الفهرس 
Acute Kidney InjuryOnly 14 pages are availabe for public view
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Abstract
In 2002, the Acute Dialysis Quality Ini¬tiative (ADQI) group proposed a standard definition and classification system for the syndrome of acute renal failure through a broad consequences of experts across international boundaries. The cla¬ssification system coins the acronym RIFLE and has three levels: Risk, Injury, and Failure; and two outcomes:Persistent acute renal failure (termed Loss) and End stage kidney disease Classically, the causes of AKI have been subdivided into three groups: prerenal, intrinsic, and post renal. While there is considerable overlap between these, especially the first two, it remains a useful clinical guide.
Current diagnostic parameters for AKI are limited by reliance on serum creatinine, which is affected by age, gender and muscle mass. In addition, elevations in serum creatinine may occur several days after the actual injury. The search for AKI biomarkers has focused on identifying alternatives to serum creatinine. Urinary neutrophil gelatinase associated lipocalin (NGAL) and interleukin-18 may provide insights into the cause of AKI . Similarly, urinary and serum NGAL, serum cystatin C and urinary kidney injury molecule-1 (KIM-1) may facilitate the early diagnosis of AKI. KIM-1 also shows promise in predicting adverse events in patients with established AKI.
Management is directed at treating any life threatening features, attempting to halt or reverse the decline in renal function, and if unsuccessful providing support by renal replacement therapy anticipating renal recovery. Hyperkalaemia, pulmonary oedema, and severe acidosis require immediate attention. Fluid balance, the treatment of less severe acidosis, the use of diuretics and dopamine, as well as the relief of obstruction are all issues in the further management of the patient some more controversial than others. Provided the patient can be maintained through the period of non function, and no further insults accrue, the kidney is remarkable in its ability to recover its normal homoeostatic role.
Pharmacological interventions in AKI have targeted the prevention of renal ischemia or modulation of the ongoing inflammatory or hormonal insults. Low dose dopamine, historically thought to improve renal perfusion and thus prevent AKI, has recently been shown in a meta analysis to have no effect on mortality and RRT requirement. Similarly, atrial natriuretic peptide (ANP), a vasoactive endogenous hormone that increases glomerular filtration by dilating afferent and constricting efferent arterioles, was felt to be a promising therapeutic option. Anaritide, an ANP analogue, was initially shown to have no effect on dialysis free survival and caused increased rates of hypotension, anaritide at a lower dose (50 ng/kg/min) was found to significantly increase the rate of 21 day dialysis free survival.
Intermittent hemodialysis (IHD), continuous renal replacement therapies (CRRT) and sustained low efficiency dialysis (SLED) are the principal RRT modalities that are used in the acute setting. Although institutional policies may determine the local availability of these modalities, CRRT and SLED tend to be used in patients with greater hemodynamic instability. There is likely substantial intercenter variability with respect to how each of these forms of RRT is utilized and prescribed.