Despite not being formally approved, fondaparinux has occasionally been used for alternative anticoagulation in HIT patients (see Chapter 17). As fondaparinux is predominantly excreted by the kidneys, its dose is to be reduced for anticoagulation in patients with renal insufficiency and for HD procedures. Recently, successful anticoagulation with fondaparinux has been described in a maintenance HD patient with symptomatic HIT (Haase et al., 2005). The role of fondaparinux for anticoagulation in HD procedures of HIT patients requires further evaluation.


HIT antibodies are surprisingly transient, and usually become undetectable within a few weeks or months following an episode of HIT (Warkentin and Kelton, 2001). Moreover, after their disappearance, the antibodies do not usually recur (or are regenerated in low levels) if a deliberate rechallenge with heparin is administered, such as for cardiac or vascular surgery (see Chapters 12 and 19) (Pötzsch et al., 2000; Warkentin and Kelton, 2001). This experience at least suggests the possibility that resumption of heparin for HD may be feasible too following an episode of HIT. Recently, Hartman et al. (2006) reported such a strategy in three patients who developed HD-associated HIT. Once the HIT antibodies became undetectable, the investigators resumed anticoagulation of HD using the LMWH, nadroparin (the standard anticoagulant used at their center in Antwerp, Belgium). More recently, Matsuo and colleagues (2007) successfully reintroduced HD with UFH in a patient who had developed HIT in the setting of acute HD about 6 mo earlier. These rechallenges were successful, with none of the patients developing recurrent HIT. However, before rechallenge with LMWH or UFH for HD anticoagulation can be recommended more generally, carefully designed systematic studies are necessary, balancing the costs and risks of indefinite anticoagulation with non-heparin agents against the potential risk of recurrent HIT.


An alternative anticoagulant is required for HD in patients with HIT. Appropriate agents include danaparoid sodium, r-hirudin derivatives such as lepirudin, or argatroban, as these appear to suppress clot formation in HD at doses that do not substantially increase bleeding risk. As these results are based on experience with a limited number of patients, larger prospective trials are needed to define the best treatment options in this setting. Even today, though, HIT should no longer be a life-threatening problem for patients requiring dialysis.

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