Substantial evidence indicates that hypertension plays a predominant role i
n the progression of most chronic renal diseases including diabetic nephrop
athy. Nevertheless, significant differences are observed in the susceptibil
ity to develop hypertension-associated renal damage between individuals, ra
cial groups and animal strains despite comparable hypertension. Recent stud
ies employing a variety of genetic methods both in humans and in experiment
al models, have provided strong support for the potential importance of gen
etic factors and have suggested that genes influencing susceptibility to re
nal damage may be inherited separately from genes that influence blood pres
sure. However, due to the genetic complexity involved in a multifactorial t
rait such as the susceptibility to hypertensive renal damage, very limited
progress has been achieved thus far in attempts to link such susceptibility
to specific genetic mechanisms, chromosome regions and/or candidate genes.
It is anticipated that the rapid recent advances in molecular genetic tech
niques and the simultaneous use of multiple complementary strategies, as is
currently under way, will greatly facilitate this search and provide funda
mental new insights into the pathogenesis of hypertensive renal damage. Cop
yright (C) 2001 S. Karger AG, Basel.