Plasma cystatin C, a new marker of glomerular filtration rate (GFR), was prospectively evaluated in surgical intensive care. Cystatin C was measured (immunonephelometry, Dade-Behring) in 10 patients selected to cover a full range of GFR (phase I) and in 28 unselected consecutive patients followed for 5 days post-admission (phase II). Results were compared with (51)Cr-EDTA clearance (phase I only), plasma creatinine (kinetic Jaffe, Roche), 24-h or estimated by Cockcroft and Gault (CG) creatinine clearance (CrCl), and modified diet in renal disease (MDRD)-estimated GFR. In phase I, the highest correlation with(51)Cr-EDTA clearance (22-198 mL/min) was noted for CG CrCl (r(2): 0.883, p<0.001). During phase II follow-up, 24-h CrCl could not be calculated in 25% of daily evaluations. Cystatin C correlated with creatinine (0.856, p<0.0001) and CG CrCl with MDRD GFR (0.926, p<0.0001) in renal failure (10-78 mL/min, n=60). There was a +40% (p<0.001) median difference between cystatin C and creatinine (as a % of upper normal cut-off). Sensitivity/specificity to detect a <80 mL/min CG CrCl was 88/97% for cystatin C vs. 48/100% for creatinine (laboratory cut-off). In patients with normal and stable renal function (n=14), day-to-day intra-individual variation was 7.4% for cystatin C (vs. 10.6% for creatinine). In intensive care unit surgical adult patients, CG CrCl provides an easy and cost-effective estimate of GFR. Superior to creatinine, plasma cystatin C can be measured in selected patients where CG CrCl is known to be inaccurate.

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.

The pharmacokinetic analysis of sufentanil for ICU sedation revealed increased volume of distribution and elimination half-life. Nevertheless the rapid distribution and elimination processes suggest that the rapid reversibility of sedation with sufentanil is maintained after long duration of infusion. Further studies should be carried out to evaluate the clinical relevance of these results.

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