- Clinical science
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.
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., )
In patients with reduced renal perfusion (e.g., congestive heart failure, renal artery stenosis), co-administering ACE inhibitors and NSAIDs can significantly decrease GFR. ACE inhibitors inhibit the angiotensin II-mediated vasoconstriction of the efferent arterioles, reducing GFR, while NSAIDs constrict the afferent arteriole, reducing renal perfusion and further decreasing GFR.
Intrinsic (∼ 35% of cases)
Any disease causing severe direct kidney damage:
- Acute tubular necrosis (causes approximately 85% of intrinsic AKIs)
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:
| || |
Hours to days
Oliguric or anuric phase
Generally < 2 weeks
∼ 3 weeks
Up to 2 years
- Patients have a higher risk of secondary infection throughout all phases (most common reason for a fatal outcome).
- Causes ∼ 85% of intrinsic AKIs
- 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.
- 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)
- Definition: acute kidney injury after IV administration of iodinated contrast medium
- Risk factors
- Clinical features/diagnostics: See “Symptoms/clinical findings” above and “Diagnostics” below.
- 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 )
- Blood test findings:
- Urine microscopy:
- Ultrasound: may reveal urinary tract obstruction and increased kidney size in postrenal AKI
- Biopsy: in suspected
|Types of AKI||Prerenal||Intrinsic||Postrenal|
|BUN/Cr ratio||> 20:1||< 20:1||< 20:1|
|< 1%||> 1%|| |
Acute: Normal (< 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|
- Treat underlying cause.
- General measures
- Monitor pH, water, and electrolyte balance
- Remove outflow obstructions (urinary catheter)
- If necessary, dialysis (see )