الفهرس 
RENAL PHYSIOLOGYOnly 14 pages are availabe for public view
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Abstract
In 2004, the term Acute Kidney Injury was firstly proposed to represent the entire spectrum of acute renal failure with clinical manifestations ranging from a minimal elevation in serum creatinine to anuric renal failure.
The incidence of acute kidney injury in the ICU has been estimated at 25–30% and carries a mortality of 50 to 70%.
The etiology of acute kidney injury is best considered divided into three main categories, pre-renal, intrinsic and post-renal acute kidney injury. Prerenal failure is mainly due to renal hypoperfusion. Postrenal failure may be caused by obstruction occurring anywhere from the renal pelvis to the external urethral meatus. Intrarenal failure is due to multifactorial renal insults. For example, in the patient with sever inflammatory response syndrome, factors such as hypotension, inadequate volume status and hypoperfusion may all contribute to oliguria.
Early clinical recognition of oliguria in adults requires the detection of urine flow of less than 0.5 ml/kg/h for six consecutive hours.
Traditional tools to diagnose AKI are serum creatinine (SCr) and determine etiology of AKI (clinical history, physical examination, renal ultrasound, fractional excretion of sodium [FeNa], fractional excretion of urea, blood urea nitrogen [BUN], and urine microscopy).
The recent development of novel biomarkers for the early detection of AKI promises to be a real advance in critical care and acute nephrology. The most promising of these include: Cystatin C, NGAL (neutrophil gelatinase-associated lipocalin), Interleukin-18 (IL-18), and Kidney Injury Molecule-1 (KIM-1).
General principles of AKI prevention include recognition of underlying risk factors, maintenance of renal perfusion, avoidance of hyperglycemia, and avoidance of nephrotoxins in these high-risk patients.
The basic goals for the management of established acute renal failure are the maintenance of fluid and electrolyte balance, avoidance of nephrotoxic medications, adequate nutrition, treatment of infections, correction of reversible prerenal (eg, hypovolemia) and postrenal factors, close monitoring, and proper dosing of medications.
The management of AKI remains primarily supportive; RRT and its modalities serve as the cornerstone of treatment in patients who have persistent severe acute renal dysfunction.
Modern practice is to initiate RRT sooner rather than later, unless there is clear evidence that renal function is about to recover. Indications for initiation of RRT in ARF include volume overload, hyperkalemia, severe metabolic acidosis, overt uremic symptoms and the presence of progressive azotemia.
RRTs for AKI can be classified as intermittent or continuous, based on the duration of treatment. In an ICU, continuous renal replacement therapies predominate which is associated with reduced mortality due to slower rate of solute or fluid removal per unit of time.
Discontinuation of renal support with recovering renal function is even less clear than that for its initiation. Urine output at the time of first stopping CRRT was the most important predictor of sustained discontinuation, especially if not enhanced by diuretics.