Abstract: TH-PO223
A Case of Rapid Remission Proteinuria with Ace Inhibitor Monotherapy in HIV Associated Minimal Change Disease
Session Information
- Fellows/Residents Case Reports: Glomerulonephritis
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Moreno, Alfonso D, St Barnabas Hospital, Bronx, New York, United States
- Desir, Janice Berthe, St Barnabas Hospital, Bronx, New York, United States
- Vera-Gomez, Juan Pablo, St Barnabas Hospital, Bronx, New York, United States
- Rueda prada, Libardo, St Barnabas Hospital, Bronx, New York, United States
Background
The use of antiretroviral drugs among HIV patients has been associated with a number of renal toxicities including proteinuria. Minimal-change disease (MCD) with nephrotic syndrome in this population has also been described, though uncommon. First line therapy includes corticosteroids with a need for prompt and efficient management since this is linked with increased mortality and poor outcomes. However, there is a higher chance for opportunistic infections with HIV. Here we report an atypical case of HIV associated MCD on Atripla (tenofovir/emtricitabine/efavirenz) with rapid remission of proteinuria on monotherapy with angiotensin converting enzyme (ACE) inhibition.
Methods
A 45-years old man with HIV-1/AIDS (diagnosed 2011) initially presented July 2016 to HIV clinic with three-week bilateral lower extremity edema. Screening labs showed creatinine 0.9 mg/dl, albumin 2.2 mg/dl, proteinuria >500 mg/dl and total cholesterol 274 mg/dl. His antiretroviral therapy with Atripla was switched to Triumeq (abacavir/dolutegravir/lamivudine). He returned September 2016 with temporal resolution of his peripheral edema and nephrotic range proteinuria at 13 g/L. He was hospitalized October 2016 with an unremarkable physical exam,and negative autoimmune workup. Pertinent findings included albumin 1.1 mg/dl and creatinine 0.9 mg/dl. Nephrology was consulted for ongoing nephrotic syndrome and renal biopsy showed podocytes with 90% foot process effacement consistent with MCD. The patient was discharged home with Lisinopril 2.5 mg and Lasix 40 mg daily. On November 2016 labs showed significant improvement of his proteinuria to 0.74 g/L. His Lisinopril was increased to 10 mg daily and he continued with Lasix. Recent follow up documented on April 2017 showed a urinalysis with 100 mg/dl.
Conclusion
In closing, it is important to consider optimization of ACE inhibitors or angiotensin II blockers as alternate therapy to corticosteroids among HIV infected patients with MCD. One isolated case of rapid decline of proteinuria exists in a diabetic patient with no literature seen in HIV. This case illustrates the need for additional research into the impact of therapy with sole ACE inhibition in lieu of corticosteroids for the treatment of MCD and other glomerular diseases associated with nephrotic proteinuria among this group.