ABSTRACT
Medical records of 523 nephrotic children followed up atAIexandria University Children's Hospital during the period from 1988 to 2002 were retrospectively studied for presence of clinically apparent thromboembolic complications [TECs]. Thirteen cases [2.5%] had evidences of 20 episodes of TECs. The frequency of TECs was 1.4% among steroid sensitive cases and 8.3% in steroid resistant cases. The TECs were predominantly venous [65%]. The most commonly affected vessels were; deep leg veins [45%]. Renal vein thrombosis was reported in 10% of the episodes. These cases were treated with heparin followed by oral anticoagulant therapy. The outcome was a full recovery in 8 patients and death in 5 patients. The commonest renal histopathology associated with TECs was MPGN. Moreover, we studied 50 children with nephrotic syndrome [NS] during their proteinuric phase. They included 10 cases with steroid resistant NS [SRNS], 20 with steroid dependent NS [SDNS] and 20 with infrequently relapsing NS. Plasminogen activity, plasma level of fibrinogen and plasminogen activator inhibitor-1[PAI-1] were measured in them and in 20 healthy control children. All studied nephrotic cases had proteinuria, hypoalbuminemia and hypercholesterolemia. Microcytic hypochromic anemia and high platelet count were evident in most cases. Fibrinogen levels were significantly elevated in all nephrotic groups [p< 0.005]. Plasminogen activity was in the normal range in all nephrotic groups. The means of PAH were significantly higher in all nephrotic groups than in the control group and in SRNS than other nephrotic groups [p< 0.005]. Elevated PAI-1 depresses tibrinolytic activity and thus increases the risk of thrombosis. We screened these cases for TECs by conventional and colored Doppler ultrasonography. Pulmonary perfusion scintigraphy was done in 6 cases with unexplained pulmonary symptoms. Two cases out of 50 [4%] developed TECs; the first had SDNS and got right femoral artery occlusion, the second had SRNS and developed left pulmonary embolism
Conclusion: TECs are life threatening complications of childhood NS. Their prevalence in our study was 2.5%. They are predominantly venous but can affect any vessel and might recur in the same patient. TECs can complicate any type of renal histopathology in childhood NS. The enhanced risk of TECs in nephrotic children is most likely a multitactorial problem, with hypoalbuminemia, hyperlipidemia, thrombocytosis, hyperfibrinogenemia and increased PAI-1 all playing a role. We recommend adequate evaluation of all children with active NS for presence of subclinical TECs to allow early treatment and thus prevention of morbidity and mortality caused by this serious complication