A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 45-year-old woman with a history of morbid obesity presents with generalized edema and weight gain over the past month. She does not have diabetes or hypertension and denies any illicit drug use. Her medications include a daily multivitamin. Physical examination reveals an obese woman with bilateral lower extremity edema and no jugular venous distension. Laboratory studies show serum creatinine of 1.2 mg/dL, serum albumin of 2.8 g/dL, and 24-hour urine protein excretion of 4.5 g. Which of the following mechanisms is most likely contributing to this patient's renal condition?
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A
Circulating nephrotoxic antibodiesIncorrect. Nephrotoxic antibodies define primary immune-mediated disease, not the hyperfiltration-driven obesity FSGS pattern.
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B
Direct tubular toxicity from obesityIncorrect. Direct tubular toxicity does not explain glomerular proteinuria with hypoalbuminemia.
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C
Glomerular hyperfiltration injuryCorrect. Obesity raises glomerular pressures and causes hyperfiltration injury, the mechanism of secondary FSGS.
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D
Immune complex deposition in glomeruliIncorrect. Immune complex deposition is the mechanism of membranous and lupus nephropathy, not obesity-related FSGS.
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E
Hypoperfusion-related ischemic injuryIncorrect. Hypoperfusion causes acute tubular necrosis, not nephrotic-range glomerular proteinuria.
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Answer: C. The patient has nephrotic syndrome with significant proteinuria and hypoalbuminemia. Morbid obesity is known to cause secondary FSGS due to glomerular hyperfiltration injury from increased glomerular pressures and hyperfiltration. Immune complex deposition and circulating nephrotoxic antibodies are not associated with secondary FSGS in obesity.