73 m-2). Through a logistic regression analysis, only two factors (age and trauma patients) remained significantly correlated with a CLCR above normal and for a moderate renal impairment. In the current selleck inhibitor results, 12% of elderly patients (over 65 years) have a CLCR greater than 120 mL minute-1 1.73 m-2. The impact of age on CLCR is well known and this parameter was, therefore, introduced in the formulas estimating CLCR (Cockcroft-Gault, Robert and simplified MDRD) [13-15]. The decrease in glomerular filtration, the involution of nephronic units and the reduction of the renal blood flow explain the high frequency of renal impairement in elderly patients. However, it should be kept in mind that glomerular ageing is correlated to age in only two-thirds of the patients, and this phenomenon accounts for the inaccuracy of the CLCR estimated by calculated formulae [20].
Current evidence suggests that PT (mainly, young patients without significant comorbidities) present with a CLCR increase. However, this phenomenon as received little attention in the literature, and dose modification are therefore rarely considered. The present results clearly demonstrate for the first time that trauma is a major factor for CLCR increase. Several factors may explain this increase in CLCR in PT patients. First, urinary creatinine excretion may be involved in such a phenomenon. A higher creatinine urinary excretion was observed in PT compared with NPT patients whereas serum creatinine was similar in both groups. However, the higher creatinine urinary excretion observed in PT patients was within a normal range.
Serum protein variations may impact our results. However, all the patients had a serum protein value between 50 and 55 gL-1. It is, therefore, very unlikely that serum protein variations interfere with the present results. Also, regarding hemodynamics, CLCR were studied and measured at a steady state in both groups (that is, distant from the admittance). It should be noted that our patients were hemodynamically stable at the time of data collection with no sign of dehydration. Although interference due to some cephalosporin has been described when the creatininemia was measured by using the Jaffe method [21]; no changes in this parameter were observed during the overall period of the study. Sepsis can also reduce creatinine production as described in mice [22].
Moreover, in critically-ill patients, a positive fluid balance may lead to underestimation of the severity of AKI and delay the recognition of a 50% relative increase in sCr [23]. Finally, it should be hypothesized Dacomitinib that humoral and inflammatory mechanisms encountered after severe trauma [24] or burn [1] are involved in the observed CLCR increase.The present study encountered some limitations. Increased CLCR is related with enhanced renal elimination of circulating drugs.