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3. Recovery of dialysis patients with COVID-19: health outcomes 3 months after diagnosis in ERACODA

Author

Hemmelder, M. H., Noordzij, M., Vart, P., Hilbrands, L. B., Jager, K. J., Abrahams, A. C., Arroyo, D., Battaglia, Y., Ekart, R., Mallamaci, F., Malloney, S. -R., Oliveira, J., Rydzewski, A., Sridharan, S., Vogt, L., Duivenvoorden, R., Gansevoort, R. T., Franssen, C. F. M., van der Net, J. B., Essig, M., du Buf-Vereijken, P. W. G., van Ginneken, B., Maas, N., van Jaarsveld, B. C., Bemelman, F. J., Klingenberg-Salahova, F., Heenan-Vos, F., Vervloet, M. G., Nurmohamed, A., Abramowicz, D., Verhofstede, S., Maoujoud, O., Malfait, T., Fialova, J., Melilli, E., Fava, A., Cruzado, J. M., Perez, N. M., Lips, J., Krepel, H., Adilovic, H., Hengst, M., Konings, C. J. A. M., Braconnier, P., Weis, D., Gellert, R., Alferes, D. G., Radulescu, D., Zakharova, E. V., Ambuehl, P. M., Guidotti, R., Walker, A., Lepeytre, F., Rabate, C., Rostoker, G., Marques, S., Azasevac, T., Majstorovic, G. S., Katicic, D., Dam, M. T., Kruger, T., Brzosko, S., Liakopoulos, V., Zanen, A. L., Logtenberg, S. J. J., Fricke, L., Kuryata, O., Slebe, J. J. P., Abd ElHafeez, S., Kemlin, D., van de Wetering, J., Reinders, M. E. J., Hesselink, D. A., van Gestel, J. K., Eiselt, J., Kielberger, L., El-Wakil, H. S., Verhoeven, M. A. M., Logan, I., Canal, C., Facundo, C., Ramos, A. M., Debska-Slizien, A., Veldhuizen, N. M. H., Tigka, E., Polyzou Konsta, M. A., Panagoutsos, S., Postorino, A., Cambareri, F., Matceac, I., Nistor, I., Covic, A., Groeneveld, J. H. M., Jousma, J., Diekmann, F., Oppenheimer, F., Blasco, M., Pereira, T. A., dos Santos Junior, A. C. S., Arias-Cabrales, C., Crespo, M., Llinas-Mallol, L., Buxeda, A., Tarrega, C. B., Redondo-Pachon, D., Arenas Jimenez, M. D., Mendoza-Valderrey, A., Martins, A. C., Mateus, C., Alvila, G., Laranjinha, I., Hofstra, J. M., Siezenga, M. A., Franco, A., Castellano, S., Rodriguez-Ferrero, M. L., Manzanos, S. B., Haridian Sosa Barrios, R., Lemahieu, W., Bartelet, K., Dirim, A. B., Demir, E., Sever, M. S., Turkmen, A., Safak, S., Hollander, D. A. M. J., Kerckhoffs, A., Buttner, S., de Vries, A. P. J., Meziyerh, S., van der Helm, D., Mallat, M., Bouwsma, H., Petruliene, K., Verberk, I., van der Sande, F. M., Christiaans, M. H. L., Mohankumar, N., Luca, M. D., Tuglular, S. Z., Kramer, A., Beerenhout, C., Luik, P. T., Kerschbaum, J., Tiefenthaler, M., Watschinger, B., Adema, A. Y., Stepanov, V. A., Zulkarnaev, A. B., Turkmen, K., Gandolfini, I., Maggiore, U., Fliedner, A., Asberg, A., Mjoen, G., Miyasato, H., de Fijter, C. W. H., Mongera, N., Pini, S., de Biase, C., van de Logt, A. E., Maas, R., Lebedeva, O., Lopez, V., Reichert, L. J. M., Verhave, J., Titov, D., Parshina, E. V., Zanoli, L., Marcantoni, C., van Kempen, G., van Gils-Verrij, L. E. A., Harty, J. C., Meurs, M., Myslak, M., Lentini, P., den Deurwaarder, E., Stendahl, M., Rahimzadeh, H., Schouten, M., Rychlik, I., Cabezas-Reina, C. J., Roca, A. M., Nauta, F., Sahin, I., Goffin, E., Kanaan, N., Labriola, L., Devresse, A., Diaz-Mareque, A., Coca, A., de Arriba, G., Meijers, B. K. I., Naesens, M., Kuypers, D., Desschans, B., Tonnerlier, A., Wissing, K. M., Dedinska, I., Pessolano, G., Malik, S., Dounousi, E., Papachristou, E., Berger, S. P., Meijer, E., Sanders, J. S. F., Ozyilmaz, A., Ponikvar, J. B., Pernat, A. M., Kovac, D., Arnol, M., Molenaar, F. M., van Zuilen, A. D., Meijvis, S. C. A., Dolmans, H., Tantisattamo, E., Esposito, P., Krzesinski, J. -M., Barahira, J. D., Gallieni, M., Martin-Moreno, P. L., Guglielmetti, G., Guzzo, G., Toapanta, N., Soler, M. J., Luik, A. J., van Kuijk, W. H. M., Stikkelbroeck, L. W. H., Hermans, M. M. H., Rimsevicius, L., Righetti, M., Islam, M., Heitink-Ter Braak, N., Nephrology, ACS - Microcirculation, ACS - Diabetes & metabolism, UCL - SSS/IREC/NEFR - Pôle de Néphrologie, UCL - (SLuc) Service de néphrologie, Clinical sciences, Faculteit Medische Wetenschappen/UMCG, Groningen Kidney Center (GKC), Cardiovascular Centre (CVC), Groningen Institute for Organ Transplantation (GIOT), Interne Geneeskunde, RS: Carim - V02 Hypertension and target organ damage, Medical Informatics, APH - Aging & Later Life, APH - Quality of Care, APH - Global Health, ACS - Pulmonary hypertension & thrombosis, APH - Health Behaviors & Chronic Diseases, and Internal Medicine

Subjects
Male, Outcome Assessment, survival, mental health status, COVID-19 Testing, SDG 3 - Good Health and Well-being, Renal Dialysis, functional health status, Outcome Assessment, Health Care, 80 and over, Humans, KIDNEY-TRANSPLANT, AcademicSubjects/MED00340, Aged, Aged, 80 and over, Transplantation, SARS-CoV-2, MORTALITY, COVID-19, Middle Aged, Health Care, Intensive Care Units, Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Nephrology, dialysis, Original Article, Female, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11]
Abstract

Background Coronavirus disease 2019 (COVID-19)-related short-term mortality is high in dialysis patients, but longer-term outcomes are largely unknown. We therefore assessed patient recovery in a large cohort of dialysis patients 3 months after their COVID-19 diagnosis. Methods We analyzed data on dialysis patients diagnosed with COVID-19 from 1 February 2020 to 31 March 2021 from the European Renal Association COVID-19 Database (ERACODA). The outcomes studied were patient survival, residence and functional and mental health status (estimated by their treating physician) 3 months after COVID-19 diagnosis. Complete follow-up data were available for 854 surviving patients. Patient characteristics associated with recovery were analyzed using logistic regression. Results In 2449 hemodialysis patients (mean ± SD age 67.5 ± 14.4 years, 62% male), survival probabilities at 3 months after COVID-19 diagnosis were 90% for nonhospitalized patients (n = 1087), 73% for patients admitted to the hospital but not to an intensive care unit (ICU) (n = 1165) and 40% for those admitted to an ICU (n = 197). Patient survival hardly decreased between 28 days and 3 months after COVID-19 diagnosis. At 3 months, 87% functioned at their pre-existent functional and 94% at their pre-existent mental level. Only few of the surviving patients were still admitted to the hospital (0.8–6.3%) or a nursing home (∼5%). A higher age and frailty score at presentation and ICU admission were associated with worse functional outcome. Conclusions Mortality between 28 days and 3 months after COVID-19 diagnosis was low and the majority of patients who survived COVID-19 recovered to their pre-existent functional and mental health level at 3 months after diagnosis.

Published
2022

5. Clinical triage of patients on kidney replacement therapy presenting with COVID-19: An ERACODA registry analysis

Author

Mitra, S., Jayanti, A., Vart, P., Coca, A., Gallieni, M., Ovrehus, M. A., Midtvedt, K., Abd Elhafeez, S., Gandolfini, I., Buttner, S., Franssen, C. F. M., Hemmelder, M. H., Van Der Net, J. B., Essig, M., Du Buf-Vereijken, P. W. G., Van Ginneken, B., Maas, N., Vogt, L., Van Jaarsveld, B. C., Jager, K. J., Bemelman, F. J., Klingenberg-Salahova, F., Heenan-Vos, F., Vervloet, M. G., Nurmohamed, A., Abramowicz, D., Verhofstede, S., Maoujoud, O., Malfait, T., Fialova, J., Melilli, E., Fava, A., Cruzado, J. M., Perez, N. M., Lips, J., Krepel, H., Adilovic, H., Hengst, M., Rydzewski, A., Gellert, R., Oliveira, J., Alferes, D. G., Zakharova, E. V., Ambuehl, P. M., Walker, A., Winzeler, R., Lepeytre, F., Rabate, C., Rostoker, G., Marques, S., Azasevac, T., Katicic, D., Dam, M. T., Kruger, T., Brzosko, S., Zanen, A. L., Logtenberg, S. J. J., Fricke, L., Slebe, J. J. P., Kemlin, D., Van De Wetering, J., Reinders, M. E. J., Eiselt, J., Kielberger, L., El-Wakil, H. S., Verhoeven, M. A. M., Canal, C., Facundo, C., Ramos, A. M., Debska-Slizien, A., Veldhuizen, N. M. H., Tigka, E., Konsta, M. A. P., Panagoutsos, S., Mallamaci, F., Postorino, A., Cambareri, F., Covic, A., Matceac, I., Nistor, I., Cordos, M., Groeneveld, J. H. M., Jousma, J., Marjolijn Van Buren, Diekmann, F., Tiago Assis Pereira, Santos, A. C. S., Arias-Cabrales, C., Crespo, M., Llinas-Mallol, L., Buxeda, A., Tarrega, C. B., Redondo-Pachon, D., Jimenez, M. D. A., Hofstra, J. M., Franco, A., Arroyo, D., Rodriguez-Ferrero, M. L., Manzanos, S. B., Barrios, R. H. S., Avila, G., Laranjinha, I., Mateus, C., Lemahieu, W., Bartelet, K., Dirim, A. B., Sever, M. S., Demir, E., Safak, S., Turkmen, A., Hollander, D. A. M. J., De Vries, A. P. J., Meziyerh, S., Van Der Helm, D., Mallat, M., Bouwsma, H., Sridharan, S., Petruliene, K., Maloney, S. -R., Verberk, I., Van Der Sande, F. M., Christiaans, M. H. L., Mohankumar, N., Di Luca, M., Tuglular, S. Z., Kramer, A., Beerenhout, C., Luik, P. T., Kerschbaum, J., Tiefenthaler, M., Watschinger, B., Adema, A. Y., Stepanov, V. A., Zulkarnaev, A. B., Turkmen, K., Fliedner, A., Asberg, A., Mjoen, G., Miyasato, H., De Fijter, C. W. H., Mongera, N., Pini, S., De Biase, C., Duivenvoorden, R., Hilbrands, L., Kerckhoffs, A., Van De Logt, A. -E., Maas, R., Lebedeva, O., Lopez, V., Verhave, J., Reichert, L. J. M., Titov, D., Parshina, E. V., Zanoli, L., Marcantoni, C., Van Gils-Verrij, L. E. A., Harty, J. C., Meurs, M., Myslak, M., Battaglia, Y., Lentini, P., Den Deurwaarder, E., Stendahl, M., Rahimzadeh, H., Schouten, M., Rychlik, I., Cabezas-Reina, C. J., Roca, A. M., Nauta, F., Goffin, E., Kanaan, N., Labriola, L., Devresse, A., Diaz-Mareque, A., Meijers, B. K. I., Naesens, M., Kuypers, D., Desschans, B., Tonnelier, A., Wissing, K. M., De Arriba, G., Dedinska, I., Pessolano, G., Maggiore, U., Malik, S., Papachristou, E., Gansevoort, R. T., Noordzij, M., Berger, S. P., Meijer, E., Ozyilmaz, A., Sanders, J. S. F., Ponikvar, J. B., Arnol, M., Pernat, A. M., Kovac, D., Ekart, R., Abrahams, A. C., Molenaar, F. M., Van Zuilen, A. D., Meijvis, S. C. A., Dolmans, H., Tantisattamo, E., Esposito, P., Krzesinski, J. -M., Barahira, J. D., Sabiu, G., Martin-Moreno, P. L., Guglielmetti, G., Guzzo, G., Toapanta, N., Soler, M. J., Luik, A. J., Van Kuijk, W. H. M., Stikkelbroeck, L. W. H., Hermans, M. M. H., Rimsevicius, L., Righetti, M., Islam, M., Braak, N. H. -T., Nephrology, UCL - SSS/IREC/NEFR - Pôle de Néphrologie, UCL - (SLuc) Service de néphrologie, Interne Geneeskunde, RS: Carim - V02 Hypertension and target organ damage, Groningen Kidney Center (GKC), ACS - Diabetes & metabolism, AII - Inflammatory diseases, AII - Infectious diseases, Internal Medicine, and Clinical sciences

Subjects
kidney, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), medicine.medical_treatment, Pulmonary insufficiency, infectious diseases, Kidney, Second presentation, Interquartile range, Internal medicine, medicine, Humans, Registries, Mortality, AcademicSubjects/MED00340, Dialysis, Aged, Transplantation, second presentation, business.industry, SARS-CoV-2, COVID-19, medicine.disease, mortality, Triage, Hospitalization, Renal Replacement Therapy, Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Nephrology, Oxygen Saturation, dialysis, Original Article, Hemodialysis, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], Presentation (obstetrics), business, transplantation
Abstract

Background Patients on kidney replacement therapy (KRT) are at very high risk of coronavirus disease 2019 (COVID-19). The triage pathway for KRT patients presenting to hospitals with varying severity of COVID-19 illness remains ill-defined. We studied the clinical characteristics of patients at initial and subsequent hospital presentations and the impact on patient outcomes. Methods The European Renal Association COVID-19 Database (ERACODA) was analysed for clinical and laboratory features of 1423 KRT patients with COVID-19 either hospitalized or non-hospitalized at initial triage and those re-presenting a second time. Predictors of outcomes (hospitalization, 28-day mortality) were then determined for all those not hospitalized at initial triage. Results Among 1423 KRT patients with COVID-19 [haemodialysis (HD), n = 1017; transplant, n = 406), 25% (n = 355) were not hospitalized at first presentation due to mild illness (30% HD, 13% transplant). Of the non-hospitalized patients, only 10% (n = 36) re-presented a second time, with a 5-day median interval between the two presentations (interquartile range 2–7 days). Patients who re-presented had worsening respiratory symptoms, a decrease in oxygen saturation (97% versus 90%) and an increase in C-reactive protein (26 versus 73 mg/L) and were older (72 vs 63 years) compared with those who did not return a second time. The 28-day mortality between early admission (at first presentation) and deferred admission (at second presentation) was not significantly different (29% versus 25%; P = 0.6). Older age, prior smoking history, higher clinical frailty score and self-reported shortness of breath at first presentation were identified as risk predictors of mortality when re-presenting after discharge at initial triage. Conclusions This study provides evidence that KRT patients with COVID-19 and mild illness can be managed effectively with supported outpatient care and with vigilance of respiratory symptoms, especially in those with risk factors for poor outcomes. Our findings support a risk-stratified clinical approach to admissions and discharges of KRT patients presenting with COVID-19 to aid clinical triage and optimize resource utilization during the ongoing pandemic.

Published
2021

8. Influence of exogenous growth hormone administration on circulating concentrations of α-klotho in healthy and chronic kidney disease subjects: A prospective, single-center open case-control pilot study 11 Medical and Health Sciences 1103 Clinical Sciences

Author

Adema, Aaltje Y., de Roij van Zuijdewijn, Camiel L. M., Hoenderop, Joost G., de Borst, Martin H., ter Wee, Piet M., Heijboer, Annemieke C., Vervloet, Marc G., Bindels, R., Hoenderop, J. G., de Borst, M. H., Hillebrands, J. L., Navis, G. J., ter Wee, P. M., Vervloet, M. G., Laboratory for Endocrinology, Amsterdam Gastroenterology Endocrinology Metabolism, AMS - Musculoskeletal Health, Nephrology, AII - Inflammatory diseases, ACS - Diabetes & metabolism, VU University medical center, Clinical chemistry, AGEM - Endocrinology, metabolism and nutrition, Amsterdam Movement Sciences - Rehabilitation & Development, and NCA - Brain mechanisms in health and disease

Subjects
urologic and male genital diseases, female genital diseases and pregnancy complications
Abstract

Background: The CKD-associated decline in soluble α-Klotho (α-Klotho) levels is considered detrimental. Some studies suggest a direct induction of α-Klotho concentrations by growth hormone (GH). In the present study, the effect of exogenous GH administration on α-Klotho concentrations in a clinical cohort with mild chronic kidney disease (CKD) and healthy subjects was studied. Methods: A prospective, single-center open case-control pilot study was performed involving 8 patients with mild CKD and 8 healthy controls matched for age and sex. All participants received subcutaneous GH injections (Genotropin®, 20 mcg/kg/day) for 7 consecutive days. α-Klotho concentrations were measured at baseline, after 7 days of therapy and 1 week after the intervention was stopped. Results: α-Klotho concentrations were not different between CKD-patients and healthy controls at baseline (554 (388-659) vs. 547 (421-711) pg/mL, P = 0.38). Overall, GH therapy increased α-Klotho concentrations from 554 (405-659) to 645 (516-754) pg/mL, P < 0.05). This was accompanied by an increase of IGF-1 concentrations from 26.8 ± 5.0 nmol/L to 61.7 ± 17.7 nmol/L (P < 0.05). GH therapy induced a trend toward increased α-Klotho concentrations both in the CKD group (554 (388-659) to 591 (358-742) pg/mL (P = 0.19)) and the healthy controls (547 (421-711) pg/mL to 654 (538-754) pg/mL (P = 0.13)). The change in α-Klotho concentration was not different for both groups (P for interaction = 0.71). α-Klotho concentrations returned to baseline levels within one week after the treatment (P < 0.05). Conclusions: GH therapy increases α-Klotho concentrations in subjects with normal renal function or stage 3 CKD. A larger follow-up study is needed to determine whether the effect size is different between both groups or in patients with more severe CKD. Trial registration: This trial is registered in EudraCT (2013-003354-24).

Published
2018

9. Mortality reduction by post-dilution online-haemodiafiltration: a cause-specific analysis

Author

Nubé, Menso J., Peters, Sanne A E, Blankestijn, Peter J., Canaud, Bernard, Davenport, Andrew, Grooteman, Muriel P C, Asci, Gulay, Locatelli, Francesco, Maduell, Francisco, Morena, Marion, Ok, Ercan, Torres, Ferran, Bots, Michiel L., Moreso, Francesc, Pons, Mercedes, Ramos, Rosa, Mora-Macià, Josep, Carreras, Jordi, Soler, Jordi, Campistol, Josep M., Martinez-Castelao, Alberto, Insensé, B., Perez, C., Feliz, T., Barbetta, M., Soto, C., Mora, J., Juan, A., Ibrik, O., Foraster, A., Nin, J., Fernández, A., Arruche, M., Sánchez, C., Vidiella, J., Barbosa, F., Chiné, M., Hurtado, S., Llibre, J., Ruiz, A., Serra, M., Salvó, M., Poyuelo, T., Maduell, F., Carrera, M., Fontseré, N., Arias, M., Merín, A., Ribera, L., Galceran, J. M., Mòdol, J., Moliner, E., Ramirez, A., Aguilera, J., Alvarez, M., De La Torre, B., Molera, M., Casellas, J., Martín, G., Andres, E., Coll, E., Valles, M., Martínez, C., Castellote, E., Casals, J. M., Gabàs, J., Romero, M., Martinez-Castelao, A., Fulladosa, X., Ramirez-Arellano, M., Fulquet, M., Pelegrí, A., El Manouari, M., Ramos, N., Bartolomé, J., Sans, R., Fernández, E., Sarró, F., Compte, T., Marco, F., Mauri, R., Bronsoms, J., Arnaiz, J. A., Beleta, H., Pejenaute, A., Ríos, J., Lara, J., Ter Wee, P. M., Van Den Dorpel, M. A., Dorval, M., Lévesque, R., Koopman, M. G., Konings, C. J A M, Haanstra, W. P., Kooistra, M., Van Jaarsveld, B., Noordzij, T., Feith, G. W., Peltenburg, H. G., Van Buren, M., Offerman, J. J G, Hoogeveen, E. K., De Heer, F., Van De Ven, P. J., Kremer Hovinga, T. K., Bax, W. A., Groeneveld, J. O., Lavrijssen, A. T J, Schrander-Van Der Meer, A. M., Reichert, L. J M, Huussen, J., Rensma, P. L., Schrama, Y., Van Hamersvelt, H. W., Boer, W. H., Van Kuijk, W. H., Vervloet, M. G., Wauters, I. M P M J, Sekse, I., Toz, Huseyin, Ok, Ebru Sevinc, Kircelli, Fatih, Yilmaz, Mumtaz, Hur, Ender, Demirci, Meltem Sezis, Demirci, Cenk, Duman, Soner, Basci, Ali, Adam, Siddig Momin, Isik, Ismet Onder, Zengin, Murat, Suleymanlar, Gultekin, Yilmaz, Mehmet Emin, Ergin, Mehmet Ozkahya Pinar, Sagdic, Alfert, Kayali, Erkan, Boydak, Can, Colak, Taskin, Caliskan, Sihli, Kaplan, Hakan, Ulas, Hasibe, Kirbiyik, Sait, Berktas, Hakan, Dilbaz, Necati, Cristol, Jean Paul, Leray-Moragues, Hélène, Chenine, Leïla, Picot, Marie Christine, Jaussent, Audrey, Belloc, Claire, Lagarrigue, Mélodie, Chalabi, Lotfi, Debure, Alain, Ouziala, Messaoud, Lefevre, Jean Jacques, Thibaudin, Damien, Mohey, Hesham, Broyet, Christian, Afiani, Aida, Serveaux, Marie Odile, Patrier, Laure, Maurice, François, Rivory, Jean Pierre, Nicoud, Philippe, Durand, Claude, Normand, Michel, Seigneuric, Bruno, Magnant, Eric, Azzouz, Lynda, Islam, Mohamed Shariful, Vido, Sandor, Nzeyimana, Hilaire, Simonin, Danièle, Azymah, Yamina, Farah, Ibrahim, Coindre, Jean Philippe, Puyoo, Olivier, Chabannier, Marie Hélène, Ibos, Richard, Rouleau, Fabienne, Vela, Carlos, Joule, Josiane, Combarnous, François, Turc-Baron, Cécile, Ducret, Francis, Pointet, Philippe, Rey, Isabelle, Potier, Jacky, Bendini, Jean Christophe, Perrin, Franck, Kunz, Kristian, Lefrancois, Gaëlle, Colin, Angélique, Parahy, Sophie, Dancea, Irima, Coupel, Stéphanie, Testa, Angelo, Brunet, Philippe, Lebrun, Gaétan, Jaubert, Dominique, Delcroix, Catherine, Lavainne, Frédéric, Lefebvre, Anne, Guillodo, Marie Paule, Le Grignou, Dominique, Djema, Assia, Maaz, Mehadji, Chiron, Sylvie, Hoffmann, Maxime, Depraetre, Pascale, Haddj-Elmrabet, Atman, Joyeux, Véronique, Fleury, Dominique, Vrigneaud, Laurence, Lemaitre, Vincent, Aguilera, Didier, Guerraoui, Abdallah, Cremault, Alain, Laradi, Achour, Babinet, Francois, VU University Medical Center [Amsterdam], University of Oxford [Oxford], University Medical Center [Utrecht], Fresenius Medical Care Deutschland, University College of London [London] (UCL), Ege university, Alessandro Manzoni Hospital, Hospital Clinic Barcelona, Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Universitat Autònoma de Barcelona (UAB), Ege Üniversitesi, Nephrology, ICaR - Circulation and metabolism, Herrada, Anthony, and University of Oxford

Subjects
Male, medicine.medical_specialty, 030232 urology & nephrology, Hemodiafiltration, 030204 cardiovascular system & hematology, haemodiafiltration, Convection, Lower risk, Sudden death, convection volume, [SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, haemo-diafiltration, 03 medical and health sciences, 0302 clinical medicine, Renal Dialysis, cardiovascular disease, Cause of Death, Internal medicine, Journal Article, medicine, Humans, Intensive care medicine, Aged, Proportional Hazards Models, Randomized Controlled Trials as Topic, Transplantation, integumentary system, business.industry, Mortality rate, Hazard ratio, Middle Aged, [SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology, mortality, Confidence interval, 3. Good health, meta-analysis, Cardiovascular Diseases, Nephrology, Meta-analysis, Cardiology, Number needed to treat, Kidney Failure, Chronic, Female, business
Abstract

WOS: 000398117600023, PubMed ID: 28025382, Background. From an individual participant data (IPD) meta-analysis from four randomized controlled trials comparing haemodialysis (HD) with post-dilution online-haemodiafiltration (ol-HDF), previously it appeared that HDF decreases all-cause mortality by 14% (95% confidence interval 25; 1) and fatal cardiovascular disease (CVD) by 23% (39; 3). Significant differences were not found for fatal infections and sudden death. So far, it is unclear, however, whether the reduced mortality risk of HDF is only due to a decrease in CVD events and if so, which CVD in particular is prevented, if compared with HD. Methods. The IPD base was used for the present study. Hazard ratios and 95% confidence intervals for cause-specific mortality overall and in thirds of the convection volume were calculated using the Cox proportional hazard regression models. Annualized mortality and numbers needed to treat (NNT) were calculated as well. Results. Besides 554 patients dying from CVD, fatal infections and sudden death, 215 participants died from 'other causes', such as withdrawal from treatment and malignancies. In this group, the mortality risk was comparable between HD and ol-HDF patients, both overall and in thirds of the convection volume. Subdivision of CVD mortality in fatal cardiac, non-cardiac and unclassified CVD showed that ol-HDF was only associated with a lower risk of cardiac casualties [0.64 (0.61; 0.90)]. Annual mortality rates also suggest that the reduction in CVD death is mainly due to a decrease in cardiac fatalities, including both ischaemic heart disease and congestion. Overall, 32 and 75 patients, respectively, need to be treated by high-volume HDF (HV-HDF) to prevent one all-cause and one CVD death, respectively, per year. Conclusion. The beneficial effect of ol-HDF on all-cause and CVD mortality appears to be mainly due to a reduction in fatal cardiac events, including ischaemic heart disease as well as congestion. In HV-HDF, the NNT to prevent one CVD death is 75 per year., EuDial working group; European Nephrology and Dialysis Institute; Catalan Society of Nephrology; Fresenius Medical Care; Dutch Kidney Foundation [C02.2019]; Fresenius Medical Care, Netherlands; Gambro Lundia AB, Sweden; Dr E.E. Twiss Fund; International Society of Nephrology/Baxter Extramural Grant Program; Netherlands Organization for Health Research and DevelopmentNetherlands Organization for Health Research and Development [170882802]; national grant from the Health Ministry (Programme Hospitalier de Recherche Clinique, PHRC); Gambro through the Catalan Society of Nephrology; Roche Netherlands, The HDF Pooling project was designed, conducted and analysed independently of the financial contributors of the individual studies as listed below. Study data were collected and retained by the investigators and were not available for the financial contributors of the individual studies. S.A.E.P. and the meetings of the representatives of the combined authors of the four studies were financially supported by the EuDial working group. EuDial is an official working group of the European Renal Association-European Dialysis Transplant Association (ERA-EDTA, http://era-edta.org/eudial/European_Dialysis_Working_Group.html). No industry funding was received for any part of or activity related to the present analysis.; The Turkish HDF study was supported by European Nephrology and Dialysis Institute with an unrestricted grant. The study was performed in Fresenius Medical Care haemodialysis clinics in Turkey. ESHOL was supported by The Catalan Society of Nephrology and by grants from Fresenius Medical Care and Gambro through the Catalan Society of Nephrology. The CONTRAST study was supported by a grant from the Dutch Kidney Foundation (Nierstichting Nederland Grant C02.2019), and unrestricted grants from Fresenius Medical Care, Netherlands, and Gambro Lundia AB, Sweden. Additional support was received from the Dr E.E. Twiss Fund, Roche Netherlands, the International Society of Nephrology/Baxter Extramural Grant Program, and the Netherlands Organization for Health Research and Development (ZONMw Grant 170882802). The French HDF study was supported by a national grant from the Health Ministry (Programme Hospitalier de Recherche Clinique, PHRC) as a means to improve care and outcome of elderly chronic disease patients.

Published
2017

10. Circulating markers of bone turnover

Author

Vervloet, M. G., Brandenburg, V. M., Bover, J., Brandenburg, V., Covic, A., Cozzolino, M., Evenepoel, P., Goldsmith, D., Massy, Z., Mazzaferro, S., Urena-Torres, P., and Vervloet, M.

Subjects
Nephrology, medicine.medical_specialty, Bone turnover, Bone disease, 030232 urology & nephrology, Physiology, Parathyroid hormone, 030209 endocrinology & metabolism, Review, urologic and male genital diseases, Collagen Type I, Bone remodeling, 03 medical and health sciences, 0302 clinical medicine, Chronic kidney disease-mineral and bone disorder, Internal medicine, Chronic kidney disease, Bone cell, medicine, CKD-MBD, Humans, Renal osteodystrophy, ddc:610, Renal Insufficiency, Renal Insufficiency, Chronic, Chronic, Chronic Kidney Disease-Mineral and Bone Disorder, business.industry, Tartrate-Resistant Acid Phosphatase, medicine.disease, Alkaline Phosphatase, Peptide Fragments, Endocrinology, Parathyroid Hormone, Bone Remodeling, business, Peptides, Biomarkers, Procollagen, Kidney disease
Abstract

Symposium on Bone in Chronic Kidney Disease (CKD), CKD 2016, Amsterdam, Netherlands, 13 Sep 2016 - 13 Sep 2016; Journal of nephrology 30(5), 663-670 (2017). doi:10.1007/s40620-017-0408-8 special issue: "Special issue on “Bone in Chronic Kidney Disease” an activity of the ERA-EDTA WG on CKD-MBD", Published by Springer, Milano

Published
2017

13. Proatherogenic changes due to haemodialysis as a possible consequence of bio-incompatibility in the dialyzer

Author

Nubé, M. J. and Vervloet, M. G.

Abstract

Chronic haemodialysis patients have a disproportionately high risk for developing cardiovascular disease, which can only in part be explained by known risk factors such as dyslipidaemia, hypertension, hyperhomocysteinemia, diabetes mellitus and chronic volume expansion. A possible cause is that the haemodialysis treatment itself contributes to the accelerated atherosclerosis, observed in these patients. Nowadays, atherosclerosis is considered an inflammatory process, mediated by a dysfunction of the vascular endothelium. As a result, blood cells adhere to the vascular surface and release a variety of vasoactive mediators, cytokines, growth factors and free radicals. Due to the contact between blood and dialyzer, humoral systems and cellular elements are stimulated, and this may be viewed as an inflammatory reaction. As a consequence of this, the vascular surface of haemodialysis patients is repeatedly exposed to the influences of cytokines, coagulation products, vasoactive mediators, stimulated leukocytes and thrombocytes, and oxidative stress. It is therefore conceivable that the haemodialysis treatment itself enhances the greatly increased cardiovascular risk in chronic haemodialysis patients.

Published
2000

14. The role of antacids in gastrotonometry:An in vitro study

Author

Vervloet, M. G., Groeneveld, A. B J, Kolkman, J. J., Zwaarekant, L. J., Nephrology, ACS - Diabetes & metabolism, AII - Inflammatory diseases, and Intensive care medicine

Abstract

Objective: To evaluate in vitro the value of antacids as an alternative to H2 blockers to raise gastric juice pH for reliable PCO2 tonometry in the human stomach. Design and setting: Laboratory study in a university hospital. Interventions: A bath was filled with 0.1 M hydrochloric acid at pH 1.3 and CO2 was gassed through the acid to simulate an intragastric environment. Experiments were performed in duplicate. Both the manual saline technique and the new semi-continuous, semi-automated air technique of PCO2 tonometry were used to evaluate the effects of adding i) aluminium oxide/magnesium hydroxide (Antagel®) and ii) sodium bicarbonate on the PCO2. The latter technique was done to simulate intragastric CO2 production following buffering of gastric acid by bicarbonate in the mucosa, or in the saliva or pancreatic/duodenal juice entering the stomach, an effect that can be prevented in vivo by prior administration of H2 blockers. Endpoints: Changes in tonometrically determined PCO2 after the addition of alkali. A secondary endpoint was the difference between the manual saline and the semicontinuous air tonometry techniques. Measurements and main results: The mean pH increased from 1.3 to 4.0 after adding 40 ml aluminium oxide/magnesium hydroxide. The subsequent addition of sodium bicarbonate, dosed to increase pH above 6.5, caused a steep rise in PCO2 from 34 and 39 mmHg to 134 and 99 mmHg, for each experiment respectively, as measured by conventional tonometry, and from 37 and 38 mmHg to 116 and 115 mmHg, respectively, for the air technique. These changes were transient. Air tonometry detected changes in PCO2 more rapidly than the manual technique. Conclusions: Adding antacids elevates the PCO2 in hydrochloric acid and does not prevent CO2 generation after the addition of sodium bicarbonate, even though the pH is raised from about 1 to 4. The clinical use of antacids instead of H2 blockers to prevent spurious PCO2 elevations following buffering of acid by bicarbonate, and thereby increase the reliability of gastric tonometry, should be discouraged.

Published
1998

15. Cardiovascular disease in CKD

Author

van den Broek, J. S., primary, Hoekstra, T., additional, Drechsler, C., additional, Brandenburg, V. M., additional, Dekker, F. W., additional, Vervloet, M. G., additional, Albrizio, P., additional, Sepe, V., additional, Gnecchi, M., additional, Cervio, E., additional, Mangione, F., additional, Fiorini, F., additional, Rampino, T., additional, Libetta, C., additional, Dal Canton, A., additional, Di Marco, G., additional, Reuter, S., additional, Kentrup, D., additional, Tiemann, K., additional, Fobker, M., additional, Engelbertz, C., additional, Breithardt, G., additional, Reinecke, H., additional, Brand, E., additional, Pavenstadt, H., additional, Brand, M., additional, De Mauri, A., additional, Conti, N., additional, Chiarinotti, D., additional, David, P., additional, Capurro, F., additional, De Leo, M., additional, Delanaye, P., additional, Krzesinski, J.-M., additional, Warling, X., additional, Smelten, N., additional, Cavalier, E., additional, Hayashi, M., additional, Kanno, Y., additional, Iwai, M., additional, Yoshida, T., additional, and Abe, T., additional

Published
2013
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23. The effect of six-month oral vitamin K supplementation on calcification propensity time in individuals with type 2 diabetes mellitus: A post hoc analysis of a randomized, double-blind, placebo-controlled trial.

Author

Meer R, Romero Prats ML, Vervloet MG, van der Schouw YT, de Jong PA, and Beulens JWJ

Subjects
Humans, Male, Double-Blind Method, Female, Aged, Middle Aged, Administration, Oral, Time Factors, Treatment Outcome, Positron Emission Tomography Computed Tomography, Biomarkers blood, Vitamin K, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Vascular Calcification diagnostic imaging, Vascular Calcification blood, Vascular Calcification drug therapy, Vascular Calcification prevention & control, Dietary Supplements, Vitamin K 2 administration & dosage, Vitamin K 2 therapeutic use, Vitamin K 2 analogs & derivatives
Abstract

Background and Aims: Experimental studies suggested that vitamin K supplementation may retard arterial calcification. Recently, serum calcification propensity time (T 50 ) has been suggested as a functional biomarker for arterial wall calcification propensity. In this post-hoc analysis of a clinical trial, we evaluated the effect of six-month oral vitamin K supplementation on T 50 and assessed the correlation between T 50 and imaging arterial calcification parameters in people with type 2 diabetes (T2DM)., Methods: This double-blind, randomized, placebo-controlled trial included 68 participants (age = 69 ± 8 years, 76% male) with T2DM. Participants were assigned to menaquinone-7 (360 μg/day; n = 35) or placebo (n = 33). T 50 was measured via nephelometry in serum collected at baseline, three and six months. Arterial calcification was measured at baseline and six months via 18 F-Na PET-CT and conventional CT using Target-to-Background ratio (TBR) and Agatston score. Longitudinal analysis of covariance adjusted for baseline T 50 was used to study the treatment effect. Spearman's correlation was used to assess the correlation between T 50 and imaging calcification parameters., Results: Median baseline T 50 was similar in the vitamin K (350 [321-394] minutes) and placebo groups (363 [320-398]). There was no significant difference in T 50 between treatment arms over time (ẞ = 1.00, 95%C.I. = 0.94-1.07, p = 0.982). The correlation coefficient of T 50 with TBR and Agatston score at baseline were -0.185 (p = 0.156) and -0.121 (p = 0.358), respectively., Conclusions: No effect of vitamin K supplementation on T 50 was observed in T2DM. Moreover, T 50 did not correlate with TBR and Agatston score. Further research on vitamin K in arterial calcification and on the validity of T 50 as arterial calcification marker is warranted., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Published
2024
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24. Clinical utility of bone markers in various diseases.

Author

Vlot MC, den Heijer M, de Jongh RT, Vervloet MG, Lems WF, de Jonge R, Obermayer-Pietsch B, and Heijboer AC

Subjects
Biomarkers blood, Biomarkers urine, Bone Diseases diagnosis, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 diagnosis, Diabetes Mellitus, Type 2 urine, Fibroblast Growth Factor-23, Humans, Osteitis Deformans blood, Osteitis Deformans diagnosis, Osteoporosis blood, Osteoporosis diagnosis, Osteoporosis urine, Bone Diseases blood, Bone Diseases urine, Bone Remodeling physiology
Abstract

Measurements of bone markers (BMs) in peripheral blood or urine are a pivotal part of bone research within modern clinical medicine. In recent years the use of BMs increased substantially as they can be useful either to diagnose bone (related) disease and to follow its natural history, but also to monitor the effects of interventions. However, the use of BMs is still complicated mainly due to (pre)analytical variability of these substances, limited accessibility of assays, variable cut-off values in different countries and laboratories and heterogeneous results with regard to clinical implications of measuring BMs in several studies. This review will provide the clinician with a practical guide, based on current evidence, in which circumstances to test which bone markers for optimal diagnostic purposes, in order to improve patient care in different areas of bone diseases including Paget's disease, primary osteoporosis, tumor induced osteomalacia, hypophosphatemic rickets, van Buchem disease, chronic kidney disease, rheumatoid arthritis, neoplasma/multiple myeloma, type 2 diabetes mellitus and primary hyperparathyroidism. The clinician should consider fasting state, recent fractures, aging, menopausal status, concomitant liver and kidney disease when ordering and interpreting BM measurements as these factors might result in misleading BM concentrations. We found that BMs are clearly useful in the current diagnosis of tumor induced osteomalacia, van Buchem disease, Paget's disease and hypophosphatemic rickets. In addition, BMs are useful to monitor disease activity in chronic kidney disease, Paget's disease and are useful to monitor treatment adherence in osteoporosis., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Published
2018
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25. Feasibility of long-term continuous subcutaneous magnesium supplementation in a patient with irreversible magnesium wasting due to cisplatin.

Author

Vermeulen EA, Vervloet MG, Lubach CH, Nurmohamed SA, and Penne EL

Subjects
Adult, Feasibility Studies, Female, Humans, Infusions, Subcutaneous, Renal Tubular Transport, Inborn Errors chemically induced, Time Factors, Treatment Outcome, Cisplatin adverse effects, Dietary Supplements, Magnesium administration & dosage, Renal Tubular Transport, Inborn Errors therapy
Abstract

A 39-year-old woman presented with severe, uncontrolled and irreversible hypomagnesaemia, following cisplatin treatment in her childhood. Because high-dose oral magnesium supplementation therapy was insufficient and not tolerated, continuous subcutaneous magnesium supplementation was successfully instituted and continued in the outpatient setting. This case demonstrates that continuous subcutaneous magnesium supplementation is effective in maintaining magnesium levels within the normal range, is well tolerated and may provide a long-term solution for chronic hypomagnesaemia due to intractable renal losses.

Published
2017

26. Fish and omega-3 fatty acid intake in relation to circulating fibroblast growth factor 23 levels in renal transplant recipients.

Author

Baia LC, Van den Berg E, Vervloet MG, Heilberg IP, Navis G, Bakker SJ, Geleijnse JM, Kromhout D, Soedamah-Muthu SS, and De Borst MH

Subjects
Adult, Aged, Animals, Cohort Studies, Cross-Sectional Studies, Female, Fibroblast Growth Factor-23, Humans, Male, Middle Aged, Transplant Recipients, Diet, Fatty Acids, Omega-3 pharmacology, Fibroblast Growth Factors blood, Fishes, Kidney Transplantation
Abstract

Background and Aims: A high circulating fibroblast growth factor 23 (FGF23) level is an independent risk factor for cardiovascular mortality in renal transplant recipients and the general population. N-3 fatty acids eicosapentaenoic (EPA) and docosahexaenoic acid (DHA) may contribute to cardiovascular risk reduction. We investigated whether fish and EPA-DHA intake are related to FGF23 levels in renal transplant recipients., Methods and Results: We performed a cross-sectional analysis in 619 stable renal transplant recipients (mean age 53 years, 57% male, estimated glomerular filtration rate [eGFR] 53 ± 20 mL/min/1.73 m(2)). Dietary intake was assessed by a 177-item food frequency questionnaire. Serum intact FGF23 was measured by ELISA. We examined differences in FGF23 levels across categories of fish and EPA-DHA intake using analysis of variance models adjusted for age, sex, dietary and lifestyle factors and key determinants of FGF23. Patients consumed on average 15 g of fish and 139 mg EPA-DHA/day. Median FGF23 was 62 pg/mL (IQR 43-98 pg/mL). Higher dietary EPA-DHA and fish intake were associated with lower serum FGF23 levels. Subgroup analyses revealed that particularly in patients with reduced renal function (eGFR <60 mL/min/1.73 m(2)), adjusted FGF23 levels (114, 79, 75 pg/mL, P = 0.0001) were inversely associated with tertiles of EPA-DHA intake. Similarly, we observed an inverse association between fish consumption and serum FGF23 levels in adjusted analyses., Conclusion: A higher intake of fish and dietary n-3 fatty acids (EPA-DHA) is related to lower circulating FGF23 levels in renal transplant recipients. Further research is needed to assess the causality of this association and the clinical implications., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Published
2014
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27. Cinacalcet for secondary hyperparathyroidism: from improved mineral levels to improved mortality?

Author

Vervloet MG, du Buf-Vereijken PW, Potter van Loon BJ, Manamley N, Reichert LJ, and Smak Gregoor PJ

Subjects
Bone Density drug effects, Calcinosis drug therapy, Calcium blood, Cinacalcet, Heart Valve Diseases drug therapy, Humans, Hyperparathyroidism, Secondary blood, Parathyroid Hormone blood, Calcimimetic Agents therapeutic use, Hyperparathyroidism, Secondary drug therapy, Naphthalenes therapeutic use
Abstract

Secondary hyperparathyroidism is an almost inevitable complication of advanced kidney failure. The introduction of the calcimimetic cinacalcet for the treatment of secondary hyperparathyroidism in patients on dialysis was based on its ability to reduce elevated levels of parathyroid hormone (PTH). Subsequent clinical studies confirmed the beneficial effects of cinacalcet on biochemical parameters reflecting mineral disturbances and bone disease. In this review we summarise the impact of cinacalcet on biochemical, intermediate and clinical outcomes. We also present previously unpublished mineral metabolism data from 144 Dutch dialysis patients treated with cinacalcet who participated in the pan-European ECHO observational study. Although secondary hyperparathyroidism tended to be more severe in our Dutch cohort, compared with the entire ECHO cohort, cinacalcet was nevertheless effective in reducing PTH in these patients. Two recent clinical studies evaluated, respectively, the efficacy of cinacalcet in improving the intermediate endpoint of cardiovascular calcifications (ADVANCE trial), and its impact on clinical outcomes, including all-cause mortality and cardiovascular events (EVOLVE trial). The ADVANCE trial provided evidence that cinacalcet may indeed improve calcification in both large arteries and cardiac valves. The EVOLVE trial, however, did not meet its clinical primary endpoint (time to all-cause mortality, myocardial infarction, hospitalisation for unstable angina, heart failure or a peripheral vascular event), although secondary and sensitivity analysis suggested a beneficial effect. The clinical implications of these important studies are also addressed in this review.

Published
2013

28. Dutch guidelines for diagnosis and therapy of proliferative lupus nephritis.

Author

van Tellingen A, Voskuyl AE, Vervloet MG, Bijl M, de Sévaux RG, Berger SP, Derksen RH, and Berden JH

Subjects
Antirheumatic Agents therapeutic use, Azathioprine therapeutic use, Biopsy, Cyclophosphamide therapeutic use, Disease Progression, Humans, Immunosuppressive Agents therapeutic use, Lupus Erythematosus, Systemic complications, Lupus Erythematosus, Systemic pathology, Lupus Nephritis diagnosis, Lupus Nephritis pathology, Mycophenolic Acid analogs & derivatives, Mycophenolic Acid therapeutic use, Netherlands, Prognosis, Treatment Outcome, Lupus Nephritis drug therapy, Practice Guidelines as Topic
Abstract

Proliferative lupus nephritis is a strong predictor of morbidity and mortality in patients with systemic lupus erythematosus. Despite improvements in the management of lupus nephritis, a significant number of the patients do not respond to immunosuppressive therapy and progress to end-stage renal failure. In order to optimise the diagnostic strategy and treatment of patients with proliferative lupus nephritis, guidelines are needed. In this review, the Dutch Working Party on Systemic Lupus Erythematosus provides recommendations regarding four important areas in patients with proliferative lupus nephritis: I) indications for a first renal biopsy, II ) definitions of treatment response, III ) selection of treatment options, and IV) indications for a repeat biopsy.

Published
2012

29. [Proatherogenic changes induced by hemodialysis; probably a result of bio-incompatibility].

Author

Nubé MJ and Vervloet MG

Subjects
Acute-Phase Reaction chemically induced, Anticoagulants therapeutic use, Arteriosclerosis immunology, Arteriosclerosis prevention & control, Chronic Disease, Humans, Kidneys, Artificial, Risk Factors, Acute-Phase Reaction immunology, Arteriosclerosis etiology, Coated Materials, Biocompatible, Dialysis Solutions adverse effects, Renal Dialysis adverse effects
Abstract

Chronic haemodialysis patients have a disproportionately high risk for developing cardiovascular disease, which can only in part be explained by known risk factors such as dyslipidaemia, hypertension, hyperhomocysteinemia, diabetes mellitus and chronic volume expansion. A possible cause is that the haemodialysis treatment itself contributes to the accelerated atherosclerosis, observed in these patients. Nowadays, atherosclerosis is considered an inflammatory process, mediated by a dysfunction of the vascular endothelium. As a result, blood cells adhere to the vascular surface and release a variety of vasoactive mediators, cytokines, growth factors and free radicals. Due to the contact between blood and dialyzer, humoral systems and cellular elements are stimulated, and this may be viewed as an inflammatory reaction. As a consequence of this, the vascular surface of haemodialysis patients is repeatedly exposed to the influences of cytokines, coagulation products, vasoactive mediators, stimulated leukocytes and thrombocytes, and oxidative stress. It is therefore conceivable that the haemodialysis treatment itself enhances the greatly increased cardiovascular risk in chronic haemodialysis patients.

Published
2000

30. Derangements of coagulation and fibrinolysis in critically ill patients with sepsis and septic shock.

Author

Vervloet MG, Thijs LG, and Hack CE

Subjects
Animals, Disseminated Intravascular Coagulation epidemiology, Disseminated Intravascular Coagulation physiopathology, Humans, Sepsis physiopathology, Shock, Septic complications, Shock, Septic physiopathology, Disseminated Intravascular Coagulation etiology, Fibrinolysis, Sepsis complications
Abstract

In patients with sepsis and septic shock, both coagulation and fibrinolysis are activated frequently leading to the syndrome of diffuse intravascular coagulation (DIC). The different mechanisms leading to abnormalities in coagulation and fibrinolysis are discussed in detail. The coagulation and fibrinolytic system appear to be influenced by the septic process largely independently, leading to a procoagulant imbalance between these systems. Coagulation is initiated by mediator-induced expression of tissue factor and is associated with consumption of the natural coagulation inhibitors antithrombin III, protein C, and protein S. As a result, high plasma levels of thrombin-antithrombin complex (TAT) can be found. The effects on fibrinolysis are dominated by (highly) increased levels of plasminogen activator inhibitor type 1 (PAI-1), leading to inadequate fibrinolysis. Although levels of plasminogen activator antigen are increased, its activity is almost completely inhibited by PAI-1. The resulting effects predispose to a procoagulant state, with widespread fibrin deposition, which may be an important mechanism contributing to multiple organ failure. A thorough understanding of the pathophysiological mechanisms underlying the DIC-syndrome is a prerequisite for a rational approach and future therapy for this severe complication of sepsis.

Published
1998
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