Genetic susceptibility of the donor kidney contributes to the development of renal damage alter syngeneic transplantation

Solitary kidneys, especially in rats, appear vulnerable to develop function al and structural damage. However, differences in susceptibility exist betw een strains. It is not clear whether this is intrinsic to the kidney or due to environmental factors. Therefore, the aim of the present study was to i nvestigate possible differences in genetic susceptibility for renal damage. By transplanting different rat donor kidneys into a normotensive, histocom patible recipient, the kidneys were exposed to the same blood pressure prof iles, metabolic and hormonal environment. Kidneys from young adult hyperten sive fawn-hooded (FHH) rats, a strain showing early onset renal damage, nor motensive, renal damage-resistant August x Copenhagen-Irish (ACI), and (ACI x FHH) F-1 donors were transplanted into male F-1 recipients. The native k idneys of the recipients were removed 1 week after transplantation. The res ults were mutually compared and to their unilaterally nephrectomized litter mates. Systolic blood pressure (SBP) and albuminuria (UaV) were determined at the time of transplantation and at 8 and 16 weeks. The histomorphologic analysis included the incidence of focal glomerulosclerosis (FGS), and dete rmination of chronic transplant dysfunction according to the BANFF criteria . A negative impact of the transplantation technique in this syngeneic situ ation could not be detected as F-1 transplants did not differ functionally and morphologically from their UNx controls. Transplanting an ACI kidney di d not result in significant changes of SEP, UaV, and incidence of FGS compa red to F-1 transplants and ACI-UNx. In contrast, FHH kidneys did show a pro gressive increase of UaV and glomerulosclerosis and a significantly higher BANFF score, whereas the SEP did not differ from F-1 transplants. The moder ate hypertension seen in FHH did not travel with the kidney. Compared to th e FHH-UNx rats, transplantation of a FHH kidney did significantly attenuate the increase of UaV and FGS. The susceptibility of the donor kidney appear s to be an important factor in the development of chronic renal damage. Thi s may play a role in the longterm functional changes seen after clinical re nal transplantation. (C) 1999 American Journal of Hypertension, Ltd.