Clinical and subclinical acute kidney injury in multidrug‐resistant septic patients treated with colistimethate sodium: Incidence and clinical outcomes

Abstract

Aim Colistimethate sodium (CMS) has been postulated as the principal cause of high incidence of clinical acute kidney injury (AKI) in multidrug‐resistance (MDR) septic patients with normal baseline serum creatinine (sCr) who were treated with CMS. This prospective observational study was conducted to examine the incidence and clinical outcomes of clinical and subclinical AKI in MDR septic patients receiving CMS. Methods Forty‐two MDR septic patients with normal sCr who required CMS were included. Clinical AKI was diagnosed by increased sCr levels according to the KDIGO2012 criteria while subclinical AKI was identified by elevated levels of urinary neutrophil gelatinase‐associated lipocalin (uNGAL > 150 ng/mL) or urinary liver‐type fatty‐acid‐binding protein (uL‐FABP > 10.5 ng/mL). Results Clinical AKI was noted in 47.6% of patients on day 5 and 38.1% on day 7 after initiating CMS. By using uL‐FABP, subclinical AKI was observed in 45.2% and 54.8% on day 5 and 7, respectively. At baseline prior to CMS treatment, subclinical AKI was already present in 90%. The baseline uL‐FABP was superior to the baseline uNGAL in early prediction of clinical AKI on day 5. The subclinical AKI patients had comparable worse outcomes as clinical AKI patients. Conclusion The incidence of subclinical AKI in MDR septic patients before CMS treatment was extremely high. The baseline uL‐FABP provided the best predictive capacity of clinical AKI. The causes of clinical AKI might include the persistence of sepsis process, subclinical AKI and CMS nephrotoxicity. Proper management of subclinical AKI patients before CMS initiation should be concerned to prevent further renal damage and improve patient and renal outcomes.

NGAL/hepcidin-25 ratio and AKI subtypes in patients following cardiac surgery: a prospective observational study

“…In contrast, Moledina et al coined the term 'hemodynamic AKI' (here 'clinical AKI') to describe a serum creatinine increase in the absence of increased kidney biomarker concentration, as may occur in cardiorenal syndrome or with renin-angiotensin-aldosterone system inhibition [19]. Recently, several original studies have used urinary biomarkers to define AKI subtypes in different patient populations including the Emergency Department, critical care and cardiac settings [3][4][5][6][7][8][9]. For example, Albert et al reported on NGAL and AKI consensus criteria-based AKI subtypes including subclinical (21.1%), clinical (4.5%) and combined AKI (7.5%) in patients following cardiac surgery [5].…”

“…Recently, however, serum creatinine-independent kidney biomarkers have been investigated to help improve AKI diagnosis and prognosis. The combination of classical renal function parameters with biomarker levels, e.g., kidney injury molecule-1, interleukin 6, midkine and neutrophil gelatinase-associated lipocalin (NGAL), has led to the introduction of the concept of biomarker-based subtypes of AKI [3][4][5][6][7][8][9]. Some of these biomarkers may be particularly relevant to cardiac surgery patients undergoing cardiopulmonary bypass.…”

Utilization of Colistin Versus β-Lactam and β-Lactamase Inhibitor Agents in Relation to Acute Kidney Injury in Patients with Severe Gram-Negative Infections

“…Recent reports have described higher incidence of acute kidney injury (AKI) in patients treated with colistin, but most have small sample sizes, are not population-based, or study only one type of GNI [ 5 , 6 ]. AKI occurs in approximately 25–50% of patients treated with colistin [ 7 – 10 ], but has been reported as high as 90% in certain patients [ 11 ]. Those with comorbid conditions, including existing kidney disease, have increased risk of AKI while receiving colistin [ 7 , 12 ].…”