TY  - JOUR
A1  - Gecht, Judith
A1  - Tsoukakis, Ioannis
A1  - Kricheldorf, Kim
A1  - Stegelmann, Frank
A1  - Klausmann, Martine
A1  - Griesshammer, Martin
A1  - Schulz, Holger
A1  - Hollburg, Wiebke
A1  - Göthert, Joachim Rudolf
A1  - Sockel, Katja
A1  - Heidel, Florian
A1  - Gattermann, Norbert
A1  - Maintz, Christoph
A1  - Al-Ali, Haifa Kathrin
A1  - Platzbecker, Uwe
A1  - Hansen, Richard
A1  - Hänel, Mathias
A1  - Parmentier, Stefani Barbara
A1  - Bommer, Martin
A1  - Pahl, Heike L.
A1  - Lang, Fabian Magnus Eugen
A1  - Kirschner, Martin
A1  - Isfort, Susanne
A1  - Brümmendorf, Tim Henrik
A1  - Döhner, Konstanze
A1  - Koschmieder, Steffen
T1  - Kidney dysfunction is associated with thrombosis and disease severity in myeloproliferative neoplasms: implications from the German Study Group for MPN Bioregistry
T2  - Cancers
N2  - 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.
KW  - myeloproliferative neoplasms (MPN)
KW  - renal dysfunction
KW  - chronic kidney disease
KW  - thrombosis
KW  - thromboembolism
KW  - bleeding
KW  - JAK2V617F
KW  - essential thrombocythemia (ET)
KW  - polycythemia vera (PV)
KW  - primary myelofibrosis (PMF)
Y1  - 2021
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/62188
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-621887
SN  - 2072-6694
N1  - 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).
N1  - 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.
VL  - 13
IS  - 16, art. 4086
SP  - 1
EP  - 21
PB  - MDPI
CY  - Basel
ER  -