7.1 Definition of AKI
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Increase in serum creatinine (SCr) by ≥0.3 mg/dL within 48 hours; or
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Increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
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Urine volume <0.5 mL/kg/hr for 6 hours.
7.2 Epidemiology of AKI
Incidence of acute kidney injury (AKI) can be thought of in three different ways:
- 1.
Contacts with the healthcare system with a primary diagnosis of AKI,
- 2.
AKI arising among hospitalized patients, especially those in the intensive care unit (ICU), or
- 3.
AKI leading to dialysis requirement.
Overall, data suggest an increase in the incidence of AKI across all three categories over the past 3 decades. This increase is thought to be driven by a number of factors :
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Aging population with more comorbidities;
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New medications which have nephrotoxic side effects, and greater degree of polypharmacy (see sections 7.10 and 7.11 );
- ■
Increased frequency of procedures that place risk to kidney function; and
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Changing definitions of AKI (see section 7.3 );
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Changing diagnostic practices (e.g., urinary biomarkers for AKI).
The diagnosis of AKI, whether requiring dialysis or not, carries with it an increased risk for mortality both in-hospital and post-hospitalization. However, mortality among individuals hospitalized with AKI has trended in the opposite direction of AKI incidence. Among those with AKI requiring dialysis, mortality fell from more than 40% in 1988 to less than 25% in 2009. , However, no improvement in mortality rates, and even higher death rates in the critically ill, have been reported over the past decade . AKI also increases the subsequent risk for chronic kidney disease (CKD), , cardiovascular disease, and hypertension (HTN).
Because of these long-term effects, patients who develop AKI should have ongoing monitoring for kidney-related and other sequelae after their hospitalization, even if their creatinine (Cr) returns to baseline.
7.3 Staging of AKI
The KDIGO (Kidney Disease: Improving Global Outcomes) staging system has largely replaced the RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease) and AKIN (Acute Kidney Injury Network) staging systems as a means of diagnosing and categorizing the severity of AKI. Note the use of SCr rather than estimated glomerular filtration rate (eGFR): remember that formulae designed for calculating eGFR or creatinine clearance (CrCl) from SCr levels must not be used in patients with AKI or in any case in which the SCr level is unstable. Providers often neglect to consider urine output (UO) criteria, which can lead to missed cases and incorrect prognostic evaluation.
| Stage | SCr | UO |
|---|---|---|
| 1 | 1.5–1.9 times baseline or ≥0.3-mg/dL (≥26.5-mmol/L) increase | <0.5 mL/kg/hr for 6–12 hr |
| 2 | 2.0–2.9 times baseline | <0.5 mL/kg/hr for ≥12 hr |
| 3 | 3.0 times baseline or Increase in SCr to ≥4.0 mg/dL or Initiation of renal replacement therapy or In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m 2 | <0.3 mL/kg/hr for ≥24 hr or Anuria for ≥12 hr |
| eGFR , Estimated glomerular filtration rate; SCr , serum creatinine; UO , urine output. | ||
| Kellum J A, Lameire N, Aspelin P, et al. Kidney Disease: Improving Global Outcomes (KDIGO) acute kidney injury work group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl . 2012;2(1):1–138. doi:10.1038/kisup.2012.1. | ||
7.4 KDIGO stage-based clinical practice guideline for AKI
Using the stages of AKI severity listed above, the KDIGO guidelines suggest general evaluation and management strategies as shown in the following algorithms:
| Stage-Based Evaluation and Management of AKI | ||||||
|---|---|---|---|---|---|---|
| KDIGO AKI Stage | ||||||
| High Risk | 1 | 2 | 3 | |||
| Discontinue all nephrotoxic agents when possible | ||||||
| Ensure volume status and perfusion pressure | ||||||
| Consider functional hemodynamic monitoring | ||||||
| Monitor SCr and UO | ||||||
| Avoid hyperglycemia | ||||||
| Consider alternatives to radiocontrast procedures | ||||||
| Noninvasive diagnostic workup (US, serologies) | ||||||
| Consider invasive diagnostic workup (kidney biopsy) | ||||||
| Check for changes in drug dosing | ||||||
| Consider renal replacement therapy | ||||||
| Consider ICU admission | ||||||
| Avoid subclavian catheters if possible | ||||||
| AKI , Acute kidney injury; ICU , intensive care unit; SCr , serum creatinine; UO , urine output; US , ultrasound. | ||||||
| Kellum J A, Lameire N, Aspelin P, et al. Kidney Disease: Improving Global Outcomes (KDIGO) acute kidney injury work group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl . 2012;2(1):1–138. doi:10.1038/kisup.2012.1. | ||||||
7.5 Diagnostic steps to establish the cause of AKI
7.5.1 Determination of AKI versus CKD
The initial step in the diagnostic approach to patients with kidney insufficiency is to determine whether the injury is acute or chronic:
| Source of Information | Acute | Chronic |
| Medical history | Abrupt ↑ in SCr over days | Slow increase in SCr over weeks to months |
| Symptoms | Recent onset of symptoms (e.g., fever, flank pain, decreased or discolored urine) | No symptoms or slow onset of fatigue, anorexia, weakness, nausea, and/or pruritus |
| Labs | Further ↑ in SCr after initial evaluation | Relatively stable SCr |
| Anemia | Less typical or secondary to other than renal causes | More typical although not very specific |
| Ultrasound | Normal size or enlarged kidneys; can have findings of hydronephrosis or vascular occlusion depending on underlying cause | Small kidneys with increased echogenicity, although may be of normal or enlarged size, particularly with diabetes, amyloidosis, or polycystic kidney disease |
7.5.2 Initial diagnostic approach
7.5.3 Diagnostic algorithm for AKI
7.6 Urinary indices in AKI
Urinary indices and other signs to differentiate between prerenal azotemia and acute tubular necrosis (ATN) can be diagnostically useful in distinguishing possible causes of AKI (see below). Conceptually, these indices are ways to evaluate whether renal tubular function is intact or compromised: Are the kidneys appropriately able to hold on to Na? Can they concentrate the urine in response to hypovolemia? Does urea follow Na reabsorption appropriately in the proximal tubule?
| Lab Test | Prerenal Azotemia | ATN |
| Urine to plasma Cr ratio | >40 | <20 |
| BUN/Cr ratio | >20 | <10–12 |
| Urea nitrogen/BUN | >8 | <3 |
| UNa (mEq/L) | <20 | >40 |
| FENa (%) | <1 | >2 |
| FE urea (%); useful when on loop diuretics that alter Na handling | <35 | >50 |
| Urinalysis (see Chapter 6 ) | Hyaline casts or negative sediment | Abnormal: muddy brown granular and epithelial cell casts, free epithelial cells |
| Specific gravity | >1.020 | <1.010–1.015 |
| Uosm (mOsm/kg H 2 O) | >500 | <350–450 |
The above criteria of prerenal disease may not be present in patients with underlying CKD since the tubular function may be impaired at baseline.
7.6.1 Fractional excretion of sodium (FENa)
FENa is probably the urinary index most commonly used in the workup of AKI.
FENa=Na+excretedNa+filtered=(UNa×SCr×100)(SNa×UCr)
However, certain conditions can create altered handling of Na in the kidney, diminishing its utility as an assessment of volumetric stress or ↓ renal blood flow.
| When FENa Might not Be Helpful | |
| ↑ FENa in Prerenal ARF or Other Non-ATN Azotemia | ↓ FENa in ATN or Other Nonprerenal Azotemia |
|
|
7.6.2 BUN/Creatinine ratio
Another index is the serum BUN/Cr ratio. A normal value for the BUN/Cr ratio is between 10 and 20. However, certain conditions may alter the metabolic production of urea or its handling in the kidneys:
| Disproportional BUN/Cr Ratio | |
| ↑ BUN/Cr | ↓ BUN/Cr |
|
|
7.7 Red flags
While most cases of AKI are due to either prerenal conditions or ATN, one should be able to identify “red flags” for other potential etiologies of AKI. In addition, do not miss urinary obstruction—kidney ultrasound (US) should be done in most AKI cases.
| Signs and Symptoms | Potential Etiology |
| Proteinuria and hematuria | Glomerulonephritis, vascular causes |
| Heavy proteinuria (>3 g/day) | Glomerulonephritis, renal vein thrombosis |
| Thrombocytopenia | HUS/TTP, HELLP, DIC |
| Lung infiltrates/nodules, hemoptysis | Pulmonary renal syndromes |
| Purpura (palpable purpura) | HSP, vasculitis, cryoglobulinemia |
| Nonpurpuric skin rash | AIN, SLE |
| Very high blood pressure | Scleroderma crisis, malignant hypertension |
| Joint pain | SLE, rheumatoid arthritis, HSP |
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