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Chapter 36: Glomerular Disorders Due to Infections

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A 34-year-old African–American man who was first diagnosed as HIV positive 10 years ago but has refused antiretroviral therapy presents to an emergency room with nausea and vomiting. The symptoms started over the last few days and have worsened. Prior to the onset of nausea and vomiting, he noted a metallic taste in his mouth and anorexia. He has a previous history of injection drug use but quit 5 years ago. He takes no medications and has no allergies. His most recent serum creatinine was 1.2 mg/dL 1 year ago.

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Vital Signs:

  • Temp—37.2

  • Blood Pressure—133/86

  • Pulse—95

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Physical Examination:

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Young man in apparent distress, occasional retching.

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Head and neck examination remarkable for oral thrush. Chest is clear to auscultation, Heart rate is normal, normal rhythm, abdominal examination is without tenderness or distension. Pulses are 2+ bilaterally in both extremities. Both lower extremities with trace edema.

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Lab Results: Urinalysis:
Sodium—141 Protein—4+
Potassium—6.1 BLD—NEG
Chloride—105 LE—NEG
CO2—16 NITRITE—NEG
BUN—101 mg/dL
Creatinine—7.9 mg/dL

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Renal Ultrasound—Bilaterally enlarged echogenic kidneys without obstruction or stones.

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Which therapy is most likely to be effective in improving the patient’s renal function?

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A. Prednisone 60 mg daily for 6 months

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B. Maximum dose ACE-inhibitor

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C. Rituximab

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D. Combination antiretroviral therapy

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The answer is D. The patient in the question has heavy proteinuria without hypertension or edema. Patient has advanced kidney failure that occurred rapidly but without a nephritic presentation. The patient’s clinical history suggests long standing HIV infection that has progressed to AIDS and African–American race suggests that he is may have genetic susceptibility to developing HIVAN. The most effective treatment for HIVAN is cART (choice D). While prednisone and ACE-i may also provide benefits for some patients with HIVAN, they should be considered only after starting cART. Rituximab (choice C) has no known therapeutic effect on HIVAN.

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A 59-year-old woman diagnosed with HIV 11 years ago presents to her infectious disease specialist’s office for follow-up of lab results. The patient has been on a tenofovir-based cART regimen (tenofovir, emtricitabine, and raltegravir for the past 3 years and has had undetectable HIV plasma RNA. Her serum creatinine has been stable at 0.7 mg/dL over the last 3 years. Recently, to decrease her pill burden, she was prescribed a fixed-dose combination therapy with Stribild (elvitegravir, cobicistat, emtricitabine, and tenofovir).

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Lab Results:

  • HIV Viral Load—Undetectable

  • Sodium—139

  • Potassium—4.2

  • Chloride—105

  • CO2—28

  • BUN—25 mg/dL

  • Creatinine—1.0 mg/dL

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Urinalysis:

  • Protein—None

  • Blood—None

  • RBC—0/hpf

  • WBC—0/hpf

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