardiomyocytes was analyzed. In human myocardial infarcts, clusterin was found on scattered, morphologically viable cardiomyocytes within the infarcted area that were negative for complement. In H9c2 cells, clusterin was rapidly expressed after ischemia. Its expression was reduced after reperfusion. Clusterin bound to single annexin V-positive or annexin V and propidium iodide-positive H9c2 cells. Clusterin inhibited ischemia-induced death in H9c2 cells as well as in isolated adult ventricular rat cardiomyocytes in the absence of complement. We conclude that ischemia induces the upregulation of clusterin in ischemically challenged, but viable, cardiomyocytes. Our data suggest that clusterin protects cardiomyocytes against ischemic cell death via a complement-independent pathway. ischemia; acute myocardial infarction; membrane flip-flop

Published
2005

17. Type II secretory phospholipase [A.sub.2] binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death

Author

Nijmeijer, R., Willemsen, M., Meijer, C.J.L.M., Visser, C.A., Verheijen, R.H., Gottlieb, R.A., Hack, C.E., and Niessen, H.W.M.

Subjects
Phospholipases -- Research, Biological sciences
Abstract

Nijmeijer, R., M. Willemsen, C. J. L. M. Meijer, C. A. Visser, R. H. Verheijen, R. A. Gottlieb, C. E. Hack, and H. W. M. Niessen. Type II secretory phospholipase A2 binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death. Am J Physiol Heart Circ Physiol 285: H2218-H2224, 2003. First published June 12, 2003; 10.1152/ ajpheart.00887.2002.-Type II secretory phospholipase [A.sub.2] (sPL[Asub.2]) is a cardiovascular risk factor. We recently found depositions of sPL[A.sub.2] in the necrotic center of infarcted human myocardium and normally appearing cardiomyocytes adjacent to the border zone. The consequences of binding of sPLA[sub.2] to ischemic cardiomyocytes are not known. To explore a potential effect of sPLA[sub.2] on ischemic cardiomyocytes at a cellular level we used an in vitro model. The cardiomyocyte cell line H9c2 or adult cardiomyocytes were isolated from rabbits that were incubated with sPL[A.sub.2] in the presence of metabolic inhibitors to mimic ischemia-reperfusion conditions. Cell viability was established with the use of annexin V and propidium iodide or 7-aminoactinomycin D. Metabolic inhibition induced an increase of the number of flip-flopped cells, including a population that did not stain with propidium iodide and that was caspase-3 negative, sPL[A.sub.2] bound to the flip-flopped cells, including those negative for caspase-3, sPL[A.sub.2] binding induced cell death in these latter cells. In addition, sPL[A.sub.2] potentiated the binding of C-reactive protein (CRP) to these cells. We conclude that by binding to flip-flopped cardiomyocytes, including those that are caspase-3 negative and presumably reversibly injured, sPL[A.sub.2] may induce cell death and tag these cells with CRP. myocardial infarction; inflammation

Published
2003

18. Longstanding obliterative panarteritis in Kawasaki disease: lack of cyclosporin A effect

Author

Kuijpers, Taco W., Biezeveld, Maarten, Achterhuis, Annemiek, Kuipers, Irene, Lam, Jan, Hack, C.E., Becker, Anton E., and Van Der Wal, Allard C.

Subjects
Cyclosporine -- Physiological aspects, Salicylates -- Physiological aspects, Aminosalicylate sodium -- Physiological aspects, Kawasaki disease -- Health aspects, Kawasaki disease -- Diagnosis, Kawasaki disease -- Care and treatment, Kawasaki disease -- Demographic aspects, Kawasaki disease -- Complications, Sick children -- Care and treatment, Sick children -- Health aspects, Sick children -- Medical examination, Sick children -- Case studies, Pediatrics -- Research
Abstract

Kawasaki disease is a childhood vasculitis of medium-sized vessels, affecting the coronary arteries in particular. We have treated a therapy-resistant child who met all diagnostic criteria for Kawasaki disease. After the boy was given intravenous immunoglobulins and salicylates, as well as several courses of pulsed methylprednisolone, disease recurred and coronary artery lesions became progressively detectable. Cyclosporin A was started and seemed clinically effective. In contrast to the positive effect on inflammatory parameters, ie, C-reactive protein and white blood ceil counts, a novel plasma marker for cytotoxicity (granzyme B) remained elevated. Coronary disease progressed to fatal obstruction and myocardial infarction. Echocardiography, electrocardiograms, and myocardial creatine phosphokinase did not predict impending death. At autopsy an obliterafive panarteritis was observed resulting from massive fibrointimal proliferation, affecting the aorta and several large and medium-sized arteries. Immunophenotypic analysis of the inflammatory infiltrates in arteries revealed mainly granzyme-positive cytotoxic T cells and macrophages in the intima and media, as well as nodular aggregates of T cells, B cells, and plasma cells in the adventitia of affected arteries. These findings further endorse the role of specific cellular and humoral immunity in Kawasaki disease. Unremitting coronary arteritis and excessive smooth muscle hyperplasia resulted in coronary occlusion despite the use of cyclosporin A. Pediatrics 2003;112:986-992; Kawasaki disease, panarteritis, immunoglobulin, cyclosporin A, granzyme., ABBREVIATIONS. IVIG, intravenous immunoglobulin; CsA, cyclosporin A; CPR, C-reactive protein; WBC, white blood cell; LAD, left anterior descending; RCA, right coronary artery; ELISA, enzyme-linked immunosorbent assay; GrA, granzyme A; GrB, [...]

Published
2003

19. Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction. (Original Article)

Author

Krijnen, P.A.J., Meischl, C., Hack, C.E., Meijer, C.J.L.M., Visser, C.A., Roos, D., and Niessen, H.W.M

Subjects
Clinical pathology -- Research -- Physiological aspects -- Health aspects -- Analysis -- Methods, Cell death -- Genetic aspects -- Physiological aspects -- Health aspects -- Methods -- Research -- Analysis, Cell proliferation -- Research -- Health aspects -- Analysis -- Physiological aspects -- Genetic aspects -- Methods, Oxygen -- Physiological aspects -- Methods -- Analysis -- Research -- Health aspects, Gene expression -- Physiological aspects -- Research -- Methods -- Genetic aspects -- Analysis -- Health aspects, Mortality -- Causes of -- Health aspects -- United Kingdom, Immune system -- Testing, Heart cells -- Physiological aspects -- Genetic aspects -- Methods -- Analysis -- Health aspects -- Research, Phagocytosis -- Care and treatment -- Health aspects -- Genetic aspects -- Methods -- Physiological aspects -- Research -- Analysis, Health, Care and treatment, Physiological aspects, Analysis, Research, Genetic aspects, Methods, Causes of, Health aspects
Abstract

Background/Aims: Recent studies indicate the presence of reactive oxygen species (ROS) producing homologues of the enzymatic subunit (Nox2) of phagocytic NADPH oxidase in non-phagocytic cells. Interestingly, in these cells, ROS [...]

Published
2003

33. Toward a Sensible Single-antigen Bead Cutoff Based on Kidney Graft Survival

Author

Wisse, B.W., Kamburova, E.G., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Stephan Sanders, J., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., van Duijnhoven, E.M., Gelens, M., Christiaans, M.H., van Ittersum, F.J., Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Otten, H.G., Wisse, B.W., Kamburova, E.G., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Stephan Sanders, J., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., van Duijnhoven, E.M., Gelens, M., Christiaans, M.H., van Ittersum, F.J., Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., and Otten, H.G.

Abstract

Contains fulltext : 204258.pdf (publisher's version ) (Open Access), BACKGROUND: There is no consensus in the literature on the interpretation of single-antigen bead positive for a specific HLA antibody. METHODS: To inform the debate, we studied the relationship between various single-antigen bead positivity algorithms and the impact of resulting donor-specific HLA antibody (DSA) positivity on long-term kidney graft survival in 3237 deceased-donor transplants. RESULTS: First, we showed that the interassay variability can be greatly reduced when working with signal-to-background ratios instead of absolute median fluorescence intensities (MFIs). Next, we determined pretransplant DSA using various MFI cutoffs, signal-to-background ratios, and combinations thereof. The impact of the various cutoffs was studied by comparing the graft survival between the DSA-positive and DSA-negative groups. We did not observe a strong impact of various cutoff levels on 10-year graft survival. A stronger relationship between the cutoff level and 1-year graft survival for DSA-positive transplants was found when using signal-to-background ratios, most pronounced for the bead of the same HLA locus with lowest MFI taken as background. CONCLUSIONS: With respect to pretransplant risk stratification, we propose a signal-to-background ratio-6 (using the bead of the same HLA-locus with lowest MFI as background) cutoff of 15 combined with an MFI cutoff of 500, resulting in 8% and 21% lower 1- and 10-year graft survivals, respectively, for 8% DSA-positive transplants.

Published
2019

34. Allocation to highly sensitized patients based on acceptable mismatches results in low rejection rates comparable to nonsensitized patients

Author

Heidt, S., Haasnoot, G.W., Witvliet, M.D., Linden-van Oevelen, M.J.H. van der, Kamburova, E.G., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. Ten, Bemelman, F.J., Hoitsma, A., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Otten, H.G., Roelen, D.L., Claas, F.H., Heidt, S., Haasnoot, G.W., Witvliet, M.D., Linden-van Oevelen, M.J.H. van der, Kamburova, E.G., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. Ten, Bemelman, F.J., Hoitsma, A., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Otten, H.G., Roelen, D.L., and Claas, F.H.

Abstract

Contains fulltext : 208426.pdf (publisher's version ) (Open Access), Whereas regular allocation avoids unacceptable mismatches on the donor organ, allocation to highly sensitized patients within the Eurotransplant Acceptable Mismatch (AM) program is based on the patient's HLA phenotype plus acceptable antigens. These are HLA antigens to which the patient never made antibodies, as determined by extensive laboratory testing. AM patients have superior long-term graft survival compared with highly sensitized patients in regular allocation. Here, we questioned whether the AM program also results in lower rejection rates. From the PROCARE cohort, consisting of all Dutch kidney transplants in 1995-2005, we selected deceased donor single transplants with a minimum of 1 HLA mismatch and determined the cumulative 6-month rejection incidence for patients in AM or regular allocation. Additionally, we determined the effect of minimal matching criteria of 1 HLA-B plus 1 HLA-DR, or 2 HLA-DR antigens on rejection incidence. AM patients showed significantly lower rejection rates than highly immunized patients in regular allocation, comparable to nonsensitized patients, independent of other risk factors for rejection. In contrast to highly sensitized patients in regular allocation, minimal matching criteria did not affect rejection rates in AM patients. Allocation based on acceptable antigens leads to relatively low-risk transplants for highly sensitized patients with rejection rates similar to those of nonimmunized individuals.

Published
2019

35. A paired kidney analysis on the impact of pre-transplant anti-HLA antibodies on graft survival

Author

Michielsen, L.A., Wisse, B.W., Kamburova, E.G., Verhaar, M.C., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E, Hack, C.E., Reekum, F.E. van, Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Sanders, J.F., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K.A. van der, Weerd, N.C. van der, Berge, I.J. ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Otten, H.G., Zuilen, A.D. van, Michielsen, L.A., Wisse, B.W., Kamburova, E.G., Verhaar, M.C., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E, Hack, C.E., Reekum, F.E. van, Bots, M.L., Drop, A., Plaisier, L., Seelen, M.A., Sanders, J.F., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K.A. van der, Weerd, N.C. van der, Berge, I.J. ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Otten, H.G., and Zuilen, A.D. van

Abstract

Item does not contain fulltext, BACKGROUND: Pre-transplant donor-specific anti-human leucocyte antigen (HLA) antibodies (DSAs) are associated with impaired kidney graft survival while the clinical relevance of non-donor-specific anti-HLA antibodies (nDSAs) is more controversial. The aim of the present paired kidney graft study was to compare the clinical relevance of DSAs and nDSAs. METHODS: To eliminate donor and era-dependent factors, a post hoc paired kidney graft analysis was performed as part of a Dutch multicentre study evaluating all transplantations between 1995 and 2005 with available pre-transplant serum samples. Anti-HLA antibodies were detected with a Luminex single-antigen bead assay. RESULTS: Among 3237 deceased donor transplantations, we identified 115 recipient pairs receiving a kidney from the same donor with one recipient being DSA positive and the other without anti-HLA antibodies. Patients with pre-transplant DSAs had a significantly lower 10-year death-censored graft survival (55% versus 82%, P=0.0001). We identified 192 pairs with one recipient as nDSA positive (against Class I and/or II) and the other without anti-HLA antibodies. For the patients with nDSAs against either Class I or II, graft survival did not significantly differ compared with patients without anti-HLA antibodies (74% versus 77%, P = 0.79). Only in patients with both nDSAs Class I and II was there a trend towards a lower graft survival (58%, P = 0.06). Lastly, in a small group of 42 recipient pairs, 10-year graft survival in recipients with DSAs was 49% compared with 68% in recipients with nDSAs (P=0.11). CONCLUSION: This paired kidney analysis confirms that the presence of pre-transplant DSAs in deceased donor transplantations is a risk marker for graft loss, whereas nDSAs in general are not associated with a lower graft survival. Subgroup analysis indicated that only in broadly sensitized patients with nDSAs against Class I and II, nDSAs may be a risk marker for graft loss in the long term.

Published
2019

36. Antibodies against ARHGDIB are associated with long-term kidney graft loss

Author

Kamburova, E.G., Gruijters, M.L., Kardol-Hoefnagel, T., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Melchers, R.C., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. Ten, Hoitsma, A., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Bemelman, F.J., Otten, H.G., Kamburova, E.G., Gruijters, M.L., Kardol-Hoefnagel, T., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A., Plaisier, L., Melchers, R.C., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, K. van der, Weerd, N.C. van der, Berge, I.J. Ten, Hoitsma, A., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Bemelman, F.J., and Otten, H.G.

Abstract

Contains fulltext : 215571.pdf (publisher's version ) (Open Access), The clinical significance of non-HLA antibodies on renal allograft survival is a matter of debate, due to differences in reported results and lack of large-scale studies incorporating analysis of multiple non-HLA antibodies simultaneously. We developed a multiplex non-HLA antibody assay against 14 proteins highly expressed in the kidney. In this study, the presence of pretransplant non-HLA antibodies was correlated to renal allograft survival in a nationwide cohort of 4770 recipients transplanted between 1995 and 2006. Autoantibodies against Rho GDP-dissociation inhibitor 2 (ARHGDIB) were significantly associated with graft loss in recipients transplanted with a deceased-donor kidney (N = 3276) but not in recipients of a living-donor kidney (N = 1496). At 10 years after deceased-donor transplantation, recipients with anti-ARHGDIB antibodies (94/3276 = 2.9%) had a 13% lower death-censored covariate-adjusted graft survival compared to the anti-ARHGDIB-negative (3182/3276 = 97.1%) population (hazard ratio 1.82; 95% confidence interval, 1.32-2.53; P = .0003). These antibodies occur independently from donor-specific anti-HLA antibodies (DSA) or other non-HLA antibodies investigated. No significant relations with graft loss were found for the other 13 non-HLA antibodies. We suggest that pretransplant risk assessment can be improved by measuring anti-ARHGDIB antibodies in all patients awaiting deceased-donor transplantation.

Published
2019

37. Antibodies against ARHGDIB are associated with long-term kidney graft loss

Author

Kamburova, E. G., Gruijters, M.L., Kardol-Hoefnagel, T., Wisse, B. W., Joosten, I. (Irma), Allebes, W.A. (Wil), Meer, A.J.G.M. (Astrid) van der, Hilbrands, L.B., Baas, M. C., Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F. E., Zuilen, A.D. (Arjan) van, Verhaar, M.C. (Marianne), Bots, M.L. (Michiel), Drop, A., Plaisier, L., Melchers, R.C.A., Seelen, MAJ, Sanders, J.-S. (Jan-Stephan), Hepkema, B.G. (Bouke), Lambeck, AJA, Bungener, LB, Roozendaal, C, Tilanus, M.G.J., Voorter, CE, Wieten, L, van Duijnhoven, E. M., Gelens, M., Christiaans, M.H. (Maarten), Ittersum, F.J. (Frans) van, Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W., van der Pant, K., van der Weerd, NC, Berge, I.J.M. (Ineke) ten, Hoitsma, A., van der Boog, P. J. M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L., Claas, FH, Bemelman, F.J. (Fréderike), Otten, H.G. (Henderikus), Kamburova, E. G., Gruijters, M.L., Kardol-Hoefnagel, T., Wisse, B. W., Joosten, I. (Irma), Allebes, W.A. (Wil), Meer, A.J.G.M. (Astrid) van der, Hilbrands, L.B., Baas, M. C., Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F. E., Zuilen, A.D. (Arjan) van, Verhaar, M.C. (Marianne), Bots, M.L. (Michiel), Drop, A., Plaisier, L., Melchers, R.C.A., Seelen, MAJ, Sanders, J.-S. (Jan-Stephan), Hepkema, B.G. (Bouke), Lambeck, AJA, Bungener, LB, Roozendaal, C, Tilanus, M.G.J., Voorter, CE, Wieten, L, van Duijnhoven, E. M., Gelens, M., Christiaans, M.H. (Maarten), Ittersum, F.J. (Frans) van, Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W., van der Pant, K., van der Weerd, NC, Berge, I.J.M. (Ineke) ten, Hoitsma, A., van der Boog, P. J. M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L., Claas, FH, Bemelman, F.J. (Fréderike), and Otten, H.G. (Henderikus)

Abstract

The clinical significance of non‐HLA antibodies on renal allograft survival is a matter of debate, due to differences in reported results and lack of large‐scale studies incorporating analysis of multiple non‐HLA antibodies simultaneously. We developed a multiplex non‐HLA antibody assay against 14 proteins highly expressed in the kidney. In this study, the presence of pretransplant non‐HLA antibodies was correl

Published
2019
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38. Allocation to highly sensitized patients based on acceptable mismatches results in low rejection rates comparable to nonsensitized patients

Author

Heidt, P.J. (Peter), Haasnoot, G.W. (Geert), Witvliet, M.D. (Marian), van der Linden-van Oevelen, M.J.H. (Marissa J. H.), Kamburova, E.G., Wisse, B.W., Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F., van Zuilen, A.D. (Arjan D.), Verhaar, M.C. (Marianne), Bots, M.L. (Michiel), Drop, A.C.A.D., Plaisier, L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Otten, H.G. (Henderikus), Roelen, D.L. (Dave), Claas, F.H.J. (Frans), Heidt, P.J. (Peter), Haasnoot, G.W. (Geert), Witvliet, M.D. (Marian), van der Linden-van Oevelen, M.J.H. (Marissa J. H.), Kamburova, E.G., Wisse, B.W., Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F., van Zuilen, A.D. (Arjan D.), Verhaar, M.C. (Marianne), Bots, M.L. (Michiel), Drop, A.C.A.D., Plaisier, L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Otten, H.G. (Henderikus), Roelen, D.L. (Dave), and Claas, F.H.J. (Frans)

Abstract

Whereas regular allocation avoids unacceptable mismatches on the donor organ, allocation to highly sensitized patients within the Eurotransplant Acceptable Mismatch (AM) program is based on the patient's HLA phenotype plus acceptable antigens. These are HLA antigens to which the patient never made antibodies, as determined by extensive laboratory testing. AM patients have superior long-term graft survival compared with highly sensitized patients in regular allocation. Here, we questioned whether the AM program also results in lower rejection rates. From the PROCARE cohort, consisting of all Dutch kidney transplants in 1995-2005, we selected deceased donor single transplants with a minimum of 1 HLA mismatch and determined the cumulative 6-month rejection incidence for patients in AM or regular allocation. Additionally, we determined the effect of minimal matching criteria of 1 HLA-B plus 1 HLA-DR, or 2 HLA-DR antigens on rejection incidence. AM patients showed significantly lower rejection rates than highly immunized patients in regular allocation, comparable to nonsensitized patients, independent of other risk factors for rejection. In contrast to highly sensitized patients in regular allocation, minimal matching criteria did not affect rejection rates in AM patients. Allocation based on acceptable antigens leads to relatively low-risk transplants for highly sensitized patients with rejection rates similar to those of nonimmunized individuals.

Published
2019
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39. PIRCHE-II: A NOVEL TOOL TO IDENTIFY PERMISSIBLE HLA MISMATCHES IN KIDNEY TRANSPLANTATION

Author

Geneugelijk, K., Niemann, M., Drylewicz, J., Zuilen, A.D. van, Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Hack, C.E., Reekum, F.E. van, Verhaar, M., Kamburova, E.G., Bots, M.L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G., Lambeck, A.J., Bungener, L.B., Roozendaal, C., Tilanus, M.G.J., Vanderlocht, J., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H.L., Ittersum, F.J. van, Nurmohamed, A., Lardy, N.M., Swelsen, W., Pant, K.A. van der, Weerd, N.C. van der, Berge, I.J.M. ten, Bemelman, F.D.J., Hoitsma, A., Boog, P.J.M. van der, Fijter, J.W. de, Betjes, M.G.H., Heidt, S., Roelen, D.L., Claas, F.H.J., Otten, H.G., and Spierings, E.

Published
2017

40. DIFFERENTIAL EFFECT OF DONOR-SPECIFIC HLA ANTIBODIES IN LIVING VERSUS DECEASED DONOR KIDNEY TRANSPLANTATION

Author

Kamburova, E.G., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F. van, Zuilen, A. van, Verhaar, M.C., Bots, M.L., Drop, A.C.A.D., Plaisier, L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G., Lambeck, A.J., Bungener, L.B., Roozendaal, C., Tilanus, M.G.J., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M., Christiaans, M.H.L., Ittersum, F.J. van, Nurmohamed, A., Lardy, N.M., Swelsen, W., Pant, K.A. van der, Weerd, N.C. van der, Berge, I.J.M. ten, Bemelman, F.J., Hoitsma, A., Boog, P.J.M. van der, Fijter, H. de, Betjes, M.G.H., Heidt, S., Roelen, D.L., Claas, F.H.J., and Otten, H.G.

Published
2017

42. Predominant role of neutrophils in the inactivation of alpha 2-macroglobulin in arthritic joints

Author

Abbink, J.J., Kamp, A.M., Nieuwenhuys, E.J., Nuijens, J.H., Swaak, A.J.G., and Hack, C.E.

Subjects
Neutrophils -- Physiological aspects, Alpha 2-macroglobulin -- Physiological aspects, Arthritis -- Physiological aspects, Health
Abstract

In inflammatory joint diseases such as rheumatoid arthritis (RA), joint cartilage is progressively destroyed. This process is probably mediated by proteinases (enzymes that degrade proteins) and many of these are released from neutrophils (white blood cells that are important destroyers of invading organisms), which are predominant in synovial fluid (SF) surrounding joints. These cells also degrade joint and other tissues with very reactive molecules derived from oxygen. Normally, tissue is protected from the action of proteinases by proteinase inhibitors such as alpha 2-macroglobulin (alpha-2-M), which can block the activity of a variety of proteinases. However, some of the inhibitors can be blocked by neutrophil-derived reactive oxygen species and this then allows neutrophil proteinases to cause tissue damage. To better understand the relevance of alpha-2-M inhibition to tissue damage in arthritis, the inhibitor was studied in joint tissues from patients with RA, osteoarthritis (OA), gout, and other arthritic diseases. Blood levels of total alpha-2-M were significantly lower in patients with inflammatory joint diseases (RA, gout) than in those with OA or healthy subjects. The portion of alpha-2-M that was inhibited (i-alpha-2-M) was significantly higher in SF than in blood and was significantly higher in SF from patients with inflammatory joint diseases. Binding to proteinases accounted for only 6 to 11 percent of i-alpha-2-M. Levels of complexes between i-alpha-2-M and enzymes such as elastase and chymotrypsin correlated significantly with parameters of neutrophil function, both in OA patients and in those with inflammatory joint diseases. An inhibitor of proteinases, eglin C, only partially reduced i-alpha-2-M levels, suggesting that oxygen metabolites were responsible for much of the observed alpha-2-M inhibition. The study suggests that in patients with inflammatory arthritis, alpha-2-M is inactivated by oxygen metabolites and by proteinase binding, both caused by neutrophils, and this facilitates tissue destruction by the proteinases. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

46. Differential effects of donor-specific HLA antibodies in living versus deceased donor transplant

Author

Kamburova, E.G., primary, Wisse, B.W., additional, Joosten, I., additional, Allebes, W.A., additional, van der Meer, A., additional, Hilbrands, L.B., additional, Baas, M.C., additional, Spierings, E., additional, Hack, C.E., additional, van Reekum, F.E., additional, van Zuilen, A.D., additional, Verhaar, M.C., additional, Bots, M.L., additional, Drop, A.C.A.D., additional, Plaisier, L., additional, Seelen, M.A.J., additional, Sanders, J.S.F., additional, Hepkema, B.G., additional, Lambeck, A.J.A., additional, Bungener, L.B., additional, Roozendaal, C., additional, Tilanus, M.G.J., additional, Voorter, C.E., additional, Wieten, L., additional, van Duijnhoven, E.M., additional, Gelens, M., additional, Christiaans, M.H.L., additional, van Ittersum, F.J., additional, Nurmohamed, S.A., additional, Lardy, N.M., additional, Swelsen, W., additional, van der Pant, K.A., additional, van der Weerd, N.C., additional, ten Berge, I.J.M., additional, Bemelman, F.J., additional, Hoitsma, A., additional, van der Boog, P.J.M., additional, de Fijter, J.W., additional, Betjes, M.G.H., additional, Heidt, S., additional, Roelen, D.L., additional, Claas, F.H., additional, and Otten, H.G., additional

Published
2018
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48. Differential effects of donor-specific HLA antibodies in living versus deceased donor transplant

Author

Kamburova, E.G., Wisse, B.W., Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F., van Zuilen, A.D. (A. D.), Verhaar, M.C. (Marianne), Bots, M.L. (M. L.), Drop, A.C.A.D., Plaisier, L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L. (Dave), Claas, F.H.J. (Frans), Otten, H.G. (Henderikus), Kamburova, E.G., Wisse, B.W., Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Spierings, E. (E.), Hack, C.E. (Erik), van Reekum, F., van Zuilen, A.D. (A. D.), Verhaar, M.C. (Marianne), Bots, M.L. (M. L.), Drop, A.C.A.D., Plaisier, L., Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, S.A. (Shaikh Azam), Lardy, N.M. (Neubury), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L. (Dave), Claas, F.H.J. (Frans), and Otten, H.G. (Henderikus)

Abstract

The presence of donor-specific anti-HLA antibodies (DSAs) is associated with increased risk of graft failure after kidney transplant. We hypothesized that DSAs against HLA class I, class II, or both classes indicate a different risk for graft loss between deceased and living donor transplant. In this study, we investigated the impact of pretransplant DSAs, by using single antigen bead assays, on long-term graft survival in 3237 deceased and 1487 living donor kidney transplants with a negative complement-dependent crossmatch. In living donor transplants, we found a limited effect on graft survival of DSAs against class I or II antigens after transplant. Class I and II DSAs combined resulted in decreased 10-year graft survival (84% to 75%). In contrast, after deceased donor transplant, patients with class I or class II DSAs had a 10-year graft survival of 59% and 60%, respectively, both significantly lower than the survival for patients without DSAs (76%). The combination of class I and II DSAs resulted in a 10-year survival of 54% in deceased donor transplants. In conclusion, class I and II DSAs are a clear risk factor for graft loss in deceased donor transplants, while in living donor transplants, class I and II DSAs seem to be associated with an increased risk for graft failure, but this could not be assessed due to their low prevalence.

Published
2018
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49. PIRCHE-II is related to graft failure after kidney transplantation

Author

Geneugelijk, K. (Kirsten), Niemann, M. (Matthias), Drylewicz, J. (Julia), van Zuilen, A.D. (Arjan D.), Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Hack, C.E. (Erik), van Reekum, F., Verhaar, M.C. (Marianne), Kamburova, E.G., Bots, M.L. (Michiel L.), Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Vanderlocht, J. (Joris), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, A., Lardy, J.N.M. (Junior N.M.), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L. (Dave), Claas, F.H.J. (Frans), Otten, H.G. (Henderikus), Spierings, E. (E.), Geneugelijk, K. (Kirsten), Niemann, M. (Matthias), Drylewicz, J. (Julia), van Zuilen, A.D. (Arjan D.), Joosten, I. (Irma), Allebes, W.A. (Wil), van der Meer, A., Hilbrands, L.B. (Luuk), Baas, M.C. (Marije), Hack, C.E. (Erik), van Reekum, F., Verhaar, M.C. (Marianne), Kamburova, E.G., Bots, M.L. (Michiel L.), Seelen, M.A.J., Sanders, J.S.F., Hepkema, B.G. (Bouke), Lambeck, A.J.A. (Annechien J.A.), Bungener, L.B., Roozendaal, C., Tilanus, M.G.J. (Marcel), Vanderlocht, J. (Joris), Voorter, C.E.M. (C. E M), Wieten, L., van Duijnhoven, E., Gelens, M., Christiaans, M.H. (Maarten), van Ittersum, F., Nurmohamed, A., Lardy, J.N.M. (Junior N.M.), Swelsen, W.T., van der Pant, K.A., Weerd, N.C. (Neelke) van der, Berge, I.J.M. (Ineke) ten, Bemelman, F.J. (Fréderike), Hoitsma, A.J. (Andries), van der Boog, P.J.M., Fijter, J.W. (Johan) de, Betjes, M.G.H. (Michiel), Heidt, P.J. (Peter), Roelen, D.L. (Dave), Claas, F.H.J. (Frans), Otten, H.G. (Henderikus), and Spierings, E. (E.)

Abstract

Individual HLA mismatches may differentially impact graft survival after kidney transplantation. Therefore, there is a need for a reliable tool to define permissible HLA mismatches in kidney transplantation. We previously demonstrated that donor-derived Predicted Indirectly ReCognizable HLA Epitopes presented by recipient HLA class II (PIRCHE-II) play a role in de novo donor-specific HLA antibodies formation after kidney transplantation. In the present Dutch multi-center study, we evaluated the possible association between PIRCHE-II and kidney graft failure in 2,918 donor-recipient couples that were transplanted between 1995 and 2005. For these donors-recipients couples, PIRCHE-II numbers were related to graft survival in univariate and multivariable analyses. Adjusted for confounders, the natural logarithm of PIRCHE-II was associated with a higher risk for graft failure [hazard ratio (HR): 1.13, 95% CI: 1.04-1.23, p = 0.003]. When analyzing a subgroup of patients who had their first transplantation, the HR of graft failure for ln(PIRCHE-II) was higher compared with the overall cohort (HR: 1.22, 95% CI: 1.10-1.34, p < 0.001). PIRCHE-II demonstrated both early and late effects on graft failure in this subgroup. These data suggest that the PIRCHE-II may impact graft survival after kidney transplantation. Inclusion of PIRCHE-II in donor-selection criteria may eventually lead to an improved kidney graft survival.

Published
2018
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50. Pretransplant C3d-Fixing Donor-Specific Anti-HLA Antibodies Are Not Associated with Increased Risk for Kidney Graft Failure

Author

Kamburova, E.G., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A.C., Plaisier, L., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M.A., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, Karlijn A.M.I. van der, Weerd, N.C. van der, Berge, I.J. Ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., Otten, H.G., Kamburova, E.G., Wisse, B.W., Joosten, I., Allebes, W.A., Meer, A. van der, Hilbrands, L.B., Baas, M.C., Spierings, E., Hack, C.E., Reekum, F.E. van, Zuilen, A.D. van, Verhaar, M.C., Bots, M.L., Drop, A.C., Plaisier, L., Seelen, M.A., Sanders, J.S., Hepkema, B.G., Lambeck, A.J.A., Bungener, L.B., Roozendaal, C., Tilanus, M.G., Voorter, C.E.M., Wieten, L., Duijnhoven, E.M. van, Gelens, M.A., Christiaans, M.H., Ittersum, F.J. van, Nurmohamed, S.A., Lardy, N.M., Swelsen, W., Pant, Karlijn A.M.I. van der, Weerd, N.C. van der, Berge, I.J. Ten, Bemelman, F.J., Hoitsma, A.J., Boog, P.J. van der, Fijter, J.W. de, Betjes, M.G., Heidt, S., Roelen, D.L., Claas, F.H., and Otten, H.G.

Abstract

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Published
2018

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