Sorry for leaving this so long mrmic; I completely forgot.
We know of many mutations within the genes of the MNS, Rh, Diego and Kell Blood Group Systems, but others are beginning to "show up", as it were. We know more about the MNS, Rh, Diego and Kell Blood Group Systems simply because these systems contain the highest number of antigens, and so have been studied extensively. Indeed, more is known about the Rh Blood Group System than any other, because there are 55 different antigens within this system, and because the antigens are protein-based, and so can easily be isolated from the red cell membrane. The RHD and RHCE genes were isolated in the late 1980s/early 1990s by, amongst others, Neil Avent (a friend and colleague of mine, I am honoured to say), and from then onwards, the world of blood group serology began to change.
To give you some idea as to where we are now, there are 24 genetic backgrounds to the categorised D antigens, 88 genetic backgrounds to D Negative, 21 genetic backgrounds to apparently normal D Positive, 45 genetic backgrounds to the DEL type, 116 genetic backgrounds to known Partial D antigens that are not part of those categorised, and at least 171 genetic backgrounds to various Weak D antigens. These are just the mutations known within the RHD gene! Not all of these are clinically significant, but many will look, phenotypically, like a normal D, but can produce an allo-anti-D if immunologically challenged with blood that is either from a "normal" D Positive donor, or from blood from a donor with a different mutation.
Of more clinical importance are the mutations within the RHCE gene, many of which have been identified within the Black populations, where, of course, most sickle cell patients are found, and some of whom are transfusion-dependent. Amongst these individuals (both donors and recipients) we find many who are either hrB Negative or hrS Negative (or both), but who, phenotypically, look "normal" (for want of a better way of putting it). The antibodies directed against these two antigens are usually not considered to be particularly clinically significant (only rarely causing anything more than a delayed haemolytic transfusion reaction. They tend to result in an almost sub-clinical delayed haemolytic transfusion reaction, resulting in a need for more frequent transfusions, but no renal failure and other clinical sequelae. That notwithstanding, frequent transfusions can lead to iron overload, difficulty in finding compatible blood and increased costs in bed occupancy. If, therefore, we could match hrB Negative donors to hrB Negative recipients, even before they have made an anti-hrB, there would be benefits for the patient, in that they would undergo less frequent transfusions, leading to less in the way of iron overload, and benefits to the Health System in that the donor blood could be directed and there would be shorter bed occupancy.
I hope that helps, but, if not, get back to me.