- Clinical science
Acute kidney injury (AKI…)
Abstract
Acute kidney injury is defined as a sudden loss of renal function with a consecutive rise in creatinine and blood urea nitrogen (BUN). It is most frequently caused by decreased renal perfusion (prerenal), but may also be due to direct damage to the kidneys (intrinsic) or inadequate urine drainage (postrenal). The main symptom of acute kidney injury is oliguria or anuria; in some cases, however, polyuria may occur as a result of disturbed tubular reabsorption. In acute kidney injury (AKI), acid-base homeostasis as well as the fluid and electrolyte balance are disturbed, and the excretion of urinary waste substances, including drugs, is impaired. Patients with prerenal AKI typically present with dehydration and low blood pressure. A postrenal cause, on the other hand, may be diagnosed using ultrasound (renal tract obstruction). The causes of intrinsic AKI may be diverse, making it difficult to diagnose. Rapid evaluation, diagnosis, and treatment are crucial in order to prevent irreversible and permanent loss of renal function.
Etiology
Prerenal (∼ 60% of cases)
Any condition leading to decreased renal perfusion:
- Hypovolemia (e.g., burns, pancreatitis, diuretics)
- Hypotension (e.g., sepsis, dehydration)
- Renal vasoconstriction or stenosis (e.g., hepatorenal syndrome)
NSAIDs constrict the afferent arteriole, while ACE inhibitors cause vasodilation of the efferent arteriole – both can lead to decreased renal perfusion and a subsequent decline in GFR in patients who are at risk for prerenal AKI.
Intrinsic (∼ 35% of cases)
Any disease causing severe direct kidney damage:
- Acute tubular necrosis (causes approximately 85% of intrinsic AKIs)
- Glomerulonephritis
- Vascular
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Tubulointerstitial nephritis
- Drug-induced
- Infectious
- Immunological
Prolonged prerenal failure also leads to intrinsic renal failure, as decreased renal perfusion causes tubular necrosis!
Postrenal (∼ 5% of cases)
Any condition causing obstruction to urinary flow:
- Congenital malformations
- Acquired obstructions (e.g., iatrogenic/catheter-associated, tumors, stones, bleeding)
Clinical features
Phase | Characteristic features | Duration |
---|---|---|
Kidney injury |
| Hours to days |
Oliguric or anuric phase |
| Generally < 2 weeks |
Polyuric phase |
| ∼ 3 weeks |
Recovery phase |
| Up to 2 years |
- Patients have a higher risk of secondary infection throughout all phases (most common reason for a fatal outcome).
Subtypes and variants
Acute tubular necrosis
- Causes ∼ 85% of intrinsic AKIs
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Location
- The straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb) are especially susceptible to ischemic damage in acute tubular necrosis.
- The convoluted segment of the proximal tubule is especially susceptible to damage from toxins in acute tubular necrosis.
-
Etiology
-
Ischemic
- Prolonged hypovolemia/shock
- Thromboembolism
- Thrombotic microangiopathy
- Cholesterol embolism (atheroemboli)
-
Toxic
- Contrast-induced nephropathy
- Medication: aminoglycosides, cisplatin
-
Pigment nephropathy
- Myoglobinuria due to rhabdomyolysis (crush syndrome)
- Hemoglobinuria associated with hemolysis
- Acute uric acid nephropathy
-
Ischemic
- Clinical features: same as for AKI (see “Symptoms/clinical findings” above)
- Urinary sediment: brownish ("muddy") granular epithelial cell casts, renal tubular epithelial cells (due to denudation of tubular basement membrane)
- Management: same as for AKI (see “Treatment” below)
Contrast-induced nephropathy
- Definition: acute kidney injury after IV administration of iodinated contrast medium
-
Risk factors
- Chronic kidney disease (esp. in patients with diabetes mellitus, multiple myeloma)
- Congestive heart failure, arterial hypotension
- Nephrotoxic drugs (esp. NSAIDs)
- Anemia
- Dehydration
- Clinical features/diagnostics: See “Symptoms/clinical findings” above and “Diagnostics” below.
-
Course
- Creatinine is highest after 3–5 days and usually falls back to the patient's baseline level within 1 week.
- The course is usually mild (end-stage renal disease usually only occurs in patients with pre-existing CKD).
-
Prevention
- Always evaluate kidney function before administering contrast agent.
- Use low dose and concentration of contrast medium.
- Discontinue nephrotoxic substances before administration.
- Ensure hydration: isotonic NaCl before and after administration of contrast medium (isotonic bicarbonate can also be used
- Acetylcysteine (no clear recommendations )
References:[1][2][3][4][5][6]
Stages
Stages of acute kidney injury according to KDIGO
- There are several classifications for staging AKI and assessing the prognosis.
- The classification by the KDIGO is the newest classification and the one most often used in clinical settings. The following parameters are included:
- Increase in serum creatinine
- Urine output
Stages of KDIGO (2012) | ||
---|---|---|
Stage | Serum creatinine | Urine output |
1 |
|
|
2 |
|
|
3 |
|
|
Further classifications: RIFLE Criteria and AKIN Stages
- The KDIGO classification is currently the most commonly used. The RIFLE criteria and AKIN stages are mentioned here for the sake of completeness.
RIFLE Criteria | AKIN Stage | Creatinine increase | Urine output |
---|---|---|---|
R=Risk | 1 |
|
|
I=Injury | 2 |
|
|
F=Failure | 3 |
|
|
L=Loss | -* |
| |
E=ESRD | -* |
| |
*The AKIN stages no longer consider the RIFLE criteria "Loss" and "ESRD" long-term effects of AKI. |
Diagnostics
-
Blood test findings:
- Acute increase in serum creatinine and decrease in urine output
- Metabolic acidosis
- Hyperkalemia, hypocalcemia, and hyperphosphatemia
-
Urine microscopy:
- Hyaline casts; : non-specific finding, can be seen in prerenal AKI (e.g. due to hypovolemia resulting in concentrated urine)
- Ultrasound: may reveal urinary tract obstruction and increased kidney size in postrenal AKI
- Biopsy: in suspected rapidly progressive glomerulonephritis
Types of AKI | Prerenal | Intrinsic | Postrenal |
---|---|---|---|
BUN/Cr ratio | > 20:1 | < 20:1 | < 20:1 |
Fractional excretion of sodium FENa= (V*UNa)/(GFR*PNa), using plasma and urine sodium concentrations (PNa and UNa), urine flow rate (V), and GFR. or FENa= (SCr*UNa)/(SNa*UCr), using serum sodium (SNa), urine sodium (UNa), serum creatinine (SCr), and urine creatinine (UCr). | < 1% | > 1% | Acute: Normal (< 1%) Subacute: >1% |
Urine sodium concentration | < 10 mEq/L | > 30 mEq/L | 10–30 mEq/L |
Urine osmolality | > 500 mOsm/kg | < 300 mOsm/kg | 300–500 mOsm/kg |
Treatment
- Treat underlying cause.
- General measures
- Discontinue nephrotoxic substances
- Monitor pH, water, and electrolyte balance
- Remove outflow obstructions (urinary catheter)
- If necessary, dialysis (see indications for acute dialysis )