A 12-year-old boy is brought to the office by his mother due to nausea and headache for 2 days. The patient has no fever or neck pain. Three weeks ago, he was treated for a skin infection with 5 days of oral cephalexin. The patient has no chronic medical conditions and takes no daily medications. Temperature is 37.2 C (99 F), blood pressure is 170/98 mm Hg, pulse is 98/min, and respirations are 20/min. Physical examination shows an alert child with periorbital edema. The neck is supple. Cardiac examination reveals no murmur. The lungs are clear to auscultation bilaterally. Trace pitting edema is present on the lower extremities. Laboratory results are as follows: Which of the following is the most likely explanation for this patient's current condition?

Question

A 12-year-old boy is brought to the office by his mother due to nausea and headache for 2 days.  The patient has no fever or neck pain.  Three weeks ago, he was treated for a skin infection with 5 days of oral cephalexin.  The patient has no chronic medical conditions and takes no daily medications.  Temperature is 37.2 C (99 F), blood pressure is 170/98 mm Hg, pulse is 98/min, and respirations are 20/min.  Physical examination shows an alert child with periorbital edema.  The neck is supple.  Cardiac examination reveals no murmur.  The lungs are clear to auscultation bilaterally.  Trace pitting edema is present on the lower extremities.  Laboratory results are as follows:  Which of the following is the most likely explanation for this patient's current condition?

Quizplus · Accepted Answer

11ec25c8_d72d_c30f_bc81_efcb0ad0baca_MD0003_00 This patient most likely has acute poststreptococcal glomerulonephritis (APSGN), an immune-mediated disease that occurs several weeks after group A Streptococcus infection (eg, pharyngitis, impetigo). The postinfectious formation of nephritogenic-specific streptococcal antigens and antibody complexes causes the development of APSGN, as follows: Immune complexes are deposited between the glomerular basement membrane (GBM) and the mesangium (ie, subepithelial), causing complement system activation and accumulation of complement component C3 within the deposits. This results in low serum C3 and CH₅₀ levels but relatively normal C4. Immune complexes are deposited between the glomerular basement membrane (GBM) and the mesangium (ie, subepithelial), causing complement system activation and accumulation of complement component C3 within the deposits. This results in low serum C3 and CH₅₀ levels but relatively normal C4. ₅₀ Complement activation causes leukocytic infiltration and inflammation, resulting in a thickened GBM, decreased glomerular filtration rate (ie, elevated serum creatinine), and subsequent fluid retention (eg, edema, hypertension). Complement activation causes leukocytic infiltration and inflammation, resulting in a thickened GBM, decreased glomerular filtration rate (ie, elevated serum creatinine), and subsequent fluid retention (eg, edema, hypertension). Inflammatory damage to the glomerular podocytes causes increased glomerular proliferation and permeability, resulting in proteinuria, hematuria, and red blood cell casts (ie, nephritic syndrome). Inflammatory damage to the glomerular podocytes causes increased glomerular proliferation and permeability, resulting in proteinuria, hematuria, and red blood cell casts (ie, nephritic syndrome). Treatment is supportive (eg, blood pressure management). Most pediatric patients fully recover in several weeks. (Choice B) Renal interstitial inflammation occurs in acute interstitial nephritis (AIN), which can be triggered by antibiotics (eg, cephalexin). However, patients typically have fever, rash, eosinophilia and white blood cells (WBCs) or WBC casts on urinalysis. In addition, AIN typically appears concurrently with the offending drug and resolves with its removal; this patient stopped cephalexin 2 weeks ago. (Choice C) Renal tubular obstruction can occur with acute tubular necrosis (ATN) due to severe prerenal disease (eg, volume depletion, sepsis) or nephrotoxic agents (eg, acyclovir, aminoglycosides). ATN is not typically associated with cephalexin, and urinalysis often reveals muddy-brown granular casts and free renal tubular epithelial cells, findings not seen in this patient. (Choice D) Renal vein thrombosis can present with hematuria and proteinuria; however, severe flank pain and nausea are also typically present. Renal vein thrombosis is rare in children; risk factors include nephrotic syndrome, central venous catheters, and malignancy, none of which are present in this patient with no chronic medical conditions. (Choice E) Hemolytic uremic syndrome causes a thrombotic microangiopathy that can result in acute kidney injury (eg, elevated creatinine) in children; however, patients typically have anemia and thrombocytopenia, making this diagnosis less likely. Educational objective: Acute poststreptococcal glomerulonephritis, a complication of group A Streptococcus infection (eg, impetigo), occurs due to subepithelial deposition of streptococcal antigen/antibody immune complexes and accumulation of complement component C3 within these deposits. The subsequent glomerular damage causes hematuria, edema, acute kidney injury, and hypertension. References: Post-streptococcal glomerulonephritis. (http://www.ncbi.nlm.nih.gov/pubmed/26866231) Acute renal tubular necrosis. (http://www.ncbi.nlm.nih.gov/pubmed/29939592)

A 12-Year-Old Boy Is Brought to the Office by His