At present, there is no standard approach to determining baseline renal function.Ĭreatinine-based criteria for AKI often do not take into account underlying renal reserve.
Unfortunately, these methods can inflate as well as reduce the true incidence of AKI. These may include inpatient results or the imputation of values such as back-calculating a baseline creatinine and using an estimated glomerular filtration rate (eGFR) of 75 ml/min per 1.73 m 2 in patients with missing data. However, information on pre-hospital kidney function is not always available so that various surrogate estimates are frequently used. Ideally, this value should reflect the patient’s steady-state kidney function just before the episode of AKI. Affected patients had mortality rates similar to those with AKI that was present before adjustment.Īnother important limitation of all creatinine-based definitions of AKI is that they require a reference value to describe “baseline” renal function. It revealed that AKI was unmasked or classified differently in up to 18 % of patients after serum creatinine levels were adjusted for net fluid balance and estimated total body water. This was highlighted in a post-hoc analysis of the Fluid and Catheter Treatment Trial. As a result, the diagnosis of AKI may be delayed or missed in patients with significant fluid shifts or fluid overload. Serum creatinine is measured as a concentration and is therefore affected by variations in volume status. There is also no standardized laboratory method for quantifying serum creatinine, and substances like bilirubin or drugs may interfere with certain analytical techniques, more commonly with Jaffe-based assays. In this case, serum creatinine levels may fluctuate without a change in renal function (Table 2). Serum creatinine concentrations are also affected by drugs which compete with tubular secretion. Furthermore, a true fall in GFR may not be adequately reflected by serum creatinine in patients with sepsis, liver disease, and/or muscle wasting. As such, the serum concentration may take 24–36 h to rise after a definite renal insult. The role of creatinine as a marker of renal function is limited by the fact that its half-life increases from 4 h to 24–72 h if the glomerular filtration rate (GFR) decreases. This review will summarise the key aspects of diagnosis and diagnostic work-up with particular focus on patients in the intensive care unit (ICU). Rapid diagnosis and appropriate diagnostic workup are essential to identify those types of AKI where specific therapies and interventions are available to reverse the injurious process within the kidneys.
As such, AKI is now recognized as a major public health problem. There is increasing evidence that AKI is associated with serious short- and long-term complications, in particular increased mortality and morbidity, the development of chronic kidney disease (CKD), and high financial healthcare costs. The impact and prognosis of AKI vary considerably depending on the severity, clinical setting, comorbid factors, and also geographical location. The clinical consequences of AKI include the accumulation of waste products, electrolytes, and fluid, but also less obvious effects, including reduced immunity and dysfunction of non-renal organs (organ cross-talk). It is often diagnosed in the context of other acute illnesses and is particularly common in critically ill patients. Acute kidney injury (AKI) is a syndrome characterised by a rapid (hours to days) deterioration of kidney function. T he m edi um upon w hich t hei m a g es a re r ec o r ded will becl ea rly i denti fi abl e,st o.
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