Objective: The cold pressure test (CPT) is a classic cardiovascular stress test known to increase blood pressure and heart rate secondary to an increase in nervous sympathetic activity. Its effect on renal hemodynamics using both Doppler ultrasound (DU) and contrast-enhanced ultrasound (CEUS) has not been reported previously. We hypothesized that a CPT would induce changes in renal hemodynamics detectable by DU and CEUS. The objective was to measure the renal responses during a CPT using DU and CEUS. Design and method: This was a single center prospective study in healthy participants. Renal resistive index (RRI) and mean acceleration time (MAT) were measured 4 times during 2 minutes baseline conditions (water at body temperature) and 4 times during 2 minutes CPT conditions (water at 4°C). The same protocol was then repeated after 5 minutes washout period for the measurement of the perfusion index (PI), relative blood volume and mean transit time using CEUS. Renal hemodynamic responses during baseline and CPT were compared using a t-test or a Wilcoxon matched-pair signed-rank test if variables were not normally distributed. Results: 24 healthy participants (15 women, 9 men) were included. Mean age and body mass index were respectively (mean ± standard deviation) 33.9 ± 11.8 years and 24.3 ± 3.4 kg/m2. The CPT increased mean blood pressure by 19.8 ± 4.4 mmHg, heart rate by 14.0 ± 3.8 beats per min. The CPT decrease RRI from 0.60 ± 0.04 to 0.58 ± 0.04 (p = 0.018). This decrease was associated with the systolic blood pressure (rho: -0.43, p = 0.038) and heart rate response (rho = -0.52, p = 0.009). Mean acceleration time did not change. Perfusion index (median and interquartile range) increased from 2578 UI (1789; 4901) to 4148UI (2499; 6739) (p < 0.001). Relative blood volume increased, but mean transit time did not change. Conclusions: This is the first demonstration that the CTP induces detectable changes in renal hemodynamics using both DU and CEUS. The CPT combined to DU and CEUS may be a valuable tool to assess the renal response to increased sympathetic drive in hypertensive or chronic kidney disease patients.
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