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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.
 Previous Article | Next Article 
Submitted January 28, 2004
Accepted April 20, 2004
Renal venous thrombosis in neonates: Prothrombotic risk factors and long-term follow-up
Andrea Kosch*, Eberhard Kuwertz-Broking, Christine Heller, Karin Kurnik, Rosemarie Schobess, and Ulrike Nowak-Gottl
Department of Pediatric Hematology/Oncology, Univ. Children`s Hospital, Muenster, Germany
Department of Pediatric Nephrology, Univ. Children`s Hospital, Muenster, Germany
Department of Pediatric Hematology/Oncology, Univ. Children`s Hosp. Frankfurt a. Main, Muenster, Germany
Department of Pediatrics, Children`s Hospital, Munich, Germany
Department of Pediatrics, Univ. Children`s Hospital, Halle, Germany
* Corresponding author; email: koscha{at}uni-muenster.
The present study was designed to evaluate prothrombotic risk profiles in 59 consecutively recruited Caucasian neonates with renal venous thrombosis (RVT). The rates of prothrombotic risk factors (PR), e.g. the factor V (FV) G1691A mutation, the factor II (FII) G20210A variant, antithrombin (AT), protein C (PC), protein S (PS), elevated lipoprotein (Lp) (a), total fasting plasma homocysteine levels (tHcy) and anticardiolipin antibodies (ACA), were compared with those of 118 healthy control children. At onset 32 of the 59 neonates (54.2%) showed underlying clinical conditions, 40 (67.8%) of them and 23 of the 27 (85.2%) infants with idiopathic RVT showed at least one PR. Univariate analysis revealed significantly elevated odds ratios/95% confidence intervals (OR/CI) for FV and Lp(a). Additionally PC-/AT-deficiency and ACA were found significantly more often in the patient group (p=0.04). Multivariate analysis calculated significant OR/CI only for FV (OR/CI:9.4/3.3-26.6) and elevated Lp(a) (OR/CI:7.6/2.4-23.8). 53 of the 59 neonates investigated 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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