Reduced renal function strongly affects survival and thrombosis in patients with myelofibrosis
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ORIGINAL ARTICLE
Reduced renal function strongly affects survival and thrombosis in patients with myelofibrosis Marko Lucijanic 1 & Davor Galusic 2 & Ivan Krecak 3 & Martina Sedinic 1 & Hrvoje Holik 4 & Vlatka Perisa 5,6 & Martina Moric Peric 7 & Ivan Zekanovic 7 & Tajana Stoos-Veic 8,9 & Rajko Kusec 1,9 Received: 9 July 2020 / Accepted: 26 August 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract We retrospectively investigated a cohort of 176 myelofibrosis patients (128 primary-PMF; 48 secondary-SMF) from five hematology centers. The presence of chronic kidney disease (CKD) was determined in addition to other clinical characteristics. CKD was present in 26.1% of MF patients and was significantly associated with older age (P < 0.001), higher WBC (P = 0.015), and its subsets (neutrophil, monocyte, and basophil counts), higher platelets (P = 0.001), lower albumin (P = 0.018), higher serum uric acid (P = 0.001), higher LDH (P = 0.022), and the presence of CV risk factors (P = 0.011). There was no significant association with driver mutations, degree of bone marrow fibrosis, PMF/SMF, or DIPSS risk categories (P > 0.05 for all analyses). The presence of CKD was significantly associated with shorter time to arterial (HR = 3.49; P = 0.041) and venous thrombosis (HR = 7.08; P = 0.030) as well as with shorter overall survival (HR 2.08; P = 0.009). In multivariate analyses, CKD (HR = 1.8; P = 0.014) was associated with shorter survival independently of the DIPSS (HR = 2.7; P < 0.001); its effect being more pronounced in lower (HR = 3.56; P = 0.036) than higher DIPSS categories (HR = 2.07; P = 0.023). MF patients with CKD should be candidates for active management aimed at the improvement of renal function. Prospective studies defining the optimal therapeutic approach are highly needed. Keywords Myeloproliferative neoplasm . Survival . Thrombosis . Renal function . JAK2
Introduction Essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF) are three classical Philadelphia chromosome (bcr-abl)-negative myeloproliferative neoplasms (MPNs) developing due to acquired mutations in signal transduction pathways [1]. Constitutional activation of the JAK-STAT signaling pathway results in chronic systemic inflammation, high cardiovascular (CV) * Marko Lucijanic [email protected] 1
Hematology Department, University Hospital Dubrava, Av. Gojka Suska 6, 10000 Zagreb, Croatia
2
Department of Hematology, University Hospital of Split, Soltanska ul. 1, 21000 Split, Croatia
3
Hematology Department, General Hospital Sibenik, Ul. Stjepana Radića 83, 22000 Sibenik, Croatia
4
Department of Internal Medicine, “Dr. Josip Bencevic” General Hospital, Ul. Andrije Štampara, 35000 Slavonski Brod, Croatia
disease burden, and high risk of thrombotic incidents [2]. In contrast to ET and PV, patients with PMF and secondary post-ET/post-PV myelofibrosis (SMF) are exposed to the stronger inflammatory atmosphere and substantially increased mortality due to bone marrow failure and disease t
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