Heparin-induced
thrombocytopenia (HIT) is a clinicopathologic syndrome in which one or more clinical events, usually
thrombocytopenia or
thrombosis, are temporally related to
heparin administration and caused by HIT
antibodies. Rapid and accurate diagnosis is essential given the high incidence of
thrombosis at around the time of initial disease recognition. Discontinuation of
heparin and initiation of alternative
anticoagulants reduces HIT-associated morbidity and mortality. The clinical consequences of HIT in
hemodialysis patients remain unclear, with several studies reporting no clinical sequelae and others describing complications such as
thrombocytopenia or clotting of the extracorporeal circuit. Frequent clotting of the extracorporeal circuit has also been reported in HIT-antibody-positive patients on
continuous veno-venous hemofiltration. Several recent findings are of particular interest to nephrologists. An acute systemic reaction has been described as a presentation of HIT in
hemodialysis patients shortly after administration of an
unfractionated heparin bolus. This syndrome is important to recognize as it might mimic a dialyzer reaction. More recently, the presence of a positive HIT-antibody test or increasing titers of HIT antibody were associated with increased mortality in
hemodialysis patients, raising the question of whether these
antibodies have a role in the increased cardiovascular mortality seen in these patients. HIT-antibody production is often transient and small numbers of
hemodialysis patients with undetectable antibody levels have been rechallenged with
heparin without adverse clinical consequences.