Abstract: TH-PO0845
Two Cases of Different Crystal Nephropathy Associated with Two Different GLP-1 Receptor Agonists
Session Information
- Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
- 1900 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)
Authors
- Kumaravel, Ashwath, Comorin Kidneycare, Livonia, Michigan, United States
- Arunselvan, Sophia Kumar, Trinity Health, Livonia, Michigan, United States
- Rehman, Ahmer O., Trinity Health, Livonia, Michigan, United States
- Bhat, Zeenat Yousuf, University of Michigan, Ann Arbor, Michigan, United States
Introduction
GLP-1RAs are typically renoprotective; as such, AKI related to GLP-1RA is infrequently reported but usually stems from GI loss. Similarly, a limited number of AIN cases have been reported. Here, we present two unusual cases of AKI Stage 3 with no GI symptoms following GLP-1RA usage, with biopsies showing crystal nephropathy.
Case Description
Two patients, summarized in Table 1, presented with AKI Stage 3 six months post initiation of GLP-1 analogs.
Discussion
Roughly 6 months after initiating GLP-1RAs, both patients presented with AKI. One had an incomplete recovery and the other recovered completely. Both patients had different crystals (Fig 1a, b) and used different GLP-1RAs; however, the common factor included chronic diuretic use and other nephrotoxic medications. Due to their different crystal types, we suspect their AKI was related to intratubular volume loss, precipitating crystals. Patient 2’s biopsy also showed AIN with Focal Granulomatous features, potentially crystal-induced or medication induced.
Clinical Findings of The Two Patients with AKI
| Patient 1 (72 year old Male) | Patient 2 (51 year old Female) | |
| Creatinine (mg/dL) | Presenting: 10.4 Baseline: 0.87 | Presenting: 5.4 Baseline: 0.5 |
| Prior Medical History and Medications | T2DM, Obesity (BMI 31.6 kg/m3), Chronic venous insufficiency, HTN Denied: Any alcohol ingestion Vitamin C tablets Any history of IBD Pancreatic insufficiency Bowel resection High oxalate consumption | HTN Multiple Sclerosis GERD Enlarged left kidney (16 cm) due to partial duplication of the left-sided collecting system Denied: A history of Gout (Uric Acid: 9.3 mg/dL on admission) |
| Lisinopril (10 mg daily) Furosemide (20 mg daily) | Spironolactone/HCTZ (25/25 mg daily) Ibuprofen (800 mg daily) Omeprazole (20 mg daily) No antibiotic usage | |
| GLP-1 Analog (Weekly Injections) | Tirzepatide, 2.5 mg, with dose increased to 5 mg 3 months prior to admission | Semaglutide (obtained through a telehealth company), unknown dosage with increments at an unknown point in time |
| Biopsy Results | Acute Tubular Injury with Increased Calcium Oxalate Crystal Deposition. | Focal Yellow Pigmented Intratubular Crystals AIN with Focal Granulomatous Features |
| Treatment | 2 months of dialysis | Prednisone course and IV hydration |
| Outcomes | Incomplete recovery Currently CKD Stage 4 | Complete recovery in 1 month |
Calcium Oxalate Crystal Deposition in Patient 1 Viewed in Polarized Light
Patient 2’s Frozen Tissue Yellow Pigmented Material Polarized