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Chapter 9. Neuro-nephrology

An 88-year-old woman with a history of hypertension, osteoporosis, and rheumatoid arthritis on daily aspirin presented to the emergency department (ED) after a mechanical fall, hitting her head on concrete. A head computed tomography (CT) showed a 2-cm subdural hematoma extending along the anterior falx, with no midline shift. Admission vital signs were normal except arterial blood pressure (ABP) of 201/88 mm Hg. Given her elevated ABP, she was given intravenous hydralazine, along with her home antihypertensive medications: carvedilol, clonidine, and prazosin.

Overnight, the patient became hypotensive with ABP of 80/50 mm Hg, and she was treated with 1 L of intravenous normal saline bolus.

Pertinent lab values


Sodium (Na) 138 mmol/L, potassium (K) 3.8 mmol/L, chloride (Cl) 104 mmol/L, bicarbonate (HCO3) 23 mmol/L, blood urea nitrogen (BUN) 16 mg/dL, creatinine (Cr) 0.84 mg/dL

Hospital day 1:

Na 138 mmol/L, K 3.7 mmol/L, Cl 105 mmol/L, HCO3 27 mmol/L, BUN 29 mg/dL, Cr 1.40 mg/dL

Urine chemistry

Urine Cr 60 mg/dL

Urine osmolality 550 mOsm/kg

Urine Na 15 mmol/L

Urea nitrogen 211 mg/dL

Based on the available data, what is the etiology of this patient’s acute kidney injury (AKI)?

A. Acute tubular necrosis

B. Prerenal azotemia

C. Obstructive acute renal failure

D. Acute interstitial nephritis

E. Radiocontrast agent–induced nephropathy

B. This patient had acute kidney injury (AKI) secondary to prerenal azotemia, which is the most common cause of AKI in hospitalized patients. It is due to either a reduction in effective circulating volume or hypotension, leading to renal hypo­perfusion. If the hypoperfusion is severe and prolonged, prerenal azotemia can lead to acute tubular necrosis. This patient had a hypotensive episode after being given her home antihypertensive medications. Both prerenal azotemia and acute tubular necrosis exist as a spectrum, and there is a set of biochemical indices that might help differentiate the 2 disorders.

In patients with prerenal azotemia, we typically expect the following:

  1. Urinary osmolality is >500 mOsm/kg

  2. Urinary sodium concentration <20 mmol/L

  3. Urine-to-serum creatinine ratio >40

  4. Serum urea-to-creatinine ratio >0.1

  5. The fractional excretion of sodium (FENa), which is based on the fact that sodium reabsorption is enhanced in setting of hypovolemia, is low: <1%

FENa = [(urinary Na/serum Na)/(urinary Cr/serum Cr)] × 100.


An FENa <1% suggests prerenal azotemia as cause of AKI.

For patient on diuretics, FENa is not accurate, and one must calculate the fractional excretion of urea (FEUrea...

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