Acute kidney injury (AKI) is common in the intensive care unit (ICU) and is associated with poor outcomes. There is evidence that even minor short-term changes in serum creatinine (i.e., ≥0.3 mg/dL or 26 μmol/L) are linked to increased morbidity and mortality, and early intervention may be of benefit. It is important for ICU physicians to recognize AKI, assess its reversibility, and institute timely interventions to prevent further kidney damage and facilitate complete recovery. This chapter provides an overview of current and emerging strategies to optimize care for patients with AKI with an ultimate goal to improve outcomes from this disease.
Evaluation
History and Physical Examination
A careful history and physical examination are keystones for evaluating patients suspected to have AKI. Underlying risk factors for AKI should be documented, including chronic kidney disease (CKD), heart failure, cirrhosis, pulmonary disease, and diabetes mellitus. In the pediatric population, risk factors for AKI include being in the ICU, multiorgan dysfunction, exposure to nephrotoxic agents, hypoxemia, thrombocytopenia, and neurologic dysfunction. Recent studies have designated a renal angina index (RAI) as a method to identify patients who are at high risk for AKI ( Table 56-1 ). In combination with acute events, the RAI has a good performance in predicting the development and severity of AKI. Basu et al. have validated the RAI, and more recently have incorporated AKI biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), into the RAI and found improvement in discrimination for severe AKI. Precipitating factors for AKI should be identified ( Table 56-2 ). Imaging with radiocontrast, surgery, trauma, recent illnesses, and systemic complaints should be specifically documented.
| Risk | Injury | |||
|---|---|---|---|---|
| Risk | Score | ↓ eCCl | % FO | Score |
| Moderate (PICU admission) | 1 | No change | <5% | 1 |
| High (solid-organ or bone marrow transplant) | 2 | ↓ 0%-25% | ≥5% | 2 |
| Ventilation and inotropy (intubation + at least one vasopressor or inotrope) | 3 | ↓ 25%-50% | ≥10% | 4 |
| ↓ ≥50% | ≥15% | 8 | ||
| Patient Factors/Exposures | Procedures |
|---|---|
| Volume depletion | Cardiopulmonary bypass |
| Sepsis | Surgery involving aortic clamp |
| Nephrotoxins/contrast material | Increased intra-abdominal pressure |
| Hypertension | Large arterial catheter placement with risk for atheroembolization |
| Hypotension | Liver transplantation |
| Multiorgan failure | Kidney transplantation |
| Invasive mechanical ventilation | Stem cell transplantation |
| Neurologic dysfunction |
As the movement toward electronic health records continues, it is feasible to use electronic reporting to identify and monitor patients at risk of or who have AKI. Selby et al. reported the implementation of a hospital-wide electronic reporting system to aid in the early recognition of AKI based on Acute Kidney Injury Network (AKIN) criteria ( Table 56-3 ). Along with alerts to physicians about elevations in creatinine, AKI stages, AKI clinical guidelines, and AKIN diagnostic criteria were provided. The authors believe implementation of such an alert system could help raise the standard of care across all acute specialties involved in the care of patients with AKI. Colpaert et al. were able to implement an electronic alert based on RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease) criteria in a single ICU where physicians were notified of patients’ worsening kidney function ( Table 56-3 ). A multicenter Italian study to look at the epidemiology of AKI in the ICU developed a data collection tool with a RIFLE class alert system. The authors believe it could be used to help physicians gather AKI data and guide decision-making for institution of renal replacement therapy (RRT).
| Stage | RIFLE | AKIN | KDIGO | |
|---|---|---|---|---|
| 1 (Risk in RIFLE) | SCr | ↑ × 1.5 or GFR >25% | ↑ × 1.5-2 or ↑ ≥0.3 mg/dL | 1.5-1.9 × baseline or ↑ ≥ 0.3 mg/dL |
| UO | <0.5 mL/kg/hr × 6-12 hr | |||
| 2 (Injury in RIFLE) | SCr | ↑ × 2 or GFR >50% | ↑ SCr × > 2-3 | 2-2.9 baseline |
| UO | <0.5 mL/kg/hr × ≥12 hr | |||
| 3 (Failure in RIFLE) | SCr | ↑ × 3 or GFR >75% or if baseline SCr ≥4 mg/dL ↑ >0.5 mg/dL | ↑ SCr × >3 or if baseline SCr ≥4 mg/dL ↑ ≥0.5 mg/dL | 3 × baseline or ↑ ≥4 mg/dL or in patients <18 yr ↓ in estimated GFR to <35 mL/min/1.73 m 2 |
| Patients receiving RRT are considered to have met stage 3 criteria, irrespective of stage they are in at time of RRT | ||||
| UO | <0.3 mL/kg/hr × ≥ 24 hr or anuria ×12 hr | |||
| 4 (Loss in RIFLE) | Complete loss of renal function >4 weeks | |||
| 5 (End-stage in RIFLE) | Complete loss of kidney function >3 months | |||
Laboratory Studies
Laboratory studies are useful to recognize and confirm AKI, assess functional changes and kidney damage, and aid with the differential diagnosis. Oliguria has been validated as a diagnostic criterion for AKI, and its magnitude and duration are used to classify and stratify the severity of AKI. A study by Mandelbaum et al. in ICU patients observed for 1 to 7 days found that mortality increased quickly as urine output (UO) decreased below 0.5 mL/kg/hr and was higher when oliguria was prolonged. Currently in development are electronic monitoring sensors of urine flow that could aid clinicians to use UO as tool to improve AKI management. One caveat is to recognize that oliguria can be a normal response to a prerenal state and may not be due to kidney damage. Anuria is a relatively late event and occurs when glomerular filtration ceases or if there is complete urinary obstruction.
Urinalysis (UA) and microscopy are helpful to determine the cause of AKI (see Table 56-4 ). With reversible renal functional changes, a concentrated urine with high specific gravity and acidic pH are usually noted and cellular elements and casts are generally lacking. An abnormal UA with proteinuria, hematuria, and/or casts suggests an intrinsic renal cause for AKI.
| UA | Components | Sensitivity/Specificity (S/S) | Comments |
|---|---|---|---|
| Hematuria | Eumorphic RBC | Lower urinary tract source, malignancy | |
| Hematuria | Dysmorphic RBC or RBC casts | Glomerular source of bleeding | |
| Hematuria | No RBC Muddy brown granular casts | Pigment nephropathy ATN, vasculitis | |
| Leukocyte esterase | WBC | Pyelonephritis | |
| Leukocyte esterase | WBC and/or WBC casts (eosinophils) | Differentiating AIN from ATN :
| Classically >1% eosinophils suggests AIN |
| FeNa, % <SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='Urine sodium concentration×plasma creatininePlasma sodium concentration×urine creatinine concentration×100′>Urine sodium concentration×plasma creatininePlasma sodium concentration×urine creatinine concentration×100Urine sodium concentration×plasma creatininePlasma sodium concentration×urine creatinine concentration×100 Urine sodium concentration × plasma creatinine Plasma sodium concentration × urine creatinine concentration × 100 | Predicting transient AKI in ICU FeNa <1% :
FeNa >1% :
| Usual cutoff: <1% prerenal >2% ATN Falsely elevated: Diuretic use, CKD Falsely low: congestive heart failure, hepatic failure, severe burns, sepsis, rhabdomyolysis, contrast nephropathy | |
| FeUN, % <SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='Urine urea nitrogen concentration×plasma creatinineBlood urea nitrogen concentration×urine creatinine concentration×100′>Urine urea nitrogen concentration×plasma creatinineBlood urea nitrogen concentration×urine creatinine concentration×100Urine urea nitrogen concentration×plasma creatinineBlood urea nitrogen concentration×urine creatinine concentration×100
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