CAN THIS NOT BE CONTRAST-INDUCED NEPHROPATHY SEVERAL TIMES OVER? - CASE REPORT.

We had observed in a 2018 publication in the Journal of Nephropathology, some publications from major academic centers in the United States that had suggested that the incidence of contrast nephropathy was exaggerated and overstated. These investigators had concluded that intravenous contrast material administration was not associated with an increased risk of acute kidney injury (AKI), emergent dialysis, and short-term mortality in a cohort of patients with diminished renal function.

A 2017 very well-publicized Johns Hopkins University single-center retrospective cohort report on a large, urban, academic emergency department with an average census of 62,179 visits per year; 17,934 ED visits for patients who underwent contrast-enhanced, unenhanced, or no CT during a 5-year period (2009 to 2014) concluded that in the largest well-controlled study of acute kidney injury following contrast administration in the ED to date, intravenous contrast was not associated with an increased frequency of acute kidney injury. Another earlier 2014 single-center retrospective study of 21 346 patients (10 673 in the contrast group, 10 673 in the non-contrast group) from Medical University of South Carolina also had concluded that intravenous contrast material administration was not associated with excess risk of AKI acute kidney injury, dialysis, or death, even among patients with comorbidities reported to predispose them to nephrotoxicity. A Mayo Clinic Rochester 2015 propensity matched report on 6.902 patients similarly had concluded that intravenous contrast material administration was not associated with an increased risk of AKI, emergent dialysis, and short-term mortality in a cohort of patients with diminished renal function. 

Conversely, yet another most recent 2025 retrospective analysis from Mayo Clinic, Rochester, identified 9199 patients who underwent PCI from January 1, 2009, through June 30, 2023. A total of 856 patients (9.3%) developed AKI (increase in serum creatinine level by ≥0.3 mg/dL or ≥1.5 times baseline), with 87 (0.9%) requiring hemodialysis. In multivariable analysis, AKI was associated with among other factors, older age (odds ratio [OR], 1.01; 95% CI, 1.00 to 1.02) and contrast volume (OR, 1.28; 95% CI, 1.17 to 1.41). After adjustment, AKI remained strongly associated with in-hospital mortality (hazard ratio, 5.75; 95% CI, 4.06 to 8.13). Among hospital survivors, 1-, 5-, and 10-year all-cause mortality, repeated revascularization, myocardial infarction, and major adverse cardiovascular event rates were significantly higher in those who developed AKI.

We report a patient who had multiple intravenous contrast exposures in a span on 1 week and had developed clear-cut, albeit reversible, acute kidney injury. Ane we were forced to ask the possibly dumb question: Can this not be contrast-induced nephropathy?

Case Report.

A 34-year-old male with history of untreated hypertension and alcohol use disorder complicated by necrotizing pancreatitis (January 2025) presented to the Emergency Department about mid-2025 with abdominal pain and vomiting. He was found to be tachycardic, hypertensive, and diaphoretic. His initial creatinine was 0.93 mg/dL. Computed tomography (CT) scan with contrast revealed extensive retroperitoneal blood with pseudoaneurysm formation and necrotizing pancreatitis. Subsequent CT angiogram with contrast demonstrated acute retroperitoneal hemorrhage. Emergent embolization of the gastroduodenal artery was performed by Interventional Radiology, and he was admitted to the Medicine Service for pain control and hemoglobin monitoring. His hospital course was complicated by duodenal obstruction requiring placement of a nasogastric tube. Nephrology was consulted on hospital day eleven given concern for acute kidney injury (AKI) and a creatinine of 4.22 mg/dL. By the time nephrology was consulted, the patient had received intravenous iodinated contrast on five occasions over the course of one week. These studies included contrast-enhanced abdominopelvic CT exam on hospital day 1, followed about 2 hours later by an abdominopelvic CT angiogram. Interventional Radiology embolization with celiac and superior mesenteric angiography and embolization of the gastroduodenal artery and the bleeding superior pancreaticoduodenal branch of the gastroduodenal artery, using coils and Gelfoam to stasis, was completed on hospital day 2 (80 cc of Omnipaque 300 contrast). These were followed subsequently by another abdominopelvic CT angiogram on hospital day 3 and yet another abdominopelvic contrast-enhanced CT scan on hospital day 7. Renal ultrasound imaging did not show any obstructive etiologies, and it was felt that the cause of the acute kidney injury was multifactorial, including contrast-induced nephropathy from multiple repeated contrast-enhanced studies – as many as 5 iodinated intravenous contrast exposures over 7 days, hypovolemia from reduced oral intake and simultaneous ongoing nausea and vomiting, and possible underlying cirrhosis, as well as GI bleeding. The patient also received several Fleet enemas further confounding the acute kidney injury course with the possibility of acute phosphate nephropathy (FIGURE). Ultimately, acute kidney injury resolved with IV fluids and total parenteral nutrition (TPN) (FIGURE).

In an accompanying Editorial to the 2025 Mayo Clinic Proceedings report on contrast-induced nephropathy following PCI, it was emphatically stated that acute kidney injury after PCI remains a major clinical challenge with profound implications for patient outcomes. Physicians must beware of contrast-induced nephropathy and ways to mitigate this risk.