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Chapter 9. Neuro-nephrology

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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.

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

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Pertinent lab values

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Admission:

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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

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Hospital day 1:

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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

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Urine chemistry

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Urine Cr 60 mg/dL

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Urine osmolality 550 mOsm/kg

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Urine Na 15 mmol/L

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Urea nitrogen 211 mg/dL

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

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A. Acute tubular necrosis

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B. Prerenal azotemia

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C. Obstructive acute renal failure

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D. Acute interstitial nephritis

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E. Radiocontrast agent–induced nephropathy

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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.

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

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  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%

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

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

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

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