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A resistance index (RI) of 0.8 or higher was shown to be a strong predictor of kidney allograft and patient survival. Uncertainties persist since the intrarenal RI is closely associated with the vascular stiffness of the allograft recipient. To clarify the diagnostic value of RI further, we analyzed parameters of vascular stiffness of the recipient and intrarenal RI of the renal allograft. In a prospective study laboratory and clinical parameters, pulse wave velocity (PWV), intima media thickness (IMT) and RI were obtained in 76 kidney allograft patients. We found that the RI values significantly correlated with the PWV (p < 0.05) and the recipients age (p < 0.01) but not with the donor age and renal function. Using multiple regression analysis recipient age, PWV, pulse pressure (PP) and IMT were identified as independent factors influencing RI values. For a more correct interpretation of the RI values in renal allografts parameters of vascular stiffness such as IMT, PP or PWV should be included.

Color Doppler sonography has been introduced for graft monitoring after renal transplantation. Little is known, however, about independent factors that have an impact on intrarenal Doppler indices as indicators for transplant dysfunction. Therefore, in this study, potential determinants of the resistive index (RI) and of the pulsatility index (PI) in 110 patients with stable renal allografts were studied. The mean RI and PI were 0.70 +/- 0.07 (range, 0.53 to 0.88) and 1.36 +/- 0.21 (range, 0.91 to 1.98), respectively. In multivariate regression analysis, RI and PI correlated significantly with age and arterial pulse pressure of the recipient. There was no correlation with donor age, heart rate, mean arterial blood pressure, and cyclosporine trough levels. Furthermore, parameters of kidney function, such as serum creatinine concentration, creatinine clearance rate, 51Cr-ethylenediaminetetraacetate clearance rate, and proteinuria, showed no significant correlation with the Doppler indices. The data indicate that intrarenal Doppler indices of the grafts are hemodynamic indices, primarily depending on the recipient-related vascular compliance rather than on the function of the graft. Therefore, only intraindividual comparison of the Doppler indices may be useful to detect potential changes of graft resistance during long-term follow-up.

1. We have previously shown that ATP is a co-transmitter of noradrenaline in the rat kidney. In the present study the release of ATP and noradrenaline from human kidney cortex was investigated. Vascular effects of ATP and stable analogues were tested in human and rabbit isolated renal blood vessels. 2. Sympathetic nerve stimulation (20 Hz for 1 min) in human kidney slices released 89 +/- 16 fmol noradrenaline per mg wet weight and 99 +/- 20 fmol ATP per mg wet weight in controls (n = 12). The Na+ channel blocker tetrodotoxin (1 microM) abolished ATP and noradrenaline release. 3. In human isolated extrarenal arteries the P2X-purinoceptor agonist beta, gamma-methylene-L-ATP caused almost no constrictor responses, beta, gamma-methylene-L-ATP induced moderate constrictor responses in intrarenal arteries. In preconstricted human intrarenal arteries ATP induced vasodilation. 4. ATP and the P2Y-receptor agonist 2-methyl-thio-ATP (2-MeSATP) dilated preconstricted rabbit renal arteries. The P2Y-receptor antagonist Reactive Blue 2 (3 microM) shifted the concentration response curves of ATP and 2-MeSATP to the right. 5. In conclusion, sympathetic nerve stimulation induces the release of ATP and noradrenaline in human renal cortex. ATP activates vasoconstrictory P2X- and vasodilatory P2Y-receptors in human renal blood vessels. The net vascular response to ATP in vivo will depend on the tissue distribution of these purinoceptors.

1. Strips of human saphenous veins and of human renal arteries and veins were superfused with Krebs-Henseleit solution at 37 degrees C. Constrictor responses were elicited by exogenous noradrenaline and the P2x-purinoceptor-selective agonist, beta, gamma-methylene-L-ATP. 2. In human saphenous veins, beta, gamma-methylene-L-ATP (0.3-30 microM; EC50 2.2 microM) induced marked constrictor responses. The maximal response to beta, gamma-methylene-L-ATP was similar to the maximal response to noradrenaline. The P2-purinoceptor antagonist suramin (30 microM) shifted the concentration-response curve of beta, gamma-methylene-L-ATP to the right (apparent pKB value 4.8); suramin (100 microM) markedly inhibited the responses to beta, gamma-methylene-L-ATP. The preferential P2x-purinoceptor antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 3 microM) slightly reduced the response to beta, gamma-methylene-L-ATP. At a ten times higher concentration (30 microM), PPADS almost abolished the responses to beta, gamma-methylene-L-ATP. PPADS (30 microM), in contrast, caused no significant change in the concentration-response curve of noradrenaline. 3. In extrarenal and intrarenal arteries, EC50 values and maximal responses to noradrenaline were similar when compared with responses to noradrenaline in saphenous veins. Noradrenaline also constricted extrarenal veins. However, in contrast to the results obtained on saphenous veins, beta, gamma-methylene-L-ATP caused almost no constrictor responses in extrarenal veins and arteries and only moderate responses in intrarenal arteries. 4. The results demonstrate marked differences in responsiveness of human blood vessels to the selective P2x-purinoceptor agonist, beta, gamma-methylene-L-ATP, suggesting tissue differences in the occurrence or operation of P2x-purinoceptors in human vascular tissues. Moreover, the results indicate that PPADS blocks P2x-purinoceptors in human isolated blood vessels as previously demonstrated in animal blood vessels.