Atypical Presentation of Contrast-Induced AKI (CI-AKI) Following CT Imaging in a Patient with Unknown Baseline Kidney Function

Introduction: Contrast-Induced Acute Kidney Injury (CI-AKI) is the third most common cause of hospital-acquired AKI, following renal hypoperfusion and nephrotoxic exposures. Diagnosing true CI-AKI can be challenging, as alternate etiologies must be ruled out, and a biopsy is typically only obtained if there is a protracted course or atypical presentation. We present an unusual case of rapidly progressive non-oliguric AKI, associated with hematuria, sub-nephrotic range proteinuria, and elevated creatine kinase (CK), ultimately diagnosed as CI-AKI on renal biopsy. Case Description: We evaluated a 68-year-old male who presented with seizures. His vital signs were stable, and initial lab results showed leukocytosis with a left shift and elevated lactate. The patient's admission serum creatinine (sCr) was 1.98 mg/dL, with an estimated glomerular filtration rate (eGFR) of 36 mL/min/1.73m2, prior to contrast media (CM) exposure. His baseline renal function was unknown prior to the current acute illness. He was treated empirically for sepsis and received aggressive IV fluids due to an elevated CK, which peaked at 35,920 U/L. A CT scan was performed for stroke and sepsis workup, using 100 mL iodixanol and 145 mL iohexol. A 32% rise in sCr was observed 30 minutes later, with a peak sCr of 3.39 mg/dL reached 21 hours post-CM exposure, without the need for renal replacement therapy. Additional findings included hematuria, sub-nephrotic range proteinuria (2.3 g/24-hour collection), and an unremarkable serologic workup. Given the atypical presentation, a renal biopsy was performed, revealing features consistent with CI-AKI. The patient's renal function at discharge was a sCr of 1.36 mg/dL, with an eGFR of 57 mL/min/1.73m2. Discussion: The typical presentation of CI-AKI is a rise in sCr of at least 25% within 24-48 hours following CM exposure, after excluding other potential causes. Most cases are non-oliguric and lack active urinary sediment. Our case emphasizes that while the presence of active urinary sediment and high-grade proteinuria is unusual and may warrant consideration of a biopsy, it does not exclude the diagnosis of CI-AKI. Preventive strategies should include IV fluid expansion for high-risk groups and the use of the lowest possible dose of low-osmolar or iso-osmolar CM to achieve adequate diagnostic results.