Acute Kidney Injury from Mononuclear Cell-Predominated Interstitial Nephritis After Introduction of a Glucagon-Like Peptide-1 Receptor Agonist: A Case Report #MMPMID41353763
Itsathitpaisarn R; Suksawad N; Wongwikrom W; Surintrspanont J; Thongsricome T
Am J Case Rep 2025[Dec]; 26 (?): e949913 PMID41353763show ga
BACKGROUND Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have become important in the treatment of diabetic kidney disease (DKD). Despite their reno-protective effect, kidney injury from GLP-1 RAs has been rarely reported. The reported kidney injuries varied from mild symptoms to dialysis at presentation and occurred 2 days to 2 years after drug initiation. We report a case of a patient with DKD who developed an episode of interstitial nephritis after dulaglutide administration. CASE REPORT A 63-year-old woman with stage 3b diabetic kidney disease and depressive disorder was prescribed dulaglutide 0.75 mg/week subcutaneously in August 2023 due to persistent albuminuria despite receiving the maximum tolerated dose of azilsartan. Sodium-glucose cotransporter-2 inhibitor was not prescribed in this case due to her frequent urinary tract infections. Serum creatinine at 2-month follow-up increased and then doubled despite reduction in the azilsartan dose. Potentially nephrotoxic medications were discontinued and no other possible causes of kidney injury, including volume depletion, were presented. Kidney biopsy revealed active interstitial nephritis and diabetic nephropathy without accumulation of immune complex. After discontinuing dulaglutide, there was an almost complete recovery of kidney function without steroid therapy. Azilsartan and chlorthalidone could then be successfully rechallenged. CONCLUSIONS Despite the established renoprotective effect of GLP-1 RAs, acute-to-chronic tubulointerstitial nephritis occasionally occurs, requiring vigilant monitoring after drug initiation or titration. Nevertheless, this does not prevent the prescription of GLP-1 RAs to alleviate DKD progression in certain patients. Treatment includes drug discontinuation and steroid therapy in non-responders.
Am+J+Case+Rep 2025 ; 26 (?): e949913
