Kidney dysfunction is associated with thrombosis and disease severity in myeloproliferative neoplasms: implications from the German Study Group for MPN Bioregistry

  • Simple Summary: In patients with myeloproliferative neoplasms (MPN) and in patients with kidney dysfunction, a higher rate of thrombosis has been reported compared with the general population. Furthermore, MPN patients are more prone to develop kidney dysfunction. In our study, we assessed the importance of specific risk factors for kidney dysfunction and thrombosis in MPN patients. We found that the rate of thrombosis is correlated with the degree of kidney dysfunction, especially in myelofibrosis. Significant associations for kidney dysfunction included arterial hypertension, MPN treatment, and increased inflammation, and those for thrombosis comprised arterial hypertension, non-excessive platelet counts, and antithrombotic therapy. The identified risk factor associations varied between MPN subtypes. Our data suggest that kidney dysfunction in MPN patients is associated with an increased risk of thrombosis, mandating closer monitoring, and, possibly, early thromboprophylaxis. Abstract: Inflammation-induced thrombosis represents a severe complication in patients with myeloproliferative neoplasms (MPN) and in those with kidney dysfunction. Overlapping disease-specific attributes suggest common mechanisms involved in MPN pathogenesis, kidney dysfunction, and thrombosis. Data from 1420 patients with essential thrombocythemia (ET, 33.7%), polycythemia vera (PV, 38.5%), and myelofibrosis (MF, 27.9%) were extracted from the bioregistry of the German Study Group for MPN. The total cohort was subdivided according to the calculated estimated glomerular filtration rate (eGFR, (mL/min/1.73 m2)) into eGFR1 (≥90, 21%), eGFR2 (60–89, 56%), and eGFR3 (<60, 22%). A total of 29% of the patients had a history of thrombosis. A higher rate of thrombosis and longer MPN duration was observed in eGFR3 than in eGFR2 and eGFR1. Kidney dysfunction occurred earlier in ET than in PV or MF. Multiple logistic regression analysis identified arterial hypertension, MPN treatment, increased uric acid, and lactate dehydrogenase levels as risk factors for kidney dysfunction in MPN patients. Risk factors for thrombosis included arterial hypertension, non-excessive platelet counts, and antithrombotic therapy. The risk factors for kidney dysfunction and thrombosis varied between MPN subtypes. Physicians should be aware of the increased risk for kidney disease in MPN patients, which warrants closer monitoring and, possibly, early thromboprophylaxis.

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Author:Judith Gecht, Ioannis Tsoukakis, Kim Kricheldorf, Frank Stegelmann, Martine Klausmann, Martin Griesshammer, Holger Schulz, Wiebke Hollburg, Joachim Rudolf Göthert, Katja Sockel, Florian Heidel, Norbert Gattermann, Christoph Maintz, Haifa Kathrin Al-Ali, Uwe PlatzbeckerORCiDGND, Richard Hansen, Mathias Hänel, Stefani Barbara Parmentier, Martin Bommer, Heike L. Pahl, Fabian Magnus Eugen Lang, Martin Kirschner, Susanne Isfort, Tim Henrik Brümmendorf, Konstanze Döhner, Steffen KoschmiederORCiDGND
URN:urn:nbn:de:hebis:30:3-621887
DOI:https://doi.org/10.3390/cancers13164086
ISSN:2072-6694
Parent Title (English):Cancers
Publisher:MDPI
Place of publication:Basel
Document Type:Article
Language:English
Date of Publication (online):2021/08/13
Date of first Publication:2021/08/13
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2022/07/04
Tag:JAK2V617F; bleeding; chronic kidney disease; essential thrombocythemia (ET); myeloproliferative neoplasms (MPN); polycythemia vera (PV); primary myelofibrosis (PMF); renal dysfunction; thromboembolism; thrombosis
Volume:13
Issue:16, art. 4086
Page Number:21
First Page:1
Last Page:21
Note:
This work was in part supported by grants of the German Research Foundation (Deutsche Forschungsgemeinschaft) to SK (KO 2155/7-1) and to THB (BR 1782/5-1) within the CRU344 on MPN, by the Stiftung Universitätsmedizin of RWTH Aachen University to KK, THB, and SK for the maintenance of the bioregistry, and to THB by the Interdisciplinary Center for Clinical Research (IZKF O3-7).
Note:
S.K. reports funding from Novartis Foundation, BMS, Novartis, and Janssen; and other financial disclosures (i.e., travel support) from Alexion, Novartis, BMS, Celgene, Incyte, Ariad, AOP Pharma, Baxalta, CTI, Pfizer, Sanofi, Shire, Geron, and Janssen. T.H.B. received  received research funding from Novartis and Pfizer; received honoraria from Pfizer and Novartis. M.H. reports financial support from Novartis. F.L. reports support from the Frankfurter Förderung “Nachwuchswissenschaftler” and the EUTOS funding program. KS received honoraria from BMS/Celgene, Novartis, Takeda, and Alexion. K.D. reports honoriaria and financing of scientific research by Novartis and Celgene/BMS. F.S. reports speaker bureau and consultancy for BMS, Incyte, Novartis, and Pfizer. M.G. reports employment by the University of Bochum; consultancy for Amgen, AOP Orphan, Novartis, Celgene, CTI, Shire, Pfizer, Roche, Janssen, and Gilead; honoraria from Amgen, AOP Orphan, Novartis, Celgene, CTI, Shire, Pfizer, Roche, Janssen, and Gilead.
HeBIS-PPN:502537124
Institutes:Medizin
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Sammlungen:Universitätspublikationen
Licence (German):License LogoCreative Commons - Namensnennung 4.0