Kidney Week

Abstract: FR-PO0459

Incidental Calcium Oxalate Crystal Depositions in Antibiotic-Induced Acute Tubulointerstitial Nephritis

Session Information

• AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Cuiban, Elena, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

Elena Cuiban, MD

• Dumitrache, Bianca, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

Bianca Dumitrache, MD

• Radulescu, Daniela, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

Daniela Radulescu, MD, PhD

• Turcu, Flavia Liliana, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

Flavia Liliana Turcu, MD, PhD

• Vacaroiu, Ileana Adeala, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

Ileana Adeala Vacaroiu, MD, PhD

Introduction

Calcium oxalate crystal depositions in the kidneys are most commonly associated with primary hyperoxaluria, but may also occur secondary to metabolic, enteric, or drug-related causes. Distinguishing between primary and secondary etiologies is essential because of the major prognostic and therapeutic implications.

Case Description

A 44-year-old woman with recurrent urinary tract infections was admitted in June 2024 with stage 3 AKI (peak creatinine 5.75 mg/dL) following repeated exposure to ceftriaxone. Evaluation at hospital admission revealed non-oliguric AKI, leukocyturia without bacteriuria, and a negative immunologic work-up. Kidney biopsy revealed an acute tubulointerstitial nephritis pattern with mild focal tubular atrophy and interstitial inflammation. Notably, rare birefringent calcium oxalate crystals were identified within the tubules on LM (Fig.1) and confirmed by EM (Fig.2).
Kidney function improved following corticotherapy, with creatinine decreasing to 1.46 mg/dL at discharge. At the 2-month follow-up, kidney function had recovered completely. Given the presence of oxalate crystals, primary hyperoxaluria was considered, although the family and personal history were negative for nephrolithiasis, nephrocalcinosis, or chronic kidney disease. In addition, we excluded risk factors for enteric hyperoxaluria, and the patient denied ingestion of drugs or chemicals metabolized into oxalate, such as ascorbic acid or ethylene glycol. Genetic testing for primary hyperoxaluria was negative.

Discussion

This case highlights incidental calcium oxalate crystal deposition in the setting of drug-induced acute tubulointerstitial nephritis, likely secondary to transient metabolic imbalances during AKI. No previously published data have linked renal oxalosis with acute allergic tubulointerstitial nephritis. Nevertheless, we hypothesize that renal oxalosis could represent an epiphenomenon in drug-induced acute tubulointerstitial nephritis.
On the other hand, repeated antibiotic use in the context of recurrent urinary tract infections could be associated with antibiotic-induced depletion of intestinal Oxalobacter formigenes, thereby contributing to hyperoxaluria.