Acute Kidney Injury: Definition and Staging criteria
Acute kidney injury ( AKI) refers to a decrease in Kidney function abruptly leading to the retention of urea and nitrogenous waste products causing dysregulation of extracellular volume and electrolytes in the body. The term AKI has largely replaced acute renal failures (ARF) reflecting that smaller decrements in kidney function do not result in overt organ failures and are of substantial clinical relevance usually associated with increased morbidity and mortality.
Several consensus definitions of AKI are developed to provide a uniform definition of AKI. These definitions are exclusively based upon the serum creatinine and urine output primarily used to identify patients with AKI in epidemiologic and outcome studies. But the overall utility of these definitions and staging systems in clinical assessment and management of patients with AKI remains validated.
The various definitions of AKI have been sequentially developed but the kidney disease Improving Global outcomes (KDIGO) definition and staging systems are the most preferred ones. Other criteria include the RIFLE criteria ( Risk, Injury, Failure, Loss of kidney function, and End-stage) kidney disease with a subsequent modification proposed by the Acute Kidney Injury Network ( AKIN) and others.
The KDIGO guidelines define AKI as follows:-
- Increase in serum creatinine by >_ 0.3 mg/dL (>_26.5 micromole /L ) within 48 hours .
- Increase In serum creatinine to >_1.5 times baseline ,which is known to have occurred prior seven days.
- Urine volume <0.5mL/kg/hour for six hours.
The KDIGO criteria allow correction of volume status and obstructive causes prior to classification.
Before diagnosing or classifying AKI, one should optimize volume status and exclude obstruction. This KDIGO definition follows the AKIN criteria.
The AKIN states that these criteria should be in the context of the clinical presentation following adequate fluid resuscitation when applicable. The use of urine output criteria alone requires exclusion of urinary tract obstruction.
The time frame for an absolute increase in serum creatinine(0.3mg/dL) is retained from the AKIN definition
while the time frame for>_ 50% increase in serum creatinine reverted to seven days is included in the acute dialysis quantity initiative (ADQI)RIFLE criteria.
improving global outcomes (KDIGO)criteria, AKI stage follows:-
- Stage 1- increased serum creatinine 1.5 to 1.9 times baseline or serum creatinine increased by >_0.3 mg/dL( >_26.5micromol/L) or reduction in the urine output to <0.5 mL/kg/hour for 6 -12 hours.
- Stage 2 – increase serum creatinine 2.0 to 2.9 times baseline or reduced urine output to <0.5 mL/kg/your for >12 hours.
- Stage 3 – Increased serum creatinine to 3.0 times baseline or<0.4 mg/dL or reduced urine output to <0.3mL/kg/hour for >_24 hours or anuria for >_ 12 hours or initiated Kidney replacement therapy or in patients <18 years ,decrease in GFR to < 35 ml/ min/ 1.73 m^2.
The KDIGO criteria differ from the RIFLE classification. The KDIGO only utilizes changes in serum creatinine down urine output and not GFR changes for staging exceptionally the children under 18 years for whom an acute decrease in GFR is 35 ml/min/1.73 m^2 included in the 3rd stage.
In reference to RIFLE and acute kidney injury network (AKIN) staging systems, KDIGO suggests classifying patients on the basis of the highest state of injury.
There are many limitations to kidney diseases improving global outcomes, and criteria for AKI. These also apply to older criteria relying solely on changes in creatinine or urine output.
Many aetiologies causes AKI
A major limitation is that criteria don’t distinguish between multiple aetiologies that cause AKI. Actually, AKI is a group of hemodynamic causes and acute tubular necrosis. The KDIGO guidelines specify that patients with AKI are evaluated promptly to determine the cause. These evaluations are important as reversible causes of AKI require specific interventions. Also, different causes of AKI relate to long-term outcomes and prognosis addressed in utilizing AKI criteria. From a research perspective, therapeutic interventions require the addition of an etiologic or atomic diagnosis to the criteria.
Using urine output for defining AKI
Using urine output as a criterion is another limitation. KDIGO guidelines use changes in either serum creatinine or urine output. However, it is based on robust evidence. Evidence shows that serum creatinine criteria are strong predictors of ICU mortality whereas urine output primarily does not. The brief duration of oliguria may reflect insufficient volume resuscitation.
Other studies also suggest that urine output predicts mortality and also may be a sensitive marker for AKI.
Studies reveal that the risk of death or kidney replacement therapy was highest when both serum creatinine and urine output criteria were used. However, urine output is often omitted from studies. until the issue resolves, it is reasonable to use the criteria resulting in the least favorable strata assignment suggested by the acute dialysis quality initiative group affirmed by KDIGO.
Determination of baseline creatinine
Determining baseline creatinine is also a limitation. It becomes impossible to calculate the changes in serum creatinine in patients with AKI who do not have baseline serum creatinine measurements.
The researchers initially suggested calculating the baseline serum creatinine concentration using four-variable modifications of diet in the renal disease equation, assuming a baseline global filtration rate of 75mL/min/1.73m^2.
However, this approach should not be utilized.
The European renal best practice group, recommends that the first documented serum creatinine is used as a baseline rather than historical values prior to acute illness or a value-based upon a presumed baseline GFR of 75 ml per minute.
However, the initial hospital creatinine values may be elevated above the patient’s usual baseline if one set of AKI has occurred prior to hospital admission.
Sometimes, creatinine production reduces while setting acute illness, leading to an anti-factual fall in serum creatinine. Changes in volume of Creatinine distribution may also depress baseline creatinine values and blunt its rise in concentration during AKI. Experts also suggest an average creatinine value measured from 7 to 365 days prior to hospitalization best approximates the true baseline creatinine value. When a baseline creatinine is available, relying on small changes in serum creatinine for the diagnosis of AKI may be associated with a high rate of misdiagnosis, especially in patients with a baseline serum creatinine >_ 1.5 mg/dL.
A major concentration raised by the Kidney Disease Outcomes Quality Initiative workgroup is the use of definition based upon a biomarker such as serum creatinine or a variable such as urine output resulting in a marked increase in the number of nephrology consultations, which would be unbeneficial to the patients.
Noted by KDOQI, Discretion is required to determine the clinical significance of AKI diagnosis
Utility in epidemiology studies
Improving global outcomes criteria have the greatest utility in epidemiologic studies also for defining consistent inclusion criteria/endpoints for clinical studies. The severity of AKI stage is connected both to mortality risk and intensive care unit and hospital stay as well.
It seems these criteria will be eventually replaced at least by sensitive and specific biomarkers of renal tubular injury. Such biomarkers analogs to troponin as a marker of myocardial injury may also allow the developing of a new classification of AKI not solely depending upon serum creatinine or other markers.
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