Acute kidney injury (AKI)

Acute kidney injury (AKI)

1. Epidemiology. Estimated to occur in 12% of hospital admissions and 50% or greater of intensive care unit (ICU) patients. Risk increases with age. Perioperative acute kidney injury is common, accounting for 30% to 40% of all in-hospital cases of AKI. Development of postoperative AKI is associated independently with increased morbidity and mortality.
2. Etiology
   1. Traditional categorization is by the anatomical groups of prerenal, intrarenal, and postrenal.
      1. Prerenal. Due to decreased circulating blood volume (hypovolemia) or a perceived decrease in circulating volume (decreased cardiac output or hypotension). Early correction of the underlying cause usually results in rapid reversal of renal dysfunction, but continued renal hypoperfusion may result in intrinsic renal damage.
      2. Intrarenal. The most common cause is ATN due to ischemia. Other intrarenal causes include toxins, acute glomerulonephritis, and interstitial nephritis.
      3. Postrenal. Obstructive lesions result in disrupted emptying and can be caused by renal calculi, neurogenic bladder, prostatic disease, or an encroaching tumor. Unilateral obstruction rarely causes AKI.
   2. Modern description favors describing specific syndromes (eg, hepatorenal, cardiorenal, nephrotoxic, sepsis-associated AKI) that do not always fit the traditional classification scheme, since each has a unique treatment.
      1. Cardiorenal syndrome: Inflammation and neurohormonal activation affect blood flow autoregulation, impairing compensation for the abnormal kidney perfusion pressure caused by low cardiac output and/or renal vein congestion.
      2. Hepatorenal syndrome: Hepatic dysfunction causes systemic vasodilation, triggering a high level of activation of the RAAS and subsequent renal dysfunction. Portal hypertension-induced splanchnic vasodilation seems to play a central role. Profound oliguria and sodium retention result.
3. Classification: There are three widely used classification systems for AKI (Table 5.1):
   1. The RIFLE criteria classifies three levels of kidney injury (risk, injury, or failure) and two outcomes (loss and end-stage renal disease [ESRD]) based upon (1) the increase in serum creatinine over 7 days or (2) a decrease in urine output (UOP).
   2. The AKIN criteria modifies the RIFLE criteria by including absolute increases in serum creatinine and limiting the period of injury to a 48-hour window.
   3. The Kidney Disease: Improving Global Outcomes (KDIGO) criteria fuse the RIFLE and AKIN criteria.
4. Diagnosis: History and physical examination, in particular assessing the patient’s volume status, to determine etiology. Pertinent laboratory tests should include urinalysis, serum creatinine level and fractional excretion of sodium (FE_Na), or fractional excretion of urea (FE_Urea) if the patient has been exposed to diuretics. Imaging studies can help rule out obstruction (Table 5.2).
5. Clinical features. Depending on the severity, the condition may be silent. It can present with hypervolemia due to an impaired ability to excrete water and sodium with resultant hypertension, cardiac arrhythmia, pulmonary edema, and peripheral edema. In the setting of cardiac failure, volume overload can precipitate cardiogenic shock (sometimes referred to as falling off the Starling curve). Uremia can affect cognitive function and platelet efficacy. Urinary tract obstruction might present with pain. Inability to concentrate the urine can present with hypovolemia. AKI also can cause electrolyte derangements, impaired excretion of drugs and toxins, and potential progression to CKD. Two-thirds of cases of AKI resolve within 7 days, cases that do not resolve are associated with 47% hospital mortality.
6. Prevention. Mainly based on tradition and extrapolation from animal models. A modest goal is to keep UOP greater than 0.5 mL/kg/h and to avoid hypovolemia, hypoxia, renovascular constriction, and maintenance of renal vasodilation and renal tubular blood flow along with attenuation of renal ischemic reperfusion injury. N-acetylcysteine (NAC) and bicarbonate do not provide benefit beyond fluid hydration.
7. Management
   1. Medications Although medications such as diuretics, dopamine, and fenoldopam can increase UOP, treat hypertension, and manage electrolyte, fluid, and acid-base disturbances, they have not been proven to prevent or treat AKI.
   2. Optimization: Remove toxic drugs, renally dose medications, and favor medications that do not require renal clearance. Avoid hydroxyethyl starch, especially in septic shock. Normal saline has a higher risk for composite death, dialysis, and renal dysfunction compared with more physiological solutions (eg, lactated Ringer’s). Order imaging with contrast only if essential. Control inflammation, correct anemia (hemoglobin >7 g/dL), optimize cardiac output, and correct volume status. This may require invasive hemodynamic monitoring. If adequately intravascularly replete, vasopressors may be needed to maintain mean arterial pressure (MAP) >65 mm Hg.
   3. Specific syndromes: In addition to the above optimization, address the underlying condition.
   4. Renal replacement therapy (RRT): Incidence of patients with postoperative AKI requiring renal replacement therapy varies depending on the underlying surgical operation (eg, coronary artery bypass grafting 1.1% vs general surgery 0.6%). Indications for RRT in AKI and CKD include hyperkalemia, acidosis, volume overload, and uremic complications (pericarditis, tamponade, and encephalopathy). Best timing for RRT initiation remains controversial.
      1. Hemodialysis uses an artificial semipermeable membrane that separates the patient’s blood from the dialysate and allows the exchange of solutes by diffusion along a gradient. Vascular access (via central venous catheters or a surgically created arteriovenous fistula) and systemic or regional anticoagulation are often required. Hemodialysis typically is performed three times a week, and serum electrolyte and volume abnormalities are corrected by adjusting the dialysis bath fluid. Blood samples taken immediately after dialysis will be inaccurate, because redistribution of fluid and electrolytes takes approximately 
6 hours. Complications include arteriovenous fistula infection or thrombosis, dialysis disequilibrium or dementia, hypotension, pericarditis, and hypoxemia.
      2. Ultrafiltration and hemofiltration allow for the removal of volume with minimal removal of waste products. These techniques are useful in volume-overloaded patients. As with standard hemodialysis, anticoagulation is usually required.
         1. Ultrafiltration uses hemodialysis equipment to create a hydrostatic driving force across the membrane without a dialysate on the opposing side. Thus, an ultrafiltrate of serum is removed, and this volume is not replaced. If large volumes of fluid are removed rapidly, hypotension may ensue.
         2. Hemofiltration uses the same principle as ultrafiltration; however, replacement fluid is given to the patient either before or after the membrane filter and solutes/electrolytes are removed by convection. Volume shifts are minimized so that patients can tolerate longer periods of continuous filtration.
      3. Continuous renal replacement therapy (CRRT) refers to any continuous mode of extracorporeal solute or fluid removal. Slower blood flow rates with CRRT improve hemodynamic stability compared with regular hemodialysis.