Acute kidney injury; the focus of world kidney day in 2013

*Corresponding author: Prof. Hamid Nasri, Department of Nephrology, Division of Nephropathology, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail: [email protected] Again, the World Kidney Day in March 14 reached. In this year World Kidney Day (WKD) will focus on acute kidney injury (AKI) as a global health alert. Indeed this is the 8th WKD, will be celebrated (1). This day is a yearly event prearranged both by the International Society of Nephrology (ISN) and the International Federation of Kidney Foundations (IFKF) (1-3). In this year, the WKD committee aimed to alert the worldwide increase in AKI (4). AKI is defined by sudden decrease in kidney function by decrease in glomerular filtration rate (GFR), followed by accumulation of nitrogenous waste products and the incapability to maintain fluid and electrolyte homeostasis (5-7), which usually consistent by decrease in urine output and various clinical presentations. This condition is highly associated with increased early and long term mortality and morbidity of these patients. Additionally also there is also a risk of the development of chronic kidney failure subsequently (5-7). In spite of progress in the understanding of pathogenesis of acute kidney dysfunction, we only have an imprecise opinion as to why kidney function deteriorates so dramatically in many patients with acute illness or injury, or why, despite renal replacement therapy, mortality is so high (8,9). While the incidence of AKI has been increasing over time, alongside, the prevalence of chronic kidney failure has also been increasing. Since AKI has long been considered of as a completely reversible disease, nevertheless, over the past several years, a mass of data from experimental animals and humans have been published and pointed out that, AKI more than likely leads to permanent kidney injury as chronic kidney failure (10,11). On the other hand, the percentage of patients existing after AKI has also been increasing over time (4,10,11). Thus, if AKI really increase the risk for chronic kidney failure, then it could imply significant public health concerns with regard to the quantity of persons developing incident chronic kidney failure, progressive chronic kidney failure, end-stage kidney failure (4,10,11). The details why AKI would increase the risk of chronic kidney failure, end-stage kidney failure, and other adverse outcomes not yet fully recognized. Some animal researches imply that AKI can stimulate glomerular and interstitial fibrosis (712). Thus, despite the point that AKI is typically reversible in nature, nonetheless, there may be subclinical renal injury that persists and mediates this outcome (7-12). Therefore, an international health strategy is indispensable to diminish the huge growing load of AKI and its complications. In facts, efforts should focused on preventing AKI accompanied by early recognition and treatment, and sufficient follow up to decrease the mortality and the long term incidence of post–AKI chronic kidney failure (4-12). AKI is defined by one of the followings: rise in serum creatinine to ≥1.5 times baseline or rise in serum creatinine by ≥0.3 mg/dl during 48 hours; or urine volume <0.5 ml/kg/h for 6 hours (4-6). Early examination should consisted differentiating, pre-renal and post-renal components from intrinsic renal disease. Biological markers may give early Mohammad-Reza Ardalan1, Hamid Nasri2*