Abstract: SA-PO087
Imaging Evidence of Contrast-Induced Nephropathy: A Case Report
Session Information
- AKI: Epidemiology, Risk Factors, Prevention - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Ouyang, Jie, SUNY Downstate Health Sciences University, New York City, New York, United States
- Puri, Isha, SUNY Downstate Health Sciences University, New York City, New York, United States
- Kremer, Arye, SUNY Downstate Health Sciences University, New York City, New York, United States
- Salifu, Moro O., SUNY Downstate Health Sciences University, New York City, New York, United States
- Mallappallil, Mary C., SUNY Downstate Health Sciences University, New York City, New York, United States
Introduction
AKI after IV contrast media (CM) exposure has been reported since 1950. CKD and DM are two major risk factors associated with contrast-induced nephropathy (CIN). One of the mechanisms is that the hyperosmotic property of CM increases tubular fluid viscosity which leads to renal CM retention and eventually tubular and medullary injuries. We report a case of CIN with a CT scan visualizing the prolonged CM renal retention.
Case Description
An 85-year-old man with HTN, DM II, CAD, and BPH was admitted for syncope with poor oral intake while taking furosemide. His initial serum BUN and serum creatinine (sCr) were 32mg/dL and 1.6mg/dL (baseline 1.3mg/dL). He received IV fluids (IVF) and furosemide was continued. sCr was 2.3mg/dL on day 2 when furosemide was stopped. sCr improved to 1.9mg/dL and he had CTA of chest to rule out pulmonary embolism with Omnipaque 95 ml. His sCr rose to 3.5md/dL within 48 hours. After addition of Valsartan he became oliguric. Renal service recommended IVF, post void bladder scan and discontinuation of Valsartan, with differential diagnoses including CIN, pre-, and post-renal etiology. Urinary obstruction was ruled out. However his sCr continue to rise 3 days after IV contrast. A non-contrast CT of abdomen to evaluate lymphadenopathy revealed renal parenchyma significantly enhanced by contrast administered 5 days ago. His sCr worsened to 6.7mg/dL on day 10, with improved urine output and normal electrolytes. He had a cardiac arrest and passed away before planned RRT.
Discussion
We hypothesized that this patient developed CIN with risk factors of DM, AKI on CKD, dehydration, use of ARB and urinary retention, with CT scan 5 days after IV contrast still showing contrast in the renal parenchyma. This prolonged exposure to CM proved by imaging may have contributed to his severe renal injury. This case report provides imaging evidence and highlights the risk factors that are strongly associated with CIN.