AKI can be categorized according to the location of insult; pre-renal, intra-renal (intrinsic) and post-renal.
Pre-renal
Pre-renal injuries are caused by decreased renal blood flow, mostly due to hypovolemia and low-output heart failure, resulting in 30 – 40% of all AKI cases. The mechanism of injury could also be precipitated by drugs which cause renal ischemia (angiotensin-converting enzyme inhibitors [ACEI], angiotensin II receptor blockers [ARB], or direct renal inhibitors) or affecting glomerular hemodynamics (anti-inflammatory, calcineurin inhibitors, ARB, or ARB).
Intra-renal (Intrinsic)
Intrinsic renal injuries are responsible for 50% AKI incidences. They are generally caused by injury to the renal tubules, glomerulus, vascular structures, interstitium, or obstruction of the renal tubules. The followings are a listof agents causing renal injuries according to site of insult (these injuries may also be attributed by other non-drug
causes such as the illness itself);
Tubular injury
Intravenous contrast agents, aminoglycosides, amphotericin B, and
anti-retroviral agents
Interstitial injury
Antimicrobials (e.g., penicillins, cephalosporins, sulfonamides,
ciprofloxacin, vancomycin), NSAIDs, COX- 2 inhibitors, omeprazole,
lansoprazole, phenytoin, valproic acid, cimetidine, ranitidine,
diuretics, and cocaine
Glomerular injury (Acute glomerulonephritis)
NSAIDs, ampicillin, rifampin, lithium, penicillamine, hydralazine, gold,
mercury, and heroin
Vascular injury
More commonly caused by microvascular or macrovascular diseases
than induced by drugs
Intra-tubular obstruction
Calcium oxalate crystals associated with ethylene glycol ingestion
Post-renal
Post-renal injuries are the least common in critically ill patients, causing only about 10% of AKI cases as bladder catheters are usually in place. Medications known to cause tubular obstruction includes acyclovir, methotrexate, sulfadiazine, foscarnet, indinavir, tenofovir, and triamterene.