SAT-534 Trulicity Troubles: When Diabetes Medications Go Kidney-ward

Abstract Disclosure: R. Pendyala: None. C. Basaleli: None. Y. Jamal: None. Background: Glucagon-like peptide-1 (GLP-1) receptor agonists, like Trulicity (dulaglutide) are popular for managing type 2 diabetes mellitus (T2DM) due to their glucose control and cardiovascular benefits. However, emerging reports link these medications to acute kidney injury (AKI), including acute interstitial nephritis (AIN). To date, only two AIN cases associated with dulaglutide have been documented, one without biopsy confirmation. We present a third case of biopsy-confirmed AIN in a 65-year-old female with no prior renal disease, developing within a month of starting Trulicity, underscoring the need for awareness of this potential complication. Case Description: A 65-year-old female with T2DM and hypertension presented with decreased oral intake, chills, and weakness. One month after starting Trulicity, she experienced decreased appetite, persistent nausea/vomiting, and low blood glucose readings. Laboratory results showed severe renal impairments (creatinine 11.3 mg/dL (normal {nl} <1.25 mg/dL), Blood urea nitrogen 81 mg/dL (nl 7-18), sodium 129 mEq/L (nl 135-145), HCO3 17 mEq/L (nl 22-28) lipase 657 U/L (nl 0-160), with normal kidney ultrasound, glycated hemoglobin/A1c 6.6%, and hematuria on urinalysis. Emergent hemodialysis was initiated, and a renal biopsy confirmed AIN with calcium oxalate crystals. Patient denied use of non-steroidal anti-inflammatory medications, antibiotics, proton pump inhibitors, diuretics, and had no recent illnesses, contrast imaging, or blood transfusions. Autoimmune workup was negative. With no other cause to clarify the etiology of the acute kidney injury (AKI), Trulicity was suspected and promptly discontinued. Prednisone 50 mg daily was initiated, leading to creatinine improvement to 3.5 mg/dL after two dialysis sessions, with ongoing AIN recovery. Discussion: AIN is a rare cause of AKI, often triggered by medications like GLP-1 receptor agonists, including Trulicity. It typically presents with renal dysfunction, eosinophiluria, and interstitial inflammation on renal biopsy. The exact mechanism of Trulicity-induced AIN is unclear but thought to be immune-mediated, triggering a hypersensitivity reaction in susceptible individuals. The primary treatment is discontinuing the offending agent. In this case, Trulicity was stopped, and prednisone 50 mg daily was started. Supportive care and dialysis were also required. The patient’s creatinine improved from 11.3 mg/dL to 3.5 mg/dL, confirming recovery potential with early intervention. Though generally safe, emerging case reports associate GLP-1 receptor agonists with AKI, particularly in patients with dehydration or pre-existing kidney disease. In this case, given the timing of symptoms and lack of other causes, Trulicity-induced AIN was suspected. Clinicians should be cognizant of this rare but serious complication for timely management of AIN. Presentation: Saturday, July 12, 2025