A 78-year-old woman is brought to the office by her son for follow-up. The patient was hospitalized 5 days ago due to fever, vomiting, dysuria, and flank pain. Acute pyelonephritis was diagnosed, and she was treated with ceftriaxone and given intravenous fluids. Urine culture grew Escherichia coli, and the patient was discharged home with a prescription for levofloxacin, which she is still taking. Since hospital discharge, the patient has had nausea and loss of appetite, but her fever and urinary symptoms have resolved. Temperature is 36.4 C (97.5 F), blood pressure is 116/68 mm Hg, and pulse is 92/min. No suprapubic or flank tenderness is noted on physical examination. Laboratory results are as follows:
| Serum chemistry | ||
| Sodium | 144 mEq/L | |
| Potassium | 3.6 mEq/L | |
| Blood urea nitrogen | 44 mg/dL | |
| Creatinine | 1.7 mg/dL | |
| Urinalysis | ||
| Protein | none | |
| Blood | negative | |
| Cells | none | |
| Casts | none | |
| Urine sodium | 10 mEq/L (normal: ≥20) | |
Renal function was normal at the time of hospital discharge. A review of hospital records shows no significant hypotensive episodes or radiographic contrast exposure during the hospital stay. Which of the following is the most likely cause of this patient's renal dysfunction?
Prerenal acute kidney injury | |
Etiology |
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Clinical features |
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Treatment |
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EABV = effective arterial blood volume; NSAID = nonsteroidal anti-inflammatory drug. | |
This patient developed reduced renal function (ie, elevated creatinine) following hospitalization for acute pyelonephritis. Her appetite loss (which often persists during recovery from illness and can be worsened by antibiotic use) likely resulted in decreased oral intake with subsequent hypovolemia and decreased renal perfusion.
Impaired renal function due to hypoperfusion is termed prerenal acute kidney injury (AKI), as the pathogenesis is driven by impaired renal blood flow; the kidneys are not actually injured and renal tubular function is intact. In response to perceived hypovolemia, the renin-angiotensin-aldosterone system (RAAS) becomes activated, and there is increased reabsorption of renal solutes (namely urea and sodium) and water in an effort to restore intravascular volume. Expected laboratory findings include:
Increased ratio of blood urea nitrogen (BUN) to creatinine (>20:1) (ie, prerenal azotemia) due to increased urea reabsorption
Low urine sodium (<20 mEq/L) and low (<1%) fractional excretion of sodium (FENa) due to increased sodium reabsorption
High urine osmolality (>450 mOsm/kg) and specific gravity (>1.015), in part due to nonosmotic stimulation of antidiuretic hormone (ADH) with relatively greater reabsorption of water than solute
Unremarkable urinalysis (eg, no protein, cells, or casts) due to lack of intrinsic kidney injury
Restoration of intravascular volume (eg, isotonic intravenous fluids) normalizes RAAS and ADH activity and resolves prerenal AKI.
(Choice A) Chronic pyelonephritis can be a complication of repeated or untreated episodes of acute pyelonephritis. However, urinalysis typically shows white blood cells (WBCs) and other evidence of kidney injury (eg, hematuria, proteinuria).
(Choice B) Acute interstitial nephritis can occur following new medication exposure (eg, levofloxacin). However, urinary WBCs and WBC casts are usually present, and laboratory findings are consistent with intrinsic kidney injury (eg, BUN/creatinine ratio ~10:1, FENa >2%).
(Choice D) Renal artery stenosis is typically accompanied by underlying hypertension caused by chronic RAAS activation. Patients are at risk for developing AKI after initiation of an ACE inhibitor.
(Choice E) Untreated prerenal AKI can eventually lead to ischemic acute tubular necrosis. However, muddy brown casts are commonly present, and laboratory findings are more consistent with intrinsic (rather than prerenal) kidney injury.
(Choice F) Although common in older men due to urethral obstruction by an enlarged prostate, AKI due to urinary tract obstruction is relatively uncommon in women because it requires obstruction of both ureters (eg, advanced cervical cancer). In addition, postrenal AKI usually demonstrates a BUN/creatinine ratio <20:1.
Educational objective:
Prerenal acute kidney injury results from renal hypoperfusion (eg, dehydration due to poor oral intake). Characteristic laboratory findings include an elevated blood urea nitrogen/creatinine ratio (>20:1), low urine sodium (<20 mEq/L), low fractional excretion of sodium (<1%), high urine osmolality and specific gravity, and unremarkable urinalysis.