Renal Doppler resistance indices are associated with systemic atherosclerosis in kidney transplant recipients.

BACKGROUND

In kidney transplant recipients, increased intrarenal resistance indices measured by duplex ultrasound are associated with poor subsequent allograft performance. It remains unclear whether high resistance indices rather reflect local renal damage or systemic vessel disease. We hypothesized that resistance indices are associated with cardiovascular risk factors and with subclinical systemic atherosclerosis in transplant recipients.

METHODS

In 105 renal transplant recipients, categories of risk for coronary heart disease were determined by Framingham risk scoring. Intrarenal resistive index (RI) and pulsatility index (PI) were measured in segmental arteries at five representative locations. For assessment of subclinical atherosclerosis, common carotid intima-media thickness, and ankle-brachial blood pressure index (ABI) were determined.

RESULTS

Transplant recipients with high coronary risk had higher intrarenal resistance indices than low-risk patients. Higher age, female gender, and lower body mass index were independently associated with increased resistance indices. Renal resistance indices were correlated with common carotid intima-media thickness [RI: r= 0.270 (P= 0.005); PI: r= 0.355 (P < 0.001)]. This association remained significant after adjusting for renal function. Renal resistance indices were increased in patients with pathologic ankle-brachial-indices compared to patients with physiologic ankle-brachial-indices [RI: 73.3 +/- 7.1 vs. 70.2 +/- 6.9 (P= 0.03); PI: 146.4 +/- 29.9 vs. 131.4 +/- 25.9 (P= 0.01)]. Renal resistance indices were neither significantly correlated with glomerular filtration rate (GFR), nor with donor age.

CONCLUSION

Intrarenal resistance indices are a complex integration of arterial compliance, pulsatility, and peripheral resistance. They are associated with traditional cardiovascular risk factors as well as with subclinical atherosclerotic vessel damage and should thus not be considered specific markers of renal damage.