Urinary tract obstruction: urethral (such as benign prostatic hyperplasia), ureteral
Pre‐renal injury occurs secondary to underperfusion of an otherwise healthy kidney.
Intrinsic renal injury is caused by disease of the renal parenchyma:
Acute tubular necrosis (ATN) is the most common intrinsic cause, and can develop from renal ischemia or injury from endogenous and exogenous substances.
Acute interstitial nephritis (AIN) is frequently secondary to one of five etiologies: drug hypersensitivity reaction (most common), infection, immune‐mediated, glomerular disease, or idiopathic.
Post‐renal injury occurs in the setting of urinary tract obstruction. Causes of the obstruction can be within the urinary tract itself (clots, stones) or outside the tract (enlarged prostate, tumors, increased surrounding pressures). The increased pressure in the urinary tract alters the pressure gradient at the glomerular capillaries with a resultant decrease in glomerular filtration rate (GFR) and signs and symptoms of AKI.
Recognition of high risk patients is key to prevention of AKI. Hospitalized patients, in particular, should have their renal function assessed before any surgical procedures, imaging studies requiring contrast, or administration of any nephrotoxic agents. These patients should also be monitored for any change in urine output from baseline.
Risk factors for acute kidney injury
Acute on chronic kidney disease (CKD).
Prior history of AKI.
Oliguria (<0.5 mL/kg/h).
Nephrotoxic agent exposure.
Use of iodinated contrast.
Symptoms or history of obstruction.
Age over 65 years.
Primary prevention is focused on understanding and responding to the associated risk factor.
Key components include:
Maintaining renal perfusion by correcting for hypovolemia, decreased cardiac output, and sepsis‐related vasodilation.
Avoiding nephrotoxic agents.
Limiting iodinated contrast (especially in diabetic and CKD patients).
Ensuring adequate urine output in rhabdomyolysis (>0.5 mL/kg/h).
Alkalinizing urine in hyperuricemia.
Causes of intrinsic renal disease
Common causes of ATN
Common causes of AIN
Ischemia (shock state)
Cast nephropathy (myeloma light chains)
Proton pump inhibitors
IV iodinated contrast
Viruses (CMV, EBV, HIV, rubeola)
AKI generally presents as an increase in serum creatinine on surveillance blood work. This can be associated with a decrease in urine output. Many times, however, patients are asymptomatic, and may be diagnosed incidentally on routine blood work testing.
Key questions include pertinent prior history and details of the current illness.
Important past medical history includes prior history of renal dysfunction (acute or chronic), diabetes mellitus, and congestive heart failure.
Important current information includes NSAID use, decreased oral intake or decreased urine output, difficulty with urination, recent iodinated contrast, and severe volume loss.
The physician should conduct a physical exam directed at possible causes and consequences of AKI.
Physical exam findings for patients with AKI may include tachycardia, loss of skin turgor, or dry mucous membranes. One can also evaluate for bladder distension by checking for suprapubic tenderness. Flank tenderness could be suggestive of possible pyelonephritis.
Physical exam findings for sequelae of AKI include assessing volume overload manifested as peripheral edema, pulmonary crackles, and jugular venous distension. Also assess for uremia manifesting as altered mental status, pericardial rub in pericarditis, or distant cardiac sounds in uremic pericardial effusions.
More invasive exam techniques include measuring bladder pressure through an indwelling urinary catheter in order to assess for abdominal compartment syndrome. Ultrasound can also be used to evaluate for bladder distention.
List of diagnostic tests
Initial blood work should include blood urea nitrogen (BUN) and serum creatinine.
Urine osmolality, urine sodium, urine creatinine, and urine urea are useful to calculate FeNa and FeUrea to help differentiate the location of the injury (pre‐renal, intrinsic/ATN) (see Algorithm 50.1).
FeNa is <1% in pre‐renal injury, reflecting increased reuptake of sodium at the renal tubules. FeNa utility is limited in patients with CKD, early intrinsic injury, and in the elderly.
FeUrea has improved sensitivity and specificity in patients taking loop diuretics. A value of <35% suggests pre‐renal injury due to renal hypoperfusion.
Urinalysis is also essential for differentiating between different intrinsic diagnoses and pre‐renal AKI.
Pre‐renal and post‐renal AKI: urine sediment is usually bland.
Glomerular injury: RBC casts, dysmorphic RBCs.
Vascular injury: RBC casts.
Tubular injury: muddy brown granular casts, tubular epithelial cells.