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Abstract: SA-PO222

Nirmatrelvir Plus Ritonavir-Induced Acute Interstitial Nephritis

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Nunez, Belen A., Department of Medicine, Division of Nephrology, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Jaffer Sathick, Insara, Department of Medicine, Division of Nephrology, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Seshan, Surya V., Department of Pathology and Laboratory Medicine, Weill Cornell University Medical Center, New York, New York, United States

Drug induced acute interstitial nephritis is an idiosyncratic delayed type IV hypersensitivity reaction that manifests 7-10 days after exposure to the culprit drug. We present a case of biopsy-proven drug-induced acute interstitial nephritis in a patient who received oral antiviral therapy for the treatment of COVID-19

Case Description

73y woman with CKD stage II and resected HER 2+ Stage IIA Lung Adenocarcinoma actively treated with fam-trastuzumab and deruxtecan since December 2021, referred to our nephrology clinic for AKI noted on routine testing. One-year prior referral, baseline renal function was at 1.0-1.2 mg/dl. During initial encounter, patient reported traveling outside the US where she contracted COVID-19 and was given Paxlovid for treatment. Initial referral labs revealed WBC 8500cells/mm3 and 1.9% eosinophils, SCr 1.8mg/dl, BUN 38mg/dl and renal ultrasound with normal echogenicity of both kidneys. Follow up labs after initial encounter showed SCr of 2.3mg/dl, BUN 36 and UA with moderate leukocyte esterase, negative nitrite, 4-6 RBC per hpf, >50 WBC cells/hpf and negative urine culture. Treatment with prednisone 60mg daily was started with plan to taper based on initial response. Over the next 3 months her SCr returned to 1.4 mg/dl while receiving tapering doses of prednisone


Nirmatrelvir plus Ritonavir (Paxlovid™) was developed for the treatment and post exposure prophylaxis of COVID-19. While the exact mechanism for its association with acute interstitial nephritis is unknown, there is a distinctly dysregulating immunological response primarily a T cell–driven process. The withdrawal of the causative drug is fundamental as an initial step in management however in some cases corticosteroid therapy is initiated due to moderate to severe renal injury based on their potent anti-inflammatory effects and prevention of irreversible structural changes resulting in renal fibrosis

Fig1.Renal cortical tissue shows fairly diffuse active and chronic tubulo-interstitial inflammation. HEx200