Fluid balance-adjusted creatinine at initiation of continuous venovenous hemofiltration and mortality. A post-hoc analysis of a multicenter randomized controlled trial.

Abstract

IntroductionAcute kidney injury (AKI) requiring renal replacement therapy (RRT) is associated with high mortality. The creatinine-based stage of AKI is considered when deciding to start or delay RRT. However, creatinine is not only determined by renal function (excretion), but also by dilution (fluid balance) and creatinine generation (muscle mass). The aim of this study was to explore whether fluid balance-adjusted creatinine at initiation of RRT is related to 28-day mortality independent of other markers of AKI, surrogates of muscle mass and severity of disease.MethodsWe performed a post-hoc analysis on data from the multicentre CASH trial comparing citrate to heparin anticoagulation during continuous venovenous hemofiltration (CVVH). To determine whether fluid balance-adjusted creatinine was associated with 28-day mortality, we performed a logistic regression analysis adjusting for confounders of creatinine generation (age, gender, body weight), other markers of AKI (creatinine, urine output) and severity of disease.ResultsOf the 139 patients, 32 patients were excluded. Of the 107 included patients, 36 died at 28 days (34%). Non-survivors were older, had higher APACHE II and inclusion SOFA scores, lower pH and bicarbonate, lower creatinine and fluid balance-adjusted creatinine at CVVH initiation. In multivariate analysis lower fluid balance-adjusted creatinine (OR 0.996, 95% CI 0.993–0.999, p = 0.019), but not unadjusted creatinine, remained associated with 28-day mortality together with bicarbonate (OR 0.869, 95% CI 0.769–0.982, P = 0.024), while the APACHE II score non-significantly contributed to the model.ConclusionIn this post-hoc analysis of a multicentre trial, low fluid balance-adjusted creatinine at CVVH initiation was associated with 28-day mortality, independent of other markers of AKI, organ failure, and surrogates of muscle mass, while unadjusted creatinine was not. More tools are needed for better understanding of the complex determinants of “AKI classification”, “CVVH initiation” and their relation with mortality, fluid balance is only one.

Adjusting Acute Kidney Injury Kidney Disease: Improving Global Outcomes Urine Output Criterion for Predicted Body Weight Improves Prediction of Hospital Mortality

“…The current recommendations for staging AKI use easily ascertainable and widely available surrogates of kidney function. 8,12 In this context, the criteria for staging AKI according to the KDIGO guideline, urine output adjusted for actual body weight [13][14][15] and measured sCr, [16][17][18][19][20] are the focus of current scientific discussions. In line with this ongoing debate and to establish a basis for possible future research, this study comprehensively analyzed mainly the adjustment of urine output by PBW as well as various other adjustments of the current recommendations for staging AKI in a large collective of patients undergoing cardiac surgery.…”

Effect of hydrocortisone on the 28-day mortality of patients with septic acute kidney injury

“…In addition, SCr is not only determined by renal function (excretion), but also by hemodilution (caused by fluid accumulation). It is reported that lower SCr levels caused by fluid overload may underestimate true renal function impairment in critically ill patients [30]. The lack of cumulative fluid balance due to the retrospective nature of the study design may cause information bias.…”