Rh factor is an antigen present in RBC. This antigen was discovered by Landsteiner and Wiener. It was first discovered in Rhesus monkey and hence the name ‘Rh factor’. There are many Rh antigens but only the D antigen is more antigenic in human. The persons having D antigen are called ‘Rh positive’ and those without D antigen are called ‘Rh negative’. Among Indian population, 85% of people are Rh positive and 15% are Rh negative. Percentage of Rh positive people is more among black people.

Rh group system is different from ABO group system because, the antigen D does not have corresponding natural antibody (anti-D). However, if Rh positive blood is transfused to a Rh negative person anti-D is developed in that person. On the other hand, there is no risk of complications if the Rh positive person receives Rh negative blood.


Rhesus factor is an inherited dominant factor. It may be homozygous Rhesus positive with DD or heterozygous Rhesus positive with Dd. Rhesus negative occurs only with complete absence of D (i.e. with homozygous dd).


When a Rh negative person receives Rh positive blood for the first time, he is not affected much, since

the reactions do not occur immediately. But, the Rh antibodies develop within one month. The transfused

RBCs, which are still present in the recipient’s blood, are agglutinated. These agglutinated cells are lysed by macrophages. So, a delayed transfusion reaction occurs. But, it is usually mild and does not affect the recipient. However, antibodies developed in the recipient remain in the body forever. So, when this person receives Rh positive blood for the second time, the donor RBCs are agglutinated and severe transfusion reactions occur immediately. These reactions are similar to the reactions of ABO incompatibility.


Hemolytic disease is the disease in fetus and newborn, characterized by abnormal hemolysis of RBCs. It is due to Rh incompatibility, i.e. the difference between the Rh blood group of the mother and baby. Hemolytic disease leads to erythroblastosis fetalis. Erythroblastosis fetalis is a disorder in fetus,

characterized by the presence of erythroblasts in blood. When a mother is Rh negative and fetus is Rh

positive (the Rh factor being inherited from the father), usually the first child escapes the complications of Rh incompatibility. This is because the Rh antigen cannot pass from fetal blood into the mother’s blood through the placental barrier. However, at the time of parturition (delivery of the child), the Rh antigen from fetal blood may leak into mother’s blood because of placental detachment. During postpartum period, i.e. within a month after delivery, the mother develops Rh antibody in her blood. When the mother conceives for the second time and if the fetus happens to be Rh positive again, the Rh antibody from mother’s blood crosses placental barrier and enters the fetal blood. Thus, the Rh antigen cannot

cross the placental barrier, whereas Rh antibody can cross it. Rh antibody which enters the fetus causes

agglutination of fetal RBCs resulting in hemolysis. Severe hemolysis in the fetus causes jaundice. To

compensate the hemolysis of more and more number of RBCs, there is rapid production of RBCs, not only from bone marrow, but also from spleen and liver. Now, many large and immature cells in proerythroblastic stage are released into circulation. Because of this, the disease is called erythroblastosis fetalis.

Ultimately due to excessive hemolysis severe complications develop, viz.

1. Severe anemia

2. Hydrops fetalis

3. Kernicterus.

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