R. Rettig et al., THE KIDNEY AND PRIMARY HYPERTENSION - CONTRIBUTIONS FROM RENAL-TRANSPLANTATION STUDIES IN ANIMALS AND HUMANS, Journal of hypertension, 11(9), 1993, pp. 883-891
Clinical studies: In clinical renal transplantation studies, recipient
s of a renal graft from a donor with a genetic predisposition to hyper
tension had higher blood pressures and required more antihypertensive
treatment than recipients of a renal graft from a normotensive donor.
In addition, blood pressure normalization in patients suffering from e
ssential hypertension by bilateral nephrectomy and subsequent transpla
ntation of a kidney from a normotensive donor has been reported. The i
nterpretation of these data may be limited by the large number of diff
erent factors that can contribute to post-transplantation hypertension
in human renal transplant recipients. Experimental studies: In experi
mental renal transplantation studies the contribution of individual fa
ctors to post-transplantation hypertension can be independently assess
ed. Besides immunological graft rejection and hypertension-induced dam
age to the renal graft, a genetic predisposition to hypertension in th
e kidney donor has been demonstrated to be associated with post-transp
lantation hypertension in the recipient. Thus, normotensive recipients
of a renal graft from a genetically hypertensive donor consistently d
eveloped post-transplantation hypertension in four different animal mo
dels of genetic hypertension. Furthermore, in genetically hypertensive
rats bilateral nephrectomy together with transplantation of a kidney
from a normotensive donor has been shown to be associated with a decre
ase in blood pressure. Conclusions: Hypertension following renal trans
plantation may be due to a variety of factors, including immunological
graft rejection, hypertension-induced damage to the renal transplant
and a genetic predisposition to hypertension of the kidney donor. The
finding that blood pressure is transplanted with the renal graft in ge
netic hypertension suggests a genetically determined alteration to the
kidney as a major factor in the aetiology of primary hypertension. Th
e nature of this factor is just beginning to be understood. Renal tran
splantation studies in rat models of genetic hypertension, combined wi
th the tools of molecular biology, may help to provide further insight
s into the role of the kidney in primary hypertension.