• Johan Mårtensson, Claes-Roland Martling, Anders Oldner, and Max Bell.
• Department of Physiology and Pharmacology, Section of Anaesthesia and Intensive Care Medicine, Karolinska Institutet, Stockholm, Sweden. johan.martensson@karolinska.se
• Nephrol. Dial. Transplant. 2012 Feb 1;27(2):576-81.

BackgroundCystatin C is a marker of acute kidney injury (AKI). However, systemic inflammation associated with sepsis, a common AKI-trigger, may affect cystatin C. We studied the impact of sepsis on cystatin C levels in plasma. Furthermore, we investigated whether the presence of sepsis affects the predictive properties of cystatin C.MethodsThree hundred and twenty-seven intensive care unit (ICU) patients were categorized as having: neither AKI nor sepsis (n = 151), sepsis without AKI (n = 80), AKI without sepsis (n = 24) or AKI and sepsis (n = 72) during their first week in the ICU. Changes in cystatin C and creatinine over time in patients with and without sepsis or AKI were analysed using repeated measures analysis of variance. The performance of cystatin C on admission to predict sustained AKI, worsened AKI or death was assessed from the area under the receiver-operating characteristic curve (AUC-ROC) in septic and non-septic patients separately.ResultsIn non-AKI patients, cystatin C increased and creatinine decreased significantly over the first week. The change in cystatin C or creatinine did not differ significantly between septic and non-septic patients without AKI. Even in AKI patients, the cystatin C change did not differ significantly between septic and non-septic patients. The AUC-ROCs for prediction of the composite outcome were 0.80 and 0.78 in patients with and without sepsis, respectively, and did not differ significantly (P = 0.76).ConclusionThe inflammatory response induced by sepsis has no impact on the levels of cystatin C in plasma during the first week in the ICU.

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