Abstract: FR-PO214
AKI and Hypercalcemia: A Complicated HIV Story
Session Information
- AKI: Mechanisms - Case Reports
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Bilen, Yara, Cleveland Clinic, Cleveland, Ohio, United States
- Mehdi, Ali, Cleveland Clinic, Cleveland, Ohio, United States
- Thomas, George, Cleveland Clinic, Cleveland, Ohio, United States
- Salih Bacha, Dania, Cleveland Clinic, Cleveland, Ohio, United States
- George, Michael W., Cleveland Clinic, Cleveland, Ohio, United States
Introduction
HIV causes kidney injury through direct viral effects, antiviral therapies, immune reconstitution, and superimposed infections. We report a case of kidney dysfunction in the setting of HIV/AIDS and disseminated mycobacterial avium complex (MAC) infection.
Case Description
A 23-year-old male with history of HIV/AIDS was admitted with acute kidney injury (AKI) and hypercalcemia (hyperCa) after outpatient evalutation for failure to thrive and lymphadenopathy. Creatinine peaked at 2.48mg/dL from a baseline of 1. HyperCa and hyperphosphatemia were noted at 13.5 and 5.2mg/dL respectively. Urinalysis showed 2+ protein with a UPCR of 0.6. Sediment analysis revealed muddy brown casts. Kidney US showed non-obstructing renal calculi without hydronephrosis. Workup showed low PTH levels, 25-OH Vitamin D of 26.8ng/mL (nl: 31-80) and 1,25-Dihydroxyvitamin D of 58.4pg/mL (nl 19.9-79.3). PTHrP was elevated at 4.1pmol/L (nl: 0-2.3).
Per chart review, patient had a diagnosis of disseminated MAC and a recent kidney biopsy that showed acute on chronic interstitial nephritis. At that time, his AKI was attributed to MAC and antibiotics were started. Subsequently, patient had worsening adenopathy concerning for lymphoma, but a follow up biopsy could not be obtained. His symptoms were suggestive of uncontrolled MAC so the antibiotics and HIV therapy were adjusted. His AKI was thought to be related to the hyperCa which in turn was hypothesized to be related to the granulomatous infection due to activated vitamin D. The elevated PTHrP remained of concern. The hyperCa was managed with IV fluids and pamidronate. Patient was discharged on optimized HIV and MAC therapy with improvement of calcium level and kidney function. 9 months after admission, creatinine was down to 1.23 with a calcium of 9.7.
Discussion
HyperCa is a rare but potentially serious complication of disseminated MAC infection, with incidence ranging from 5 to 20%. The mechanism is thought to be due to increased 1-alpha hydroxylase expression in activated macrophages. A similar mechanism explains hyperCa seen with lymphomas. In the setting of HIV in general, and AIDS particularly, hyperCa should trigger an in-depth evaluation for an underlying granulomatous or lymphomatous disorder. Improvement generally follows treatment of the underlying pathology.