There may be prenatal danger to the fetus when a pregnant woman is RhD-negative and the biological father is RhD-positive. But, as discussed below, the situation is considerably more complex than that.
The Wiener system used the Rh-Hr nomenclature. This system was based on the theory that there was one gene at a single locus on each chromosome of the pair which controls production of multiple antigens. In this theory a gene R is supposed to give rise to the “blood factors” Rho, rh’, and hr” and the gene r to produce hr’ and hr”.
Notations of the two theories are used interchangeably in blood banking (e.g., Rho(D)). Wiener’s notation is more complex and cumbersome for routine use. Because it is simpler to explain, the Fisher-Race theory is more widely used.
DNA testing has shown that both theories are partially correct. There are in fact two linked genes, one with multiple specificities and one with a single specificity. Thus, Wiener's postulate that a gene could have multiple specificities (something many did not give credence to originally) has been proven correct. On the other hand, Wiener's theory that there is one gene has proven incorrect, as has the Fischer-Race theory that there are three genes.
When the condition is caused by the RhD antigen-antibody incompatibility, it is called RhD Hemolytic disease of the newborn (often called Rhesus disease or Rh disease for brevity). Here, sensitization to Rh D antigens (usually by feto-maternal transfusion during pregnancy) may lead to the production of maternal IgG anti-RhD antibodies which can pass through the placenta. This is of particular importance to RhD negative females of or below childbearing age, because any subsequent pregnancy may be affected by the Rhesus D hemolytic disease of the newborn if the baby is Rh D positive. The vast majority of Rh disease is preventable in modern antenatal care by injections of IgG anti-D antibodies (Rho(D) Immune Globulin). The incidence of Rhesus disease is mathematically related to the frequency of RhD negative individuals in a population, so Rhesus disease is rare in East Asians, South Americans, and Africans, but more common in Caucasians.
|Population||Rh(D) Neg||Rh(D) Pos||Rh(D) Neg alleles|
|European Basque||approx 35%||65%||approx 60%|
|American Blacks||approx 7%||93%||approx 26%|
|Native Americans||approx 1%||99%||approx 10%|
|African descent||less 1%||over 99%||3%|
|Asian||less 1%||over 99%||1%|
Two very similar epitopes are encoded on the same protein on the adjacent related RHCE gene, Cc and Ee. It is believed that the RHD gene arose by duplication of the RHCE gene during primate evolution. Mice have just one RH gene
The Rhesus system is much more complex than the ABO blood type system because there are more than 30 combinations possible.
In testing, D positive blood is easily identified. Units which are negative for D are often retested to rule out a weaker reaction. This was previously referred to as Du, which has fallen out of favor. In some cases, this phenotype occurs because of an altered surface protein that is more common in people of African descent. The testing is difficult, since using different anti-D reagents, especially the older polyclonal reagents, may give different results.
The practical implication of this is that people with this sub-phenotype will have a product labeled as "D positive" when donating blood. When receiving blood, they are sometimes typed as a "D negative", though this is the subject of some debate. Most "Weak D" patients can receive "D positive" blood without complications. This is important, since most blood banks have a limited supply of "D negative" blood. Patients who test as "D negative" and whose "D positive" status is detectable with an IAT are commonly given "D negative" blood, but this is also debated.
This may lead to the unusual situation where a person is "D positive" as a donor but receives "D negative" blood. Since autologous donations are labeled with the blood type and matching the blood type is part of routine pre-transfusion clerical checks, this can easily lead to confusion.
43 other Rh group antigens have been described, but they are either much less frequently encountered or are rarely clinically significant. Each is given a number, though the highest assigned number (Rh56 or CENR) is not an accurate reflection of the antigens encountered since many (e.g. Rh38) have been combined, reassigned to other groups, or otherwise removed.
Phenotype Matching of Donor Red Blood Cell Units for Nonalloimmunized Sickle Cell Disease Patients: A Survey of 1182 North American Laboratories
Feb 01, 2005; Context.-The transfusion of donor red blood cell units (RBCs) that lack certain red cell antigens (such as C, E, and K) when the...