Photomicrograph of a kidney biopsy specimen shows renal medulla, which is composed mainly of renal tubules. Features suggesting acute tubular necrosis are the patchy or diffuse denudation of the renal tubular cells with loss of brush border (blue arrows); flattening of the renal tubular cells due to tubular dilation (orange arrows); intratubular cast formation (yellow arrows); and sloughing of The diagnosis of NAGMA may be made in one of two ways (red arrows above)Patient has normal anion gap with metabolic acidosis (bicarbonate < 22 mM). Patient has an anion gap metabolic acidosis, but the decrease in bicarbonate is much greater than the elevation in anion gap (indicating the combination of an anion-gap metabolic acidosis plus a non-anion-gap metabolic acidosis). Acute kidney injury (AKI) describes a spectrum of injury to the kidneys which can result from a number of causes which may co-exist. It is characterized by a sudden decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte, and acid-base balance. The diagnosis of AKI and its staging is regarding CI-AKI – definitions and risk factors and will also try to clarify controversies of various preventive approaches including but not limited to the role of prophylactic hemodialysis. Definition and Relevance Of CI-AKI CI-AKI or CIN is defined as an absolute increase in serum creatinine of ≥0.5 mg/dl or as a relative increase Sepsis is also a well-known risk factor for AKI; 35%-50% of AKI cases in ICUs are attributable to sepsis[18,22,23]. Severe sepsis and septic shock are defined according to modified the American College of Chest Physicians and Society of Critical Care Medicine consensus criteria. Patients with proven or suspected infection, two or more systemic Acute kidney injury (AKI) is a common complication in hospitalized patients and has been consistently associated with increased long-term risk of death, de novo or worsening chronic kidney disease (CKD), and end-stage renal disease (ESRD). 1-11 Patients discharged after an episode of AKI have a 40% increased risk of death in the 2 years after Acute kidney injury (AKI) is estimated to occur in about 20–200 per million population in the community, 7–18% of patients in hospital, and approximately 50% of patients admitted to the Treatment for AKI is confounded by several variables including patient demographics, severity of AKI, and AKI associated with complex medical and surgical interventions. Therefore, there is a growing need to provide timely and accurate diagnosis to allow for the implementation of potentially novel therapeutic interventions to overcome AKI. Acute kidney injury (AKI) is a common and serious complication of cardiac surgery and is associated with increased mortality and morbidity, accompanied by a substantial economic burden. The pathogenesis of cardiac surgery-associated acute kidney injury (CSA-AKI) is multifactorial and complex, with a variety of pathophysiological theories. In addition to the existing diagnostic criteria, the Acute kidney injury (AKI) is a frequent complication of hospitalization and is associated with an increased risk of chronic kidney disease (CKD), end-stage renal disease (ESRD), and mortality. While AKI is a known risk factor for short-term adverse outcomes, more recent data suggest that the risk of mortality and renal dysfunction extends far beyond hospital discharge. However, determining TpNr8m.