Acute kidney injury (AKI) secondary to iodinated contrast media (CM) is commonly referred to as contrast-induced nephropathy (CIN). CIN is a phenomenon of increased interest in recent years for a variety of reasons [1] . The term CIN has also become controversial; recently, the Acute Kidney Injury Network (AKIN) has chosen “Acute Kidney Injury (AKI)” as a synonym for CIN in cases where AKI occurs as a result of contrast administration [2] . Contrast-induced nephropathy (CIN) is defined as an increase in the serum creatinine level of ≥0.5 mg/dl or ≥25% from baseline within 48 - 72 hours following the administration of contrast medium [3] . An absolute increase in baseline serum creatinine is considered the most useful and practical definition of CIN. The serum creatinine typically starts to increase within 24 - 48 hours of contrast medium administration, with peak elevation occurring after 3 - 5 days and returning to baseline or near baseline within 7-10 days [4] . Acute kidney injury (AKI) caused by CIN is generally non-oliguric and reversible. The exact mechanism underlying contrast-induced nephropathy (CIN) is still elusive. The leading theories propose that it stems from two primary sources: first, hypoxic injury to the renal tubules due to renal vasoconstriction; and second, direct cytotoxic effects induced by the contrast media itself [5] . Alternatively, some experts suggest that acute kidney injury following intravascular contrast administration might be linked more to pre-existing risk factors and might merely coincide with the use of contrast media, particularly when administered intravenously [6] . A recent meta-analysis found no evidence for increased risk for AKI after contrast-enhanced CT among patients with estimated glomerular filtration rate (eGFR) ≥ 45 mL/min/1.73m² [7] . Based on emerging evidence in the literature, it was suggested that caution should be exercised in patients with hypertension and eGFR ≤ 30 mL/min/1.73m² [7] . The overall incidence of CIN in the general population remains uncertain and ranges from 0.6% to 2.3% in various studies [8] . Contrast-induced nephropathy (CIN) is a known complication following the intravascular administration of iodinated contrast media (CM) in the absence of other nephrotoxic events and is often associated with both short-term and long-term morbidity and mortality [8] [9] . The reassessment of the risk of CIN among individuals referred for contrast-enhanced computed tomography (CECT) is driven by the growing usefulness of CECT in diagnostic imaging. It is a well-established practice to avoid the use of high-osmolar contrast media (HOCM) because it is linked to nephrotoxicity, cardiovascular side effects, and anaphylactoid reactions. However, the choice between using iso-osmolar contrast media (IOCM) or low-osmolar contrast media (LOCM) remains a matter of uncertainty. There are conflicting findings in the literature regarding whether IOCM carries a lower risk of contrast-induced nephropathy (CIN) compared to LOCM [9] [10] . During recent years, contrast-related investigations have been common diagnostic tools. Despite several reported complications, contrast largely increases the diagnostic yield of radiological imaging, especially in the case of malignancy. CIN is not an uncommon cause of acute renal failure. In the majority of cases, CIN remains undiscovered, particularly when the investigation is conducted in the outpatient settings. The majority of CIN episodes are transient and typically resolve within one to three weeks, but in a small number of cases, permanent renal impairment may develop, as seen by an increase in serum creatinine level [11] . It is worth noting that CIN is associated with significant morbidity and mortality after computed tomography (CT) in both inpatient and outpatient settings. There is very little data regarding CIN after contrast-enhanced computed tomography (CECT), particularly in resource-limited countries. Therefore, the present study aimed to evaluate the contrast-induced nephropathy following contrast-enhanced computed tomography at a Tertiary Care Hospital in Bangladesh.

This prospective observational study was carried out at the Department of Nephrology, Bangladesh Medical University (BMU), Dhaka, Bangladesh, from November 2022 to September 2023. A total of one hundred (100) patients who underwent contrast-enhanced computed tomography (CECT) at the Department of Radiology and Imaging, BMU, Dhaka, Bangladesh, were enrolled by a purposive sampling technique following selection criteria. Adult subjects (age >18 years) who underwent computed tomography (CT) were included. Subjects having contrast allergy or having had previous intravenous contrast scanning for any reason within 14 days before enrollment, patients with impaired renal function (serum creatinine ≥ 2 mg/dl) due to any cause, were excluded from the study. The selection criteria were scrutinized by medical history along with drug history, clinical examination, previous medical records, and recent laboratory investigations.

This prospective observational study was intended to assess the contrast-induced nephropathy (CIN) after contrast-enhanced computed tomography (CECT). The incidence of CIN was found to be 10% in this study. The study subjects were divided into 2 groups: “CIN group” and “No-CIN group”.

The mean age of the participants was 49.9 ± 14.4 years. Of them, 60% were male, while 40% were female. The age distribution showed that the majority of them fall in the 60 - 70 years (36%) and 50 - 59 years (27%) age groups. The mean BMI was (20.7 ± 1.71) kg/m² ( Table 1 ).

In this study, 29% of the participants had hypertension (HTN), while 14% had diabetes mellitus (DM), 17% had cirrhosis of the liver, 10% had chronic kidney disease (CKD), and 3% had ischemic heart disease (IHD). Of them, 10% were on different types of nephrotoxic drugs such as NSAIDs. Regarding behavioral risk factors, 16% of the study participants were smokers ( Table 2 ).

*Multiple response.

Among the study population, the majority (59%) had a CT scan of the whole abdomen. 32% of the participants had a chest CT scan, while 7% had a kidney ureter with bladder (KUB) CT scan, and 2% had a hepatobiliary system (HBS) CT scan ( Figure 1 ).

Out of 100 study participants, 10 (10%) participants had developed CIN, while 90 (90%) did not develop CIN. This data helps determine the prevalence of CIN in the study population and can be used to evaluate how contrast media affects kidney function ( Figure 2 ).

Comparison of laboratory parameters between with (CIN) or without contrast-induced nephropathy (No-CIN) among the study subjects indicated that participants with CIN had significantly higher levels of serum urea, serum creatinine, and serum potassium compared to patients without CIN at baseline, after 48 - 72 hours, and on the 7^th day of CECT ( Table 3 ).

p-value obtained by unpaired t-test, s = significant.

Table 4 presents the results of multivariate logistic regression to assess independent predictors of CIN. Baseline serum creatinine was found to be a statistically significant predictor (p = 0.013; OR = 73.86), indicating a strong association with increased risk of CIN. Although nephrotoxic drug use showed a near-significant trend (p = 0.059; OR = 0.064), it did not reach statistical significance. Other variables, including hypertension, diabetes mellitus, liver cirrhosis, and chronic kidney disease (CKD), were not significantly associated with CIN in this model (p > 0.05).

Regarding the association of anatomical region, contrast types, and volume of contrast with contrast-induced nephropathy (CIN) among the study subjects, the type of contrast had a statistically significant association with the development of CIN (p < 0.001) ( Table 5 ).

p-value obtained by Chi-square test for qualitative data, s = significant.

On the 7^th day of CIN follow-up, patients whose renal function returned to baseline had a mean serum creatinine of (1.00 ± 0.15) mg/dl, while those improving showed serum creatinine levels of (1.30 ± 0.11) mg/dl. Patients with static renal function had serum creatinine levels of (1.40 ± 0.15) mg/dl, and those deteriorating reached mean serum creatinine levels of (2.10 ± 0.2) mg/dl ( Table 6 ).

In hospitalized patients, contrast-induced nephropathy (CIN) is the third most common preventable cause of acute kidney injury (AKI) [14] . The evaluation of contrast-induced nephropathy (CIN) following computed tomography (CT) is essential for understanding the risk factors associated with this condition and for implementing preventive measures. The purpose of the present study was to assess the CIN following contrast-enhanced computed tomography (CECN). A total of 100 patients who underwent contrast-enhanced computed tomography (CECT) were selected.

In this study, hypertension (HTN), diabetes mellitus (DM), cirrhosis of the liver, chronic kidney disease (CKD), and ischemic heart disease (IHD) were the comorbidities, while nephrotoxic drugs and smoking were risk factors among the study participants. In multivariate regression analysis, baseline serum creatinine was found to be a significant predictor for CIN (p = 0.013; OR = 73.86). Although other variables, including hypertension, diabetes mellitus, liver cirrhosis, chronic kidney disease (CKD), and nephrotoxic drugs, were not significantly associated with CIN (p > 0.05). It was documented that the existence of cardiovascular disease (i.e., myocardial infarction, angina pectoris, and chronic heart failure) and pre-existing renal dysfunction were associated factors for CIN [15] [16] . Khodabandeh et al., in a systematic review, observed that acute kidney injury (AKI) is not caused by intravenous contrast media at a standard dose for CT scans unless a specific risk factor is present [17] .

In this study, the most commonly performed imaging studies were CT abdomen (58%), followed by CT chest (32%) and others (10%). These findings were consistent with one previous study where a similar anatomical distribution of contrast-enhanced CT was performed [12] . The incidence of contrast-induced nephropathy (CIN) was 10% in this current study. This information provides an understanding of the occurrence of CIN within the study population and can be used to assess the impact of contrast administration on kidney function. In accordance with this current study, Ong et al. reported that the incidence of CIN ranged from 5.69% to 36.9% [18] . The reported incidence of CIN percentage varies across the studies, with some studies reporting a high incidence of CIN [19] [20] and others reporting a low incidence [21] [22] . These findings suggest that the incidence of CIN may vary depending on the study population, the type and amount of contrast agent used, and other factors.

It was observed that participants who developed CIN had significantly higher levels of serum urea, creatinine, and potassium at baseline than those who did not (No-CIN). Although the underlying mechanism is not yet fully understood, iodinated contrast media frequently increase the strain on already impaired kidneys, lower renal blood flow and glomerular filtration rate (GFR), and permit the accumulation of contrast molecules within the kidney, exacerbating kidney injury [23] . Additional hypothesized mechanisms for CIN include activation of endothelin and other vasoconstrictor mediators, increased production of reactive oxygen species that cause lipid peroxidation and tubular damage, impairment of tubular endothelium mitochondrial function, and stimulation of cytokines and local inflammatory responses [24] .

The present study revealed that the age distribution of the study population is important, with a significant portion falling into the 50 - 59 and 60 - 70 age groups, which were 27% and 36% respectively. The mean age of the participants was approximately 50 years, with a higher proportion of males (60%). This information is important because age was found to be associated with the development of CIN. Participants in the 60 - 70 age group had a higher incidence of CIN (70%), suggesting that older individuals may be more vulnerable to contrast-induced kidney injury. Clinicians should exercise caution when administering contrast media to older participants and closely monitor their renal function. This finding was in agreement with a related study that reported the mean age of the CIN group was 54 (±14) years compared to the non-CIN group 46 (±15) years [12] . Our study population shares similarities with a study conducted by Bhatt et al. (2016) in which they also found a higher percentage of males (58.8% males compared to 41.2% females) [2] . Similar patterns of a higher male presence have been observed in other studies, although there are some studies that have reported a higher percentage of females also [12] . In a couple of previous studies, demographic factors were not identified as influential factors affecting the occurrence of CIN [2] [25] .

Among the study population, the type of contrast had a significant association with the development of CIN (p < 0.001). Specifically, participants who received iodixanol as the type of contrast had a higher incidence of CIN (60%) compared to patients who received iobitridol (40%). The anatomical region of the computed tomography scan and volume of contrast did not show any statistically significant association with the development of CIN (p > 0.05). These findings suggest that the type of contrast could be a potential risk factor for the development of CIN following CECT, and precautions should be taken while selecting a contrast media for participants. In our study, 91 participants received Iobitridol (LOCM) as contrast media, and the remaining 9 participants received iodixanol (IOCM). The result showed that in participants who received Iodixanol (IOCM), CIN developed in 6 out of 9 participants. On the other hand, participants with normal baseline renal function who received Iobitridol (LOCM) developed CIN in 4 out of 91 participants. Cheruvu et al. reported that participants who received Iodixanol (IOCM) had significantly experienced CIN (p = 0.015) [26] . Another recent study showed that the CIN rate for iohexol (LOCM) was 2% compared to 9% for iodixanol (IOCM) [27] . It was documented that participants who received iodixanol (IOCM) were almost 5 times more likely to experience CIN [27] [28] .

In this study, at the 7^th day out of 10 patients of CIN; 3 patients’ renal function (Serum creatinine) returned to baseline, 3 patients’ renal function (Serum creatinine) were improving, 2 patients’ renal function (Serum creatinine) remained static, and 2 patients’ renal function (Serum creatinine) were deteriorating. Typically, CIN is a self-resolving process, with renal function returning to normal within 7 - 14 days after administration of contrast. Less than one-third of patients with CIN experience residual renal impairment to some degree, while less than 1% of patients with CIN require renal replacement therapy, with a slightly higher rate in those with chronic renal impairment (3.1%) [29] .

This study demonstrated that the incidence of contrast-induced nephropathy (CIN) in subjects who underwent CECT is 10%. Advanced age and the type of contrast have a significant association with the development of CIN. Baseline serum creatinine is a significant predictor of CIN. Therefore, participants’ age, renal status, and the type of contrast should be taken into consideration when performing CECT.

The current study had certain limitations. It was a single-center study that included a small number of participants. Moreover, follow-up periods were relatively short.

A long-term multicenter study with close follow-up is warranted to validate the findings of this study. Preventive measures should be taken before, during, and after the CECT procedure. Follow-up should be continued at least 4 weeks following CECT.