الفهرس 
Pathophysiology of AKIOnly 14 pages are availabe for public view
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Abstract
Acute kidney injury is a clinical syndrome defined by a rise in serum creatinine and/or fall in urine output as per KDIGO classification. Future definitions are likely to incorporate novel functional and damage biomarkers to characterise AKI better. Early diagnosis and appropriate diagnostic work-up are essential to determine the underlying aetiology and to identify cases of AKI that require specific and timely therapeutic interventions. The exact diagnostic investigations depend on the clinical context and should include routine baseline tests as well as more specific and novel tools.
AKI has been linked to sepsis and inflammation, as the kidney is very sensitive to hypoperfusion. The kidney is also sensitive to many of our interventions, such as mechanical ventilation and excessive fluid resuscitation. Positive pressure ventilation can lead to hemodynamic changes and also the systemic release of cytokines that can impact renal function.
It may be time to search more closely for specific causes, assess more carefully the prevalence of aetiologies even when typical symptoms are misleadingly absent-such as acute post-infectious glomerulonephritis or AIN-and, ultimately, reshape an old-fashioned and probably outdated AKI diagnostic paradigm.
Fluid therapy during resuscitation can also result in renal impairment, including all forms of fluid therapy. Crystalloids and colloids in the form of albumin are considered equally safe, however. Crystalloids are first-line therapy followed by 5% albumin for large volume resuscitation.
Identifying and diagnosing specific causes of AKI in critically ill patients remains challenging. A high degree of suspicion must be the rule and a systematic diagnostic work-up should be undertaken in every AKI presenting without an obvious predisposing factor or following an unusual course. Although data regarding specific causes of AKI remain limited, increased recognition of the nephrotoxic contribution to AKI, and of the infrequent finding of true “acute tubular necrosis” in critically ill patients, will result in improved AKI management.
Renal replacement therapies are a supportive adjunct in the critically ill patients and more research is needed to further elucidate timing and optimal modes of replacement therapy in diverse patient groups.
The initiation of RRT should be considered early and there are data supporting early RRT in the setting of oliguria versus the traditional parameters including azotemia, fluid overload, electrolyte changes, and acidosis. The early initiation of CVVH is widely supported with the benefits occurring primarily in hemodynamically unstable patients due to its continuous nature and lack of significant fluid shifts. The benefits may be substantial in sepsis, as the removal of cytokines and perhaps the nutritional benefits, have some theoretical application.