The answer to this question, saying that Down Syndrome - a trisomy of human chromosome 21 - is caused by de novo mutation (rather than resulting from standing variation) made me think about polymorphisms in the number of autosomes (not so much for sex chromosomes because of dosage compensation). The reason for this question is that I would never have thought that an aneuploidy, in theory, could be a segregating trait because of meiotic barriers.
I found evidence of ploidy polymorphisms in plants (especially their hybrids) that occurs when plants with different karyotypes hybridise [see, for example, Vandenhout et al. (1995) and Husband (2014)]. Additionally, I also found that this also applies to some aquatic vertebrates, however, 'fish' are also known for karyotype diversity (see Zhou et al. (2007) and Zhao et al. (2016)).
In rather sharp contrast to that, mammals are (almost) strictly diploid and most mammal species are characterised by fixed chromosome numbers, even though exceptions exist, i.e in mice and other rodents that exhibit intraspecific variation in diploid numbers - these are created by Robertsonian translovations [Graphodatsky et al. (2011)].
However, all of these are diploid and variation always needs to be expressed as a chromosome number of the form $2n$ because of meiosis. The karyotype of a human with trisomie 21 cannot be expressed in that form as this person has $2n +1$ chromosomes. All cases of aneuploidiy in autosomes I am aware of cause disease. My (related) questions now are:
(1) Are there described cases of non-deleterious aneuploidies in autosomes?
Those cannot be segregating in the populations as aneuploidies are not inherited to children, so more importantly:
(2) Are there indirectly segregating aneuploidies in autosomes (i.e. some sort of heritable trisomy that e.g. result from a trisomy followed by chromosomal rearrangement)?
If so, do any of these also exist in mammals, particularly in humans?