Acute Kidney Injury (Case 12)

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Chapter 19
Acute Kidney Injury (Case 12)

Isai Gopalakrishnan Bowline MD amd Akhtar Ashfaq MD

Case: The patient is a 77-year-old man with diabetes, hypertension, and benign prostatic hypertrophy who was admitted with nausea, vomiting, and altered mental status. He was well until 2 weeks ago when he developed cough and myalgias. He was seen in a walk-in clinic and prescribed antibiotics for an upper respiratory infection (URI). Although his URI symptoms subsided, he subsequently developed loose stools and anorexia. For the past 2 days he has been unable to keep down any food, and the morning of presentation he became confused and disoriented. His family has noticed that he has not been urinating much but states that he has not been drinking much either. On exam he is hypotensive and tachycardic. Initial admission lab tests show a blood urea nitrogen (BUN) of 43 mg/dL and a creatinine (Cr) of 3.5 mg/dL.

Differential Diagnosis



Speaking Intelligently

Acute kidney injury (AKI) is defined by a sudden decline in kidney function as manifested by a decrease in glomerular filtration rate (GFR). The etiologies of AKI can be divided into three categories: prerenal azotemia, postrenal azotemia, and intrinsic renal disease. Prerenal azotemia is a physiologic response to volume depletion or renal hypoperfusion. Postrenal azotemia is due to an obstruction of the urine flow from the kidney. Intrinsic azotemia is due to dysfunction of the renal parenchyma.



Clinical Thinking

• Evaluate AKI with a systematic approach to reverse any potential causes, minimize any further injury, and initiate appropriate therapy.

• Determine whether the elevated serum creatinine is due to an acute insult or whether the creatinine is chronically elevated; our patients are often unaware of any previous disease, and it is helpful to look at their past creatinine values.

• Classify the patient based on urine output.

• Anuria is defined as a urine output less than 100 mL/day; anuria is rare and suggests complete obstruction, ATN, or a vascular event.

• Oliguria is defined as urine output less than 400 mL/day; oliguria is commonly seen with AKI, and patients with oliguria should be evaluated closely because fluid overload and electrolyte abnormalities can occur rapidly.


• When evaluating for prerenal azotemia, it is important to inquire about volume loss.

Has the patient had any diarrhea, vomiting, or burns, or is he or she taking diuretics?

Hypovolemia can cause profound renal failure especially in the setting of certain medications (nonsteroidal anti-inflammatory drugs [NSAIDs], angiotensin-converting enzyme [ACE] inhibitors or angiotensin II receptor blockers [ARBs]) and conditions (renal artery stenosis) that limit the kidneys’ ability to compensate for hypovolemia.

Evaluate for any signs of infection that may also result in hypovolemia. Has the patient had any cough, congestion, diarrhea, dysuria, fevers, or chills?

Review the patient’s medical history for any cardiac conditions that may reduce cardiac output and forward flow to the kidneys.

Inquire about liver disease, which may result in decreased renal perfusion as a consequence of arterial vasodilation in the splanchnic circulation.

• Eliminating postrenal etiologies involves assessing urine output.

Ask the patient about urgency, hesitancy, incontinence, and frequency of urination; each of these can be a symptom of incomplete bladder emptying.

Inquire about hematuria; gross hematuria can be a sign of stone disease or malignancy, and blood clots can lead to obstruction.

Review medications for use of anticholinergic medications that may cause urinary retention.

• Consider etiologies that precipitate intrinsic renal disease.

Review the patient’s medical history for systemic diseases that affect the kidney, such as systemic lupus erythematosus (SLE), diabetes, hypertension, HIV infection, or hepatitis C.

Inquire about recent trauma, which can precipitate rhabdomyolysis.

Consider atheroembolic disease in patients with recent endovascular procedures.

Inquire about symptoms of fever, rash, and arthralgias to support the diagnosis of interstitial nephritis.

Review medications that may potentially cause ATN, such as the aminoglycosides.

Physical Examination

• Physical assessment of volume status is very important in evaluating the cause of AKI.

• Vital signs are crucial; look for hypotension and tachycardia to support the diagnosis of prerenal azotemia.

• Central venous pressure (CVP) tracings and wedge pressures can give a more definitive assessment of volume status.

• Dry mucous membranes and hyperthermia support hypovolemia as a diagnosis.

• Distended neck veins, S3 gallop, bibasilar crackles, and edema support the diagnosis of heart failure with resultant renal hypoperfusion.

• Stigmata of cirrhosis may support the diagnosis of hepatorenal syndrome. Periorbital, sacral, and lower extremity edema can be signs of glomerular diseases.

• Examine the skin thoroughly to evaluate for any rash that may hint at an allergic interstitial nephritis.

• Blue toes with palpable pulses and livedo reticularis support the diagnosis of atheroembolic disease.

• Be mindful of physical exam findings associated with the systemic diseases that have renal manifestations, such as the malar rash of SLE. A palpable bladder, enlarged prostate, or palpable pelvic masses are suggestive of obstruction.

Tests for Consideration

Serum chemistries: Chemistries are essential to determine the existence and extent of AKI and the presence of associated electrolyte abnormalities. The BUN/Cr ratio is often greater than 20 : 1 in prerenal azotemia. This occurs as a result of low urinary flow allowing increased reabsorption of urea. ATN usually results in a BUN/Cr ratio less than 20 : 1.


Urine sodium (UNa) can be used to differentiate between prerenal azotemia and ATN. UNa less than 20 mmol/L is a good indicator of prerenal azotemia; maximal sodium retention is an attempt to conserve volume in the setting of hypoperfusion. ATN is usually associated with UNa greater than 40 mmol/L.


• The fractional excretion of sodium (FENa) helps to differentiate between prerenal azotemia and ATN in the setting of oliguric AKI. FENa is calculated by: (UNa)(plasma Cr) / (plasma Na)(urine Cr). FENa less than 1% is observed with prerenal azotemia, while a FENa greater than 1% is seen in ATN. FENa is variable in postrenal etiologies. It is difficult to interpret FENa in the setting of diuretic use; in these cases, the fractional excretion of urea would be more helpful.


Urinalysis is important in determining which part of the kidney is damaged. Significant proteinuria is often a sign of glomerular pathology. Isosthenuric urine is often a sign of ATN. The presence of absence of hematuria alters the differential of AKI.


Microscopic examination of the urine sediment can be very useful in diagnosing AKI. The urine sediment is usually normal in prerenal and postrenal azotemia. Renal tubular epithelial cells and muddy-brown granular casts may be visualized with ATN. Red blood cell casts exemplify glomerular injury. White blood cell (WBC) casts suggest interstitial nephritis or pyelonephritis.


Urine eosinophils are often present in the setting of allergic interstitial nephritis.



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