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[Prevention of "contrast-induced" acute kidney injury - practical considerations]

Marc Weidenbusch1, Markus Wörnle2, Philipp Kazmierczak3

  • 1Nephrologisches Zentrum, Medizinische Klinik IV, Klinikum der Universität München.

Acute kidney injury (AKI) episodes after iodine radiocontrast application are decreasing since non-ionic agents are routinely used. Retrospective studies (in total comprising more than 100 000 patients) DO NOT show increased AKI rates after CT scans with the application of radiocontrast (vs. uncontrasted CT scans). AKI rates are generally higher after intra-arterial (i. a.) compared with intra-venous (i. v.) radiocontrast application - cholesterol embolism due to catheter manipulation does play a role in this setting. Because of the multifactorial pathogenesis the term "contrast-associated AKI" (CA-AKI) should be used preferentially. The AMACING trial, which prospectively evaluated the use of i. v. volume administration before contrast application to prevent CA-AKI, DID NOT show a benefit for volume therapy. Instead, the trial found a significant increase in symptomatic heart failure episodes in patients after volume administrastion. "Hydration" before (emergency) contrasted CT scans therefore can put patients at risk through both volume overload and diagnostic delay. The PRESERVE trial prospectively evaluated the use of volume administration and N-acetyl cysteine (NAC) before i. a. contrast application to prevent CA-AKI. While NAC, which was placebo controlled, did not show any benefit (and therefore should not be used anymore), all patients in the PRESERVE trial received i. v. volume (either sodium chloride or sodium bicarbonate). Interestingly, the incidence of CA-AKI in both groups was below 5 % and hence almost half of what was expected based on previous trials. If the baseline volume status is checked in order to avoid overload, volume administration in patients with i. a. contrast application can be safely performed until definitive data are available. The type of solution can be pragmatically guided by the patient's acid base status. While preventive measures to avoid CA-AKI are limited, the clinical relevance of (any) AKI remains - new data showing increased morbidity and mortality with creatinine increments of onl 0.3 mg/dl. In order to distinguish CA-AKI from other, potentially treatably forms of AKI (e. g. pre- or post-renal AKI), early consultation of a nephrologist seems favorable.

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