To understand why Kell-mediated hemolytic disease of the fetus and newborn (HDFN) can still cause severe complications despite the presence of low titers, it is first important to understand what a Kell antigen is and how HDFN works.
How HDFN works
HDFN occurs when the pregnant mother produces antibodies that mistakenly cross the placenta and destroy the red blood cells of the fetus.
There are generally two causes for this. The first is Rhesus incompatibility. This occurs when a Rhesus-negative mother produces antibodies against the red blood cells of a Rhesus-positive fetus.
Read more about HDFN testing and diagnosis
The second is ABO incompatibility. This occurs when the pregnant mothers has an O blood type, which means that her blood has antibodies against A or B antigens that are present on the fetus’s red blood cells.
Rhesus and ABO incompatibility form the bulk of the causes of HDFN. However, Kell antigen incompatibility can also drive the disease processes associated with HDFN. In this case, the mother has anti-Kell antibodies that produce antibodies against Kell-positive red blood cells of the fetus.
How Kell-mediated HDFN works
Even if low antibody titers are present, Kell-mediated HDFN can occur because the Kell antigen is strongly immunogenic and is markedly expressed on fetal red blood cells. This differs from other forms of HDFN, in which levels of antibody titers tend to dictate the severity of HDFN experienced.
Briefly, Kell-mediated HDFN has a number of characteristics that make it so harmful, even if low antibody titers are present. The antibodies that are present can cross the placenta with efficiency to bind to fetal red blood cells and destroy them. As a result, antibody titers may appear artificially low because they are quickly bound to fetal red blood cells.
While most cases of HDFN are centered around the destruction of red blood cells, anti-Kell antibodies have the ability to inhibit red blood cell production. This means that Kell-mediated HDFN reduces the number of fetal red blood cells by limiting their production in the first place, in addition to destroying the ones that are currently circulating.
Combined, all these features can lead to fetal anemia that is more rapid and severe than typical cases of HDFN. This means that physicians have to closely monitor pregnancies affected by Kell-mediated HDFN and initiate interventions such as intrauterine transfusions when indicated. Patients who are known to have
Kell-mediated HDFN in a previous pregnancy especially deserves close monitoring during the antenatal period.
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