Kidney Attack: Overdiagnosis of Acute Kidney Injury or Comprehensive Definition of Acute Kidney Syndromes?

heart with its severe consequences and may contribute to a better understanding of this dangerous condition. In spite of the multiple causes and the complex pathophysiology, so far we have only relied on one single parameter to diagnose AKI, i.e. serum creatinine. In the literature the reported incidence and mortality for AKI ranges from 1 to 31% while mortality ranges from 28 to 82%. This depends on the used definitions since diagnostic criteria and severity of the syndrome strongly affects both epidemiology and outcome [3] . While in the past, terms such as acute tubular necrosis (ATN) or acute renal failure (ARF) were mostly descriptive and they were never based on a specific biochemical syntax, today AKI is graded in terms of severity using both serum creatinine and urine output as criteria for the diagnosis. This has been the advance produced by ADQI with the creation of RIFLE, subsequently modified by AKIN stages and finally twigged by KDIGO guidelines [3, 4] . The term ‘kidney attack’ has no biochemical reference nor does it grade the severity of the insult, but it stresses the concept that while heart attack is documented or suspected by the presence of chest pain and EKG abnormalities, the kidney is a silent organ and clinical evidence for this disorder may be scanty although a severe condition may develop [1] . Furthermore, although clinically silent Acute kidney injury (AKI) is today facing a complex phase of characterization due to a lack of an accepted definition for a long time. The same problem occurred in the past to the acute coronary syndrome (ACS). Acute myocardial infarction (AMI) has undergone a long process over the years before finding a standardization of diagnostic criteria and a rationale classification. ACS are well defined by a screening process based on symptoms (chest pain at onset), EKG abnormalities (STEMI: ST-elevation myocardial infarction and NSTEMI: non-ST elevation myocardial infarction) and biomarkers such as troponins (NSTEMI vs. renal angina). All these clinical pictures are somehow falling under the umbrella term of ‘heart attack’. Different names have been used to define a similar disorder for the kidney (acute tubular necrosis, acute renal failure, acute kidney disease) and although the commonest term is acute kidney injury/AKI, recently a consensus has been developed to call this syndrome ‘kidney attack’ [1, 2] . For the kidney, authors agree that the pathophysiology can be extremely complex and well beyond a single ischemic insult (toxic, allergic, metabolic, obstructive, septic). The final effect can be an acute structural damage (often tubular) and/or an acute dysfunction or both. There is an effort today to increase alertness and awareness about AKI; the term ‘kidney attack’ may recall what occurs in the Published online: August 20, 2013