New Frontiers in Diagnosis and Prevention of Acute Kidney Injury (AKI): The Role of Dendritic Cells and Innovative High-Throughput Techniques  
[PERSON]  
1 Department of Nephrology, Dialysis and Transplant, San Bortolo Hospital, International Renal Research Institute Vicenza, 36100 Vicenza, Italy12 TRIV-International Renal Research Institute Vicenza, 36100 Vicenza, Italy2 TRIV-International Renal Research Institute Vicenza, 361  
or decreased urine output. According to KDIGO guidelines, AKI is defined as an increase in SCr by 0.3 mg/dL within 48 h; or increase in SCr to 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or urine volume of 0.5 mL/kg/h for 6 h [3; 6]. It includes several conditions affecting kidney structure and function, encompassing various etiologies: specific kidney diseases (e.g., acute interstitial nephritis, acute glomerular and vasculitis renal diseases); non-specific conditions (e.g., ischemia, toxic injury); and extrarenal pathology (e.g., prerenal azotemia, and acute postrenal obstructive nephropathy). More than one of these conditions may coexist in the same patient [6]. According to its pathophysiology, AKI can be classified into three categories: pre-renal, intrinsic, and post-renal [6]. Table 1 summarizes the main mechanisms of AKI. In the hospital setting, pre-renal AKI and acute tubular necrosis (ATN) account for the majority of AKI cases. \begin{table}
\begin{tabular}{l l l l} \hline
**Pathophysiology** & **Mechanism** & **Causes** & **Main Examples** \\ \hline Pre renal & Reduced RBF & Absolute hypovolemia & - & Blood loss (hemorrhage) \\  & & & - & Gastrointestinal loss (vomiting, diarrhea) \\  & & & - & Renal loss (diuretic, osmotic diuresis) \\  & & & - & Extracellular sequestration (acute pancreatitis, muscle trauma) \\ \hline  & & Relative hypovolemia & - & Cardiac failure (cardiorenal syndrome) \\  & & & - & Peripheral vasodilitation (sepsis, hepatoreal syndrome) \\ \hline  & & Impaired blood supply & - & Renal artery occlusion (stenosis, thrombosis) \\  & & & - & renal vein supply (thrombosis) \\ \hline Intrinsic & Glomerular damage & Glomerulonephritis & - & Primary (e.g., FSGS, MCD, membranous nephropathy, IgA nephropathy) \\  & & & - & Secondary to systemic disease, autoimmune (lupus nephritis), infectious (post infectious, endocarditis), hematological (MGRS) \\ \hline  & Tubulointerstitial damage & Acute tubular necrosis & - & Ischemic insults \\  & & & - & Exogenous nephrotoxins (drugs, contrast media, toxic) \\  & & & - & Endogenous nephrotoxins \\  & & & (myoglobin, hemoglobin) \\ \hline  & & Acute interstitial nephritis & - & Drugs (NSAIDs, antibiotics) \\  & & & - & Infection \\  & & & - & Systemic disease (connetiviitis) \\ \hline  & Intravascular damage & Small-vessel disease & - & Trombotic microangiopathy \\  & & & - & Renal atheroembolism \\  & & & - & small-vessel vasculitis (ANCA-vascularitis, anti-GBM) \\ \hline Post renal & Intrattubular obstruction & Protein cast precipitation & - & Paraprotein (myeloma cast nephropathy) \\  & & & - & Hemoglobin, myoglobin \\ \hline  & & Crystals precipitation & - & salt overproduction (phosphate, oxalate, uric acid) \\  & & & - & drugs (methotrexate, acyclovir, sulfonamides, indinavir, triamterene \\ \hline  & Urinary tract obstruction & Kidney stones & - & Urethral, bilateral \\  & & & - & pelvic/ureteral obstruction \\  & & & - & ureteral obstruction in single kidney \\ \hline  & & & & \\ \end{tabular}
\end{table} 
Table 1: Ethiopatogenesis of AKI. Pre-renal AKI is mainly secondary to intravascular volume reduction which results in renal blood flow (RBF) impairment. It could be the consequence of net body fluid reduction, such as hemorrhage, gastrointestinal losses (diarrhea, vomiting, prolonged nasogastric drainage), renal losses (diuretics, osmotic diuresis), dermal losses (burns, extensive sweating), or from sequestration of fluid in body tissues, so-called \"third spacing\" (e.g., acute pancreatitis, muscle trauma).