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A 54-year-old African-American man was admitted after being found unconscious by emergency medical service responders following several days of reported fevers and lethargy. His girlfriend reported a past history of injection-drug use and hepatitis C virus (HCV) infection. He was afebrile but had thrush and bilateral interstitial pneumonia on chest x-ray. Because HIV infection was suspected, trimethoprim-sulfamethoxazole (TMP-SMX) was begun empirically at treatment doses for Pneumocystis jirovecii pneumonia (PCP); fluconazole was also initiated. He was unable to cooperate with induced sputum examination to confirm the diagnosis of PCP.
On the third day of hospitalization, the diagnosis of HIV infection was confirmed; the patient's CD4 count was 14 cells/mm3, and his viral load was 120,000 copies/mL. Antiretroviral therapy (ART) was started with tenofovir/FTC and ritonavir-boosted darunavir.
During the next 5 days, his creatinine levels increased from 0.79 mg/dL (estimated glomerular filtration rate [eGFR] by Modification of Diet in Renal Disease equation, ≥60 mL/minute/1.73 m2) to 2.92 mg/dL (eGFR, 23 mL/minute/1.73 m2), and then to 4.98 mg/dL (eGFR, 12 mL/minute/1.73 m2). He is now producing adequate urine and maintaining good oral intake. Urinalysis shows 1+ protein and 10 to 15 granular casts/high power field; urine sodium level is 95 mEq/L/day, creatinine level is 80 mg/dL, and osmolality is 349 mOsm/kg (normal, 390–1093 mOsm/kg). He is improving clinically, with no shortness of breath or fevers. A renal ultrasound is normal.
What do you think is causing the renal failure? Would you continue empirical treatment for PCP or try to confirm the diagnosis? If you would continue empirical treatment, would you modify it? What would you do with his ART? Specifically, would you continue the tenofovir? What would be your preferred alternative regimen?
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