Renal hemodynamic and functional effect of PEEP ventilation in human renal transplantations

Increased intrathoracic pressure with positive pressure breathing (PPB) induces renal hypoperfusion and excretion function impairment the mechanism of which may be partially related to reflex sympathetic nerve activation. The consequences of renal denervation on PPB-induced renal impairment are unknown. This study was conducted to evaluate the effects of increasing intrathoracic pressure with positive end-expiratory pressure (PEEP) on renal blood flow (RBF, pulsed Doppler implantable microprobes) and function in 12 kidney transplantation recipients during the immediate post-transplantation period. Three sets of measurements were performed during successively zero end-expiratory pressure (ZEEP), 15 cm H2O PEEP, and back to ZEEP. PEEP ventilation was associated with mean arterial pressure (MAP) and cardiac output (CO) decrease (-12%, p < 0.01; -26%, p < 0.01, respectively). RBF remained constant in the three protocol conditions. PEEP ventilation was associated with a decrease in urinary output (8.5 +/- 5.6 versus 12.9 +/- 8.6 ml/min; p < 0.01), urinary sodium concentration (115 +/- 14 versus 121 +/- 12 mmol/L; p < 0.01) sodium excretion rate (1 +/- 0.7 versus 1.6 +/- 1.1 mmol/min; p < 0.01), and creatinine clearance (17.1 +/- 10 versus 23.2 +/- 13.6 ml/min; p < 0.01). PEEP-induced urinary output decrease was correlated to renal perfusion pressure decrease (r = 0.7, p = 0.016). These results suggest that despite denervation and renal blood flow stability, renal handling of water and salt is perfusion pressure-dependent during PEEP in human renal allograft recipients.