**1. Introduction**

Acute kidney injury (AKI) is a common and mostly severe clinical syndrome complicating a number of critical illnesses. It has a highly negative impact on patient morbidity, mortality and clinical outcome. The diagnosis is generally based on evaluation of: (1) increase in serum creatinine and/or (2)

**Nadezda Petejova 1,2,3,\*, Arnost Martinek 1,2, Josef Zadrazil 3, Marcela Kanova 4, Viktor Klementa 3, Radka Sigutova 5,6, Ivana Kacirova 5,7, Vladimir Hrabovsky 1,2, Zdenek Svagera 5,6 and David Stejskal 5,6**

decrease in urinary output. According to the KDIGO (Kidney Disease Improving Global Outcomes) classification of 2012, the severity of urinary output deterioration to terminal stages and presentation of an anuria and serum creatinine increase to 353.6 μmol/L is the most serious stage 3 [1]. Further, in 2017, new forms of acute renal impairment were described with AKI lasting at least 7 days after insult and acute kidney disease (AKD) lasting up to 90 days. Renal impairment and serum creatinine levels that had not returned to baseline levels by 90 days resulted in the need for renal replacement therapy (RRT) and/or progression to chronic kidney disease (CKD) [2]. Timely AKI diagnosis, especially in critically ill patients, would enable clinicians to better initiate preventive measures to avoid the need for RRT and obviate the risk of CKD. A number of promising new biomarkers may be able to predict the development or worsening of AKI in intensive care. The most highlighted of these in recent years are noncoding microRNAs in these circumstances. This review focuses on the pathophysiology and potential biomarkers in the detection of AKI after nephrotoxic drugs and/or septic insults with emphasis on specific microRNAs.
