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Acute kidney injury, presentation and diagnosis

Acute kidney injury, pathophysiology, presentation and diagnosis

Acute kidney injury (AKI) is a clinical syndrome generally defined by an abrupt reduction in kidney functions as evidenced by changes in laboratory values, serum creatinine (Scr), blood urea nitrogen (BUN), and urine output.

RIFLE (Risk, Injury, Failure, Loss of Kidney Function, and End-Stage Renal Disease) and AKIN (Acute Kidney Injury Network) criteria are two criteria-based classification systems developed to predict patient outcomes. The Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines were developed to provide one standardized definition of AKI

KDIGO defines AKI as being present if any of the following criteria is met:
1. Increase in Scr by at least 0.3 mg/dL (27 ╬╝mol/L) within 48 hours
2. Increase in Scr by at least 1.5 times baseline within the prior 7 days
3. Decrease in urine volume to less than 0.5 mL/kg/h for 6 hours


AKI can be categorized as prerenal (resulting from decreased renal perfusion in the setting of undamaged parenchymal tissue), intrinsic (resulting from structural damage to the kidney, most commonly the tubule from an ischemic or toxic insult), and postrenal (resulting from obstruction of urine flow downstream from the kidney)


Patient presentation varies widely and depends on the underlying cause. Outpatients often are not in acute distress; hospitalized patients may develop AKI after a catastrophic event.

Symptoms in the outpatient setting include acute change in urinary habits, weight gain, and flank pain. Signs include edema, colored or foamy urine, and, in volumedepleted patients, orthostatic hypotension.


Thorough medical and medication histories, physical examination, assessment of laboratory values, and, if needed, imaging studies are important in the diagnosis of AKI.

Scr cannot be used alone to diagnose AKI because it is insensitive to rapid changes in glomerular filtration rate (GFR) and therefore may not reflect current renal function. The use of BUN in AKI is very limited because urea’s production and renal clearance are heavily influenced by extrarenal factors such as critical illness, volume status, protein intake, and medications.

Urine output measured over a specified period of time allows for short-term assessment of kidney function, but its utility is limited to cases in which it is significantly decreased.

In addition to BUN and Scr, selected blood tests, urinary chemistry, and urinary sediment are used to differentiate the cause of AKI and guide patient management

Simultaneous measurement of urine and serum electrolytes and calculation of the fractional excretion of sodium (FENa) can help determine the etiology of AKI . The FENa is calculated as
FENa = (UNa × SCr × 100)/(UCr × SNa)
where UNa = urine sodium, SCr = serum creatinine, UCr = urine creatinine, and SNa = serum sodium.
A number of new serum and urinary biomarkers are under investigation for early detection and prediction of prognosis of AKI.


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