A 3-year-old boy is brought to the emergency department due to a 3-day history of fever, vomiting, and diarrhea. His mother reports that his urine output has decreased over the last day. She has been giving him ibuprofen for fever, which has improved intermittently. The patient has no chronic medical conditions and takes no daily medications. Temperature is 38.3 C (100.9 F), blood pressure is 82/60 mm Hg, pulse is 144/min, and respirations are 24/min. Examination shows dry lips and mucous membranes. The abdomen has mild, diffuse tenderness, and bowel sounds are hyperactive. Capillary refill is 4 seconds. The remainder of the examination shows no abnormalities. Laboratory results are as follows: Which of the following is the most likely cause of this patient's decreased urine output?

Question

A 3-year-old boy is brought to the emergency department due to a 3-day history of fever, vomiting, and diarrhea.  His mother reports that his urine output has decreased over the last day.  She has been giving him ibuprofen for fever, which has improved intermittently.  The patient has no chronic medical conditions and takes no daily medications.  Temperature is 38.3 C (100.9 F), blood pressure is 82/60 mm Hg, pulse is 144/min, and respirations are 24/min.  Examination shows dry lips and mucous membranes.  The abdomen has mild, diffuse tenderness, and bowel sounds are hyperactive.  Capillary refill is 4 seconds.  The remainder of the examination shows no abnormalities.  Laboratory results are as follows:  Which of the following is the most likely cause of this patient's decreased urine output?

Quizplus · Accepted Answer

11ec25c8_d725_d3bc_bc81_2579b13ed364_MD0003_00 This child with decreased urine output in the setting of recent use of a nonsteroidal anti-inflammatory drug (NSAID) (eg, ibuprofen for fever) most likely has NSAID-induced kidney injury. The kidneys normally compensate for intravascular volume depletion (eg, vomiting, diarrhea) by secreting vasodilatory prostaglandins via increased cyclooxygenase (COX) production. This dilates the afferent arteriole, thereby maintaining renal blood flow and glomerular filtration rate. When administered in patients with hypovolemia (eg, vomiting, diarrhea), NSAIDs inhibit the COX enzymes and reduce prostaglandin synthesis, resulting in renal afferent arterial vasoconstriction and subsequent reduced glomerular filtration rate, renal ischemia, and acute kidney injury. Therefore, laboratory examination reveals prerenal azotemia with a blood urea nitrogen/creatinine (BUN/Cr) ratio of >20:1. Urine sediment is typically bland without protein, hematuria, or casts. Treatment involves stoppage of the offending agent and volume resuscitation to restore renal perfusion pressure. (Choice A) NSAIDs can cause drug-induced interstitial nephritis; however, this typically occurs after prolonged (weeks) NSAID use. Classic findings include rash, fever, and eosinophilia, with urinalysis typically showing abundant white blood cells (WBCs) and WBC casts. (Choice B) The most common causes of glomerulonephritis in children (eg, poststreptococcal glomerulonephritis, IgA nephropathy) are due to immune complex deposition that can lead to elevated creatinine and decreased urine output. However, in contrast to the laboratory values in this patient, laboratory evaluation typically shows intrinsic renal disease (eg, hematuria, proteinuria, BUN/Cr ratio <20:1). (Choice D) Gastroenteritis (typically from Shiga toxin-producing Escherichia coli) can trigger hemolytic uremic syndrome, a form of thrombotic microangiopathy in children. However, this syndrome causes intrinsic renal disease via deposition of thrombi within glomerular capillaries; therefore, laboratory examination reveals a BUN/Cr ratio of <20:1 and urinalysis with red blood cells and protein. (Choice E) Toxin-mediated renal tubular injury (acute tubular necrosis [ATN]) is caused by nephrotoxic drugs (eg, vancomycin, aminoglycosides) that directly damage renal tubules; NSAIDs are not typically associated with ATN. In addition, laboratory findings include a normal BUN/Cr ratio (<20:1) and muddy brown granular casts on urinalysis. Educational objective: Patients with intravascular volume depletion (eg, vomiting, diarrhea) normally have increased renal prostaglandin production to dilate the afferent arteriole and maintain the glomerular filtration rate. Nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which can cause prerenal azotemia. References: Prerenal failure: from old concepts to new paradigms. (http://www.ncbi.nlm.nih.gov/pubmed/19855270)

A 3-Year-Old Boy Is Brought to the Emergency Department Due