It is critical to diagnose<unk>  at an early stage in order to achieve optimal therapeutic efficacy. However, unlike markers of heart damage or stress such as troponin, creatine kinase, natriuretic peptides, reliable markers for acute kidney injury are lacking. Recently, research has found several biomarkers that can be used for early detection of acute kidney injury before serious loss of organ function may occur. Several of these biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-B-D-glucosaminidase (NAG), Cystatin C, and kidney injury molecule-1 (KIM-1) which have been shown to be involved in tubular damage. Other biomarkers that have been shown to be useful include BNP, IL-18, and fatty acid binding protein (FABP). However, there is great variability in the measurement of these biomarkers and their use in diagnosing<unk>  must be assessed. Classification Ronco et al. first proposed a five-part classification system for<unk>  in 2008 which was also accepted at ADQI consensus conference in 2010. These include: Type Inciting event Secondary disturbance Example Type 1 (acute<unk>  Abrupt worsening of heart function kidney injury acute cardiogenic shock or acute decompensation of chronic heart failure Type 2 (chronic<unk>  Chronic abnormalities in heart function progressive chronic kidney disease chronic heart failure Type 3 (acute renocardiac syndrome) Abrupt worsening of kidney function acute cardiac disorder (e.g. heart failure, abnormal heart rhythm, or pulmonary edema) acute kidney failure or glomerulonephritis Type 4 (chronic renocardiac syndrome) Chronic kidney disease decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events chronic glomerular disease Type 5 (secondary<unk>  Systemic condition both heart and kidney dysfunction diabetes mellitus, sepsis, lupus The distinction between<unk>  type 2 and<unk>  type 4 is based on the assumption that, also in advanced and chronic disease, two different pathophysiological mechanisms can be distinguished, whereas both CKD and HF often develop due to a common pathophysiological background, most notably hypertension and diabetes mellitus. Furthermore, the feasibility of the distinction between<unk>  type 2 and 4 in terms of diagnosis can be questioned. Braam et al. argue that classifying the<unk>  based on the order in which the organs are affected and the timeframe (acute vs chronic) is too simplistic and without a mechanistic classification it is difficult to study<unk> . They view the<unk>  in a more holistic, integrative manner. They defined the<unk>  as a pathophysiological condition in which combined heart and kidney dysfunction amplifies progression of failure of the individual organ, by inducing similar pathophysiological mechanisms. Therefore, regardless of which organ fails first, the same neurohormonal systems are activated causing accelerated cardiovascular disease, and progression of damage and failure of both organs. These systems are broken down into two broad categories of "hemodynamic factors" and non-hemodynamic factors or<unk>  connectors".
Cardiorenal syndrome
Conorenal syndrome
Papillorenal syndrome
Hepatorenal syndrome
Nephritic syndrome
Tumor lysis syndrome
Monofixation syndrome
Dialysis disequilibrium syndrome