Acute kidney injury in the ICU: from injury to recovery: reports from the 5th Paris International Conference

Abstract

The French Intensive Care Society organized its yearly Paris International Conference in intensive care on June 18-19, 2015. The main purpose of this meeting is to gather the best experts in the field in order to provide the highest quality update on a chosen topic. In 2015, the selected theme was: "Acute Renal Failure in the ICU: from injury to recovery." The conference program covered multiple aspects of renal failure, including epidemiology, diagnosis, treatment and kidney support system, prognosis and recovery together with acute renal failure in specific settings. The present report provides a summary of every presentation including the key message and references and is structured in eight sections: (a) diagnosis and evaluation, (b) old and new diagnosis tools,

Keywords: Acute renal failure; Anticoagulation; Biomarkers; Epidemiology; Extracorporeal epuration; Renal blood flow; Renal replacement; Therapy.

Fig. 1

RFR and baseline GFR according to patients characteristics

Fig. 2

KIDGO definition for AKI

Fig. 3

Changes in renal oxygen consumption following loop diuretics. In human or animal, use of diuretics is associated with higher renal medulla PO2 (mmHg), lower R2* BOLD MRI signal (Hz, 1/s) suggesting a higher oxygenation and lower renal oxygen consumption (RVO2, ml/min) in various conditions. *Results from selected studies (Brezis et al. Am J Physiol Renal Physiol 1994; Textor et al. J Am Soc Nephrol 2009; Warner et al. Invest Radiol 2011; Redfors et al. Intensive Care Med 2009; Sward et al. Intensive Care Med 2005). R2* is believed to be correlated with deoxyhemoglobin and therefore inversely correlated with tissue oxygenation

Fig. 4

RRT requirement and AKI occurence after biAP in patient with sepsis

Fig. 5

Schematic illustration of continuous hemofiltration, hemodialysis and hemodiafiltration circuits

Fig. 6

Decrease in perfusate flow, glomerular filtration and sodium excretion after stepwise increase in venous pressure in kidneys perfused at constant arterial pressure (from 2)

Fig. 7

Possible mechanisms leading to worsening renal failure during increased intra-abdominal pressure. ADH antidiuretic hormone, CO cardiac output, IAP intra-abdominal pressure, MAP mean arterial pressure, NS nervous system, RIP renal interstitial pressure, RPP renal perfusion pressure, RVP renal venous pressure

Fig. 8

Vicious cycle leading to fluid accumulation and worsening renal failure in patients with hypovolemia or sepsis

Fig. 9

90-day mortality of RRT-treated AKI patients who were positive versus negative for the presence of fluid overload in RENAL and FINNAKI studies

Fig. 10

a eGFR (gray boxplots) and Clcr (white boxplots) (in ml/min/1.73 m²) at ICU discharge for subgroups of AKI patients with ICU stay <7 days, 7–14 days and >14 days. Boxplots show median and IQR, whiskers 10th and 90th percentile. b eGFR (gray boxplots) and Clcr (white boxplots) (in ml/min/1.73 m²) at ICU discharge for subgroups of non-AKI patients with ICU stay <7 days, 7–14 days and >14 days. Boxplots show median and IQR, whiskers 10th and 90th percentile (from [4]—with permission)