+ Common causes
+ + hypotension causing renal hypoperfusion
+ + nephrotoxic drugs
+ is asymptomatic unless it causes renal failure
+ diagnosis is suspected when
+ + azotemia develops after a hypotensive event
+ + + distinguished from prerenal azotemia by
+ + + + laboratory testing &
+ + + + response to volume expansion
+ + severe sepsis
+ + drug exposure
+ Treatment is supportive
+ Causes
+ + Hypotension (ischemic ATN, common)
+ + Nephrotoxins (common)
+ + Sepsis (common)
+ + Major surgery
+ + Third-degree burns covering > 15% of BSA
+ + The heme pigments myoglobin & hemoglobin (uncommon)
+ + Disorders resulting in other endogenous toxins, such as tumor lysis / multiple myeloma (uncommon)
+ + Poisons, such as ethylene glycol (uncommon)
+ + Herbal & folk remedies, such as ingestion of fish gallbladder in Southeast Asia (uncommon)
+ Common nephrotoxins include the following:
+ + Aminoglycoside antibiotics
+ + Amphotericin B
+ + Cisplatin
+ + Radiocontrast (particularly agents with osmolality > 100 mL)
+ + NSAIDs
+ Massive volume loss increases the risk of ischemic ATN
+ + septic / hemorrhagic shock
+ + pancreatitis
+ + serious surgery
+ Patients with serious comorbidities are at highest risk
+ increase risk of aminoglycoside toxicity
+ + Serious surgery
+ + advanced hepatobiliary disease
+ + poor perfusion states
+ + advanced age
+ Certain drug combinations may be especially nephrotoxic
+ + eg, aminoglycosides with amphotericin B
+ NSAIDs may cause several types of intrinsic kidney disease, including ATN
+ Toxic exposures cause
+ + patchy, segmental, tubular luminal occlusion with casts
+ + cellular debris
+ + segmental tubular necrosis.
+ ATN is more likely to develop in patients with the following:
+ + Baseline creatinine clearance < 47 mL/min
+ + Diabetes mellitus
+ + Preexisting hypovolemia / poor renal perfusion
+ Symptoms & Signs
+ + usually asymptomatic
+ + may cause symptoms / signs of acute renal failure, typically oliguria
+ Diagnosis
+ + Differentiation from prerenal azotemia
+ + + based mainly on laboratory findings
+ + + in the case of blood / fluid loss, response to volume expansion
+ + suspected when serum creatinine rises ≥ 0.5 mg/dL/day above baseline after an apparent trigger (eg, hypotensive event, exposure to a nephrotoxin)
+ + + the rise in creatinine may occur days after exposure to some nephrotoxins
+ + must be differentiated from prerenal azotemia because treatment differs
+ + In prerenal azotemia
+ + + renal perfusion is decreased enough to elevate serum BUN out of proportion to creatinine, but not enough to cause ischemic damage to tubular cells
+ + + Prerenal azotemia can be caused by direct intravascular fluid loss (eg, from hemorrhage, GI tract / urinary losses) / by a relative decrease in effective circulating volume without loss of total body fluid (eg, in heart failure, portal hypertension with ascites)
+ + + If fluid loss is the cause, volume expansion using IV normal saline solution normalizes serum creatinine level
+ + + If ATN is the cause, IV saline typically causes no rapid change in serum creatinine
+ + + Laboratory findings also help distinguish ATN from prerenal azotemia
+ + + + Acute Tubular Necrosis
+ + + + + Rate of creatinine rise: 0.3–0.5 mg/dL/day
+ + + + + BUN/creatinine ratio: 10–15:1
+ + + + + Urine osmolality (mOsm/kg): < 450 (usually < 350)
+ + + + + Urine Na (mEq/L):> 40
+ + + + + Urine/plasma creatinine ratio: < 20
+ + + + + Fractional excretion of Na (%): > 2
+ + + + + Urinary sediment: Muddy brown granular casts, epithelial cell casts, free epithelial cells, / a combination
+ + + + Prerenal Azotemia
+ + + + + Rate of creatinine rise: Variable & fluctuates
+ + + + + BUN/creatinine ratio: > 20:1
+ + + + + Urine osmolality (mOsm/kg): > 500
+ + + + + Urine Na (mEq/L): < 20
+ + + + + Urine/plasma creatinine ratio: > 40
+ + + + + Fractional excretion of Na (%): < 1
+ + + + + Urinary sediment: Normal / with hyaline casts
+ Prognosis
+ + In otherwise healthy patients
+ + + prognosis is good when the underlying insult is corrected
+ + + serum creatinine typically returns to normal / near-normal within 1 to 3 wk
+ + In sick patients, even when acute renal failure is mild
+ + + morbidity & mortality are increased
+ + + prognosis is better in patients who do not require ICU care (32% mortality) than in those who do (72% mortality)
+ + + Predictors of mortality include
+ + + + mainly decreased urine volume (eg, anuria, oliguria)
+ + + + severity of the underlying illness & comorbid disorders
+ + Cause of death is usually infection / the underlying disorder
+ Treatment
+ + Supportive care
+ + includes stopping of nephrotoxins whenever possible
+ + maintenance of euvolemia
+ + nutritional support
+ + treatment of infections (preferably with drugs that are not nephrotoxic)
+ + Diuretics are commonly used to maintain urine output in oliguric ATN but are of unproven benefit
+ + there is no evidence to support use of mannitol / dopamine
+ Prevention
+ + Maintaining euvolemia & renal perfusion in critically ill patients
+ + Avoiding nephrotoxic drugs when possible
+ + Closely monitoring renal function when nephrotoxic drugs must be used
+ + Taking measures to prevent contrast nephropathy
+ + Among patients with diabetes, controlling blood sugar levels
+ + There is no evidence that loop diuretics, mannitol, / dopamine helps prevent ATN.
see also Contrast Nephropathy
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