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Blood, 1 September 2004, Vol. 104, No. 5, pp. 1356-1360.
Prepublished online as a Blood First Edition Paper on May 18, 2004; DOI 10.1182/blood-2004-01-0229.


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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Renal venous thrombosis in neonates: prothrombotic risk factors and long-term follow-up

Andrea Kosch, Eberhard Kuwertz-Bröking, Christine Heller, Karin Kurnik, Rosemarie Schobess, and Ulrike Nowak-Göttl, for the Childhood Thrombophilia Study Group

From the Department of Pediatric Hematology/Oncology and the Department of Pediatric Nephrology, University Children's Hospital Münster, Münster, Germany; the Department of Pediatric Hematology/Oncology, University Children's Hospital Frankfurt am Main, Frankfurt am Main, Germany; the Department of Pediatrics, University Children's Hospital Munich, Munich, Germany; and the Department of Pediatrics, University Children's Hospital Halle, Halle, Germany.

The present study was designed to evaluate prothrombotic risk profiles in 59 consecutively recruited white neonates with renal venous thrombosis (RVT). The rates of prothrombotic risk factors (PRs)—for example, the factor V (FV) 1691G> A mutation, the factor II (FII) 20210G> A variant, antithrombin (AT), protein C (PC), protein S (PS), elevated lipoprotein(a) (Lp(a)), total fasting plasma homocysteine (tHcy) levels, and anticardiolipin antibodies (ACAs)—were compared with those of 118 healthy control children. At onset, 32 (54.2%) of the 59 neonates showed underlying clinical conditions; 40 (67.8%) of them and 23 (85.2%) of the 27 infants with idiopathic RVT showed at least one PR. Univariate analysis revealed significantly elevated odds ratios/95% confidence intervals (ORs/95% CIs) for FV and Lp(a). Additionally, PC/AT deficiency and ACAs were found significantly more often in the patient group (P = .04). Multivariate analysis calculated significant ORs/95% CIs only for FV (OR, 9.4; 95% CI, 3.3-26.6) and elevated Lp(a) (OR, 7.6; 95% CI, 2.4-23.8). Of the 59 neonates investigated, 53 revealed renal atrophy, and 13 children additionally suffered from severe arterial hypertension. In conclusion, the present study demonstrates the significance of genetic PR—especially the FV mutation and elevated Lp(a)—for the etiology of neonatal RVT.


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