A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 44-year-old woman presents with increased thirst and frequent urination that started 6 months ago and have progressively worsened. Recently, she also notes occasional edema of the face. She has no significant past medical history or current medications. The patient is afebrile and the rest of the vital signs include: blood pressure is 120/80 mm Hg, heart rate is 61/min, respiratory rate is 14/min, and temperature is 36.6°C (97.8°F). The BMI is 35.2 kg/m2. On physical exam, there is 2+ pitting edema of the lower extremities and 1+ edema in the face. There is generalized increased deposition of adipose tissue present that is worse in the posterior neck, upper back, and shoulders. There is hyperpigmentation of the axilla and inguinal areas. The laboratory tests show the following findings:
Blood
Erythrocyte count 4.1 million/mm3
Hgb 12.9 mg/dL
Leukocyte count 7,200/mm3
Platelet count 167,000/mm3
Fasting blood glucose 141 mg/dL (7.8 mmol/L)
Creatinine 1.23 mg/dL (108.7 µmol/L)
Urea nitrogen 19 mg/dL (6.78 mmol/L)
Urine dipstick
Glucose +++
Protein ++
Bacteria Negative
The 24-hour urine protein is 0.36 g. Which of the following medications is the best treatment for this patient’s condition?
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A
EnalaprilCorrect. ACE inhibitors (enalapril) reduce intraglomerular pressure and proteinuria, slowing progression of diabetic nephropathy - first-line for this presentation.
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B
InsulinIncorrect. Insulin treats hyperglycemia but does not provide the renoprotective hemodynamic benefit of ACE inhibitors in diabetic nephropathy.
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C
FurosemideIncorrect. Furosemide is for symptomatic volume overload; her mild lower-extremity edema is more consistent with insulin resistance/obesity and does not need a loop diuretic as primary therapy.
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D
MannitolIncorrect. Mannitol is an osmotic diuretic for cerebral edema or to maintain urine output in AKI, with no role in diabetic nephropathy.
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E
MetforminIncorrect. Metformin is an oral antihyperglycemic but lacks the direct intraglomerular hemodynamic effect that makes ACE inhibitors first-line for diabetic nephropathy with proteinuria.
↑ Tap an answer to reveal the reasoning
Answer: A. An obese woman with central fat distribution (buffalo hump, supraclavicular fat), acanthosis nigricans, polyuria, polydipsia, and proteinuria with an elevated fasting glucose has type 2 diabetes mellitus with early diabetic nephropathy. The 24-hour urine protein of 0.36 g is microalbuminuria-range proteinuria (mild, sub-nephrotic), and the patient has clinical features of metabolic syndrome with insulin resistance.
First-line treatment to slow progression of diabetic kidney disease and reduce proteinuria is an ACE inhibitor (enalapril) or ARB. These drugs decrease intraglomerular pressure by dilating the efferent arteriole, reducing albumin filtration and the long-term decline in GFR. They are recommended in any diabetic with hypertension, microalbuminuria, or overt nephropathy - even at normal blood pressure if microalbuminuria is present.
Insulin and metformin treat the hyperglycemia but do not have the renoprotective glomerular-pressure effect of ACEi/ARB. Furosemide reduces edema but does not slow nephropathy progression. Mannitol is an osmotic diuretic used for cerebral edema or to maintain urine output, not for diabetic nephropathy.
**Why each option:**
**A.** Correct. ACE inhibitors (enalapril) reduce intraglomerular pressure and proteinuria, slowing progression of diabetic nephropathy - first-line for this presentation.
**B.** Insulin treats hyperglycemia but does not provide the renoprotective hemodynamic benefit of ACE inhibitors in diabetic nephropathy.
**C.** Furosemide is for symptomatic volume overload; her mild lower-extremity edema is more consistent with insulin resistance/obesity and does not need a loop diuretic as primary therapy.
**D.** Mannitol is an osmotic diuretic for cerebral edema or to maintain urine output in AKI, with no role in diabetic nephropathy.