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 μmol/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 volume depleted 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.
Treatment of Acute Kidney Injury
Currently, there is no definitive therapy for AKI (Acute Kidney Injury). Supportive care is the mainstay of AKI management regardless of etiology.
Supportive care goals include maintenance of adequate cardiac output and blood pressure to optimize tissue perfusion while restoring renal function to pre-AKI baseline. Discontinue medications associated with diminished renal blood flow. Initiate appropriate fluid and electrolyte management. Avoid use of nephrotoxins.
In severe AKI, renal replacement therapy (RRT), such as hemodialysis and peritoneal dialysis, maintains fluid and electrolyte balance while removing waste products.Intermittent and continuous options have different advantages (and disadvantages) but, after correcting for severity of illness, have similar outcomes. Consequently, hybrid approaches (eg, sustained lowefficiency dialysis and extended daily dialysis) are being developed to provide the advantages of both.
Intermittent hemodialysis (IHD) is the most frequently used RRT and has the advantage of widespread availability and the convenience of lasting only 3 to 4 hours. Disadvantages include difficult venous dialysis access in hypotensive patients and hypotension due to rapid removal of large amounts of fluid.
Several continuous RRT (CRRT) variants have been developed including continuous hemofiltration, continuous hemodialysis, or a combination. CRRT gradually removes solute, resulting in better tolerability by critically ill patients. Disadvantages include limited availability of equipment, need for intensive nursing care, and the need to individualize IV replacement, dialysate fluids, and drug therapy adjustments.
Mannitol 20% is typically started at a dose of 12.5 to 25 g IV over 3 to 5 minutes. Disadvantages include IV administration, hyperosmolality risk, and need for monitoring urine output and serum electrolytes and osmolality because mannitol can contribute to AKI.
Loop diuretics effectively reduce fluid overload but can worsen AKI. Equipotent doses of loop diuretics (furosemide, bumetanide, torsemide, and ethacrynicacid) have similar efficacy. Ethacrynic acid is reserved for sulfa-allergic patients. Continuous infusions of loop diuretics appear to overcome diuretic resistance and to have fewer adverse effects than intermittent boluses. An initial IV loading dose (equivalent to furosemide 40–80 mg) should be administered before starting a continuous infusion (equivalent to furosemide 10–20 mg/h).
Strategies are available to overcome diuretic resistance. Administration of agents from different pharmacologic classes, such as diuretics that work at the distal convoluted tubule (thiazides) or the collecting duct (amiloride, triamterene, and spironolactone), may be synergistic when combined with loop diuretics.
Metolazone is commonly used because, unlike other thiazides, it produces effective diuresis at GFR less than 20 mL/min (0.33 mL/s).
Electrolyte management and nutrition interventions
Serum electrolytes should be monitored daily. Hyperkalemia is the most common and serious electrolyte abnormality in AKI. Hypernatremia and fluid retention commonly occur, requiring calculation of daily sodium intake, including sodium contained in commonly administered antibiotic and antifungal agents.
Phosphorus and magnesium should be monitored, especially in patients with significant tissue destruction due to increased amounts of released phosphorus; neither is efficiently removed by dialysis.
Nutritional management of critically ill patients with AKI is complex due to multiple mechanisms for metabolic derangements. Nutritional requirements are altered by stress, inflammation, and injury that lead to hypermetabolic and hypercatabolic states.