Acute kidney injury (AKI) may be a clinical syndrome that complicates the course and worsens the result during a significant number of hospitalised patients. Recent advances in clinical and basic research will help with a more accurate definition of this syndrome and within the elucidation of its pathogenesis. With this data we'll be ready to conduct more accurate epidemiologic studies in an attempt to realize a far better understanding of the impact of this syndrome. AKI may be a syndrome that rarely features a sole and distinct pathophysiology. Recent evidence, in both basic science and clinical research, is beginning to change our view for AKI from one organ failure syndrome to a syndrome where the kidney plays a lively role within the progress of multi-organ dysfunction. Accurate and prompt recognition of AKI and better understanding of the pathophysiologic mechanisms underlying the numerous clinical phenotypes are of great importance to research for effective therapeutic interventions. In this review we offer the foremost recent updates within the definition, epidemiology and pathophysiology of AKI.

The concept of Acute kidney failure (ARF) has undergone significant re-examination in recent years. Traditionally, emphasis was given to the foremost severe acute reduction in kidney function, as manifested by severe azotaemia and sometimes by oliguria or anuria. However, recent evidence suggests that even relatively mild injury or impairment of kidney function manifested by small changes in serum creatinine and urine output (UO) may be a predictor of serious clinical consequences.

Acute Kidney Injury (AKI) is that the term that has recently replaced the term ARF. AKI is defined as an abrupt (within hours) decrease in kidney function, which encompasses both injury (structural damage) and impairment (loss of function). It is a syndrome that rarely features a sole and distinct pathophysiology. Many patients with AKI have a mixed aetiology where the presence of sepsis, ischaemia and nephrotoxicity often co-exist and complicate recognition and treatment. Furthermore the syndrome is sort of common among patients without critical illness and it's essential that health care professionals, particularly those without specialisation in renal disorders, detect it easily.

Classification of AKI includes pre-renal AKI, acute post-renal obstructive nephropathy and intrinsic acute kidney diseases. Of these, only ‘intrinsic’ AKI represents true kidney disease , while pre-renal and post-renal AKI are the consequence of extra-renal diseases leading to the decreased glomerular filtration rate (GFR). If these pre and post-renal conditions persist, they're going to eventually evolve to renal cellular damage and hence intrinsic renal disease.

The current diagnostic approach of AKI is predicated on an acute decrease of GFR, as reflected by an acute rise in scar levels and a decline in UO over a given time interval. Recently several biomarkers are proposed for the diagnosis of AKI and these are in various stages of development and validation. Nevertheless, it's not clear, if one or multiple biomarker approach is important to diagnose the complicated and multifactorial aspects of AKI.

However, additionally to the analytical difficulties related to each specific biomarker, there's also a problem concerning the acceptable point of reference , and more specifically about using serum creatinine as the standard, for the clinical evaluation of those biomarkers. It is known that serum creatinine is insensitive to acute changes of renal function and levels can vary widely with age, gender, muscle mass, diet, medications and hydration status. Moreover it's not an immediate marker of tubular damage, but rather a marker of GFR, and substantial increases in serum creatinine are often observed in renal hypo-perfusion even when the kidneys are structurally intact, leading to pre-renal azotaemia. For these reasons serum creatinine is considered an ‘imperfect gold standard’ for the diagnosis of AKI. Another issue with serum creatinine is that in most clinical situations its true baseline value isn't known, which makes the evaluation of patients very difficult. Moreover, given the phenotypic variability of AKI (different clinical phenotypes with distinct underlying pathophysiology’s), it's not clear whether different approaches are necessary for diagnosis and monitoring of the clinical course and therapy.

Journal of Nephrology and Urology is an Open Access peer-reviewed publication that discusses current research and advancements in diagnosis and management of kidney disorders as well as related epidemiology, pathophysiology and molecular genetics.

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Mercy Eleanor
Editorial Assistant
Journal of Nephrology and Urology