Miroslav Šašinka, Katarína Furková, Tibor Šagát
Acute tubular necrosis (ATN) is characterized with structural and functional tubular cells disturbance and various degree of the tubular function disturbance, it´s most important and most often cause of the acute kidney injury (AKI). ATN proceeds in 3 phases: phase of the initiation, maintenance and recovery regeneration. ATN etiology depends on the patient age: prerenal – ischemia (shock, sepsis, serious dehydration); renal – nephrotoxins endogenous (hemoglobin, myoglobin – rhabdomyolysis) and exogenous (cyclosporine A, tacrolimus, angiotensin converting enzyme inhibitors – ACEI, nonsteroidal anti-inflammatory drugs – NSAIDs, aminoglycosides, amphotericin B, contrast drugs); postrenal (stones, acute obstruction - hemorrhage). Pathophysiological mechanisms in ATN phases fluently goes through one to other and manage diagnostic and therapeutic progress. In morphology dominate injury of the tubular cells and interstitium. Authors analyze mechanisms of the acute kidneys injury with intention on ischemia and endogenous/exogenous nephrotoxicity.