Sodium‐Glucose Cotransporter 2 Inhibitors Use and Adverse Kidney Outcomes in Patients Receiving Contrast Media

ABSTRACT

The kidney benefits of sodium‐glucose cotransporter‐2 inhibitors (SGLT2i) in patients receiving contrast media remain unclear. This Taiwanese cohort study investigated the short‐ and long‐term effects of SGLT2i on adverse kidney outcomes in patients receiving contrast media between January 1, 2016 and December 31, 2018. Patients who had used SGLT2i in the 90 days prior to receiving contrast media were matched with non‐users. Cox proportional hazards regression was used to estimate the hazard ratio (HR) for the composite kidney outcome, which included acute kidney injury (AKI), acute kidney disease (AKD), and a sustained ≥ 30% reduction in estimated glomerular filtration rate (eGFR) confirmed after 3 months. The absolute mean change in eGFR over time was compared using a linear mixed‐effects model. The final analysis included 1032 patients (SGLT2i: 344; control: 688). During follow‐up, the overall composite adverse kidney event rate was 32.8%. Although the SGLT2i group had a lower event rate (29.94%) than the non‐SGLT2i group (34.3%), this difference was not statistically significant (HR, 0.95; 95% CI, 0.75–1.20). Crucially, SGLT2i demonstrated a significant protective effect on long‐term kidney function: the hazard for a ≥ 30% eGFR reduction was significantly lower in SGLT2i users (HR, 0.48; 95% CI, 0.29–0.81). Exploratory analyses showed that this benefit—a slower rate of kidney function deterioration—was consistent across subgroups, including men, patients under 65 years, individuals with baseline eGFR < 60 mL/min/1.73 m², and patients with diabetes. While SGLT2i showed no significant short‐term protection against AKI or AKD, these findings strongly suggest that SGLT2i confers significant long‐term reno‐protective benefits for patients receiving contrast media.

Study Highlights

• What is the current knowledge on the topic?

  • ○
    There is no optimal approach to prevent contrast media‐induced acute or chronic adverse kidney outcomes.
• What question did this study address?

  • ○
    Whether SGLT2i can attenuate contrast‐induced risk of AKI, AKD and long‐term kidney function deterioration in the real world remains unclear.
• What does this study add to our knowledge?

  • ○
    SGLT2i may not prevent contrast‐media induced immediate AKI or AKD. However, SGLT2i is beneficial for preventing long‐term kidney function deterioration, particularly in subgroups including men, patients aged under 65 years, those with baseline eGFR < 60 mL/min/1.73 m², and those with comorbid diabetes.
• How might this change clinical pharmacology or translational science?

  • ○
    Using SGLT2i in patients receiving contrast media may not have short‐term benefits but have long‐term benefits in kidney function.

1. Introduction

Contrast media administration has become increasingly common with advances in radiology, transcatheter diagnostics, and interventions. However, the increasing use of contrast media has increased the risk of post‐contrast acute kidney injury (PC‐AKI), a condition strongly associated with prolonged hospitalization, elevated mortality, and a higher likelihood of progression to chronic kidney disease (CKD) [1, 2].

The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) defined PC‐AKI as increased serum creatinine (sCr) ≥ 0.5 mg/dL (44.2 μmol/L) or ≥ 25% from baseline within 3 days after intravascular injection of iodine contrast media [3]. Subsequently, sCr peaks at 3–5 days and may drop to baseline at 10–14 days [4]. The incidence of PC‐AKI is significantly higher in patients with renal injury, particularly those with DM‐related nephropathy and CKD [5]. Epidemiological studies have revealed that the incidence of PC‐AKI is approximately 13% in patients without diabetes and 29.4% in those with diabetes [6]. Various approaches have been investigated to prevent PC‐AKI, such as fluid hydration, sodium bicarbonate, N‐acetylcysteine, and statins [7, 8, 9]; however, an optimal approach remains unknown.

Sodium‐glucose cotransporter‐2 inhibitors (SGLT2i) are a novel class of antidiabetic agents that inhibit sodium‐glucose transport protein 2 in the proximal tubule of the nephron. Besides blood sugar control, SGLT2i have been reported to provide significant cardiovascular benefits to patients with T2DM [10, 11, 12]. Despite the warning that SGLT2i may cause AKI by the U.S. Food and Drug Administration (U.S. Food and Drug Administration, 2018), recent real‐world studies suggested that patients using SGLT2i were at a lower risk of developing AKI and showed a slower estimated glomerular filtration rate (eGFR) decline than those using other glucose‐lowering agents [13]. However, little is known about the impact of SGLT2i on PC‐AKI and long‐term renal outcomes. This study aimed to evaluate the impacts of SGLT2i therapy on the prevention of AKI and other adverse kidney events following exposure to contrast media.

2. Methods

2.1. Data Source and Population

This cohort study used electronic health record data from the Chang Gung Research Database (CGRD) to identify adults who received contrast media between January 1, 2016 and December 31, 2018. The CGRD comprises data from the network of Chang Gung Memorial Hospitals—medical institutions distributed across different geographical areas of Taiwan: north (Linkou, Keelung), middle (Chiayi, Yunlin), and south (Kaohsiung). The CGRD constitutes 10%–12% of the health services covered by Taiwan's National Health Insurance. The generalizability of the CGRD data has been validated in many disease populations [14, 15], and laboratory results have been used in heart and kidney studies [16, 17, 18, 19]. This study was approved by the Institutional Review Board of Chang Gung Medical Foundation in Taipei, Taiwan (permit number: 202200995B0C501).

2.2. Exposure

Of the 75,906 adult patients (aged 30–90 years) who received a contrast medium (as detailed in Table S1) in either an in‐ or out‐patient setting. The SGLT2i therapy (empagliflozin, dapagliflozin, and canagliflozin) was confirmed to have occurred at least 7 days before the first date of contrast medium administration (the index date), with the treatment starting within the 3 months prior to that index date. The control group was defined as patients who did not receive SGLT2i in the 3 months before and 6 months after the index date. Figure 1 shows the further inclusion and exclusion criteria. The details of the study cohort, exposure, and outcome definitions are provided in Table S1.

FIGURE 1.

Flowchart of the study cohort. Index date: The earliest date of contrast media exposure; eGFR, estimated glomerular filtration rate; SCr, serum creatinine; SGLT2i, sodium‐glucose transport protein 2 inhibitor.

2.3. Outcomes and Follow‐Up

The primary composite outcome, assessed in a time‐to‐event analysis, was the first occurrence of any of the following: AKI, acute kidney disease (AKD), kidney function deterioration, or kidney replacement therapy (KRT) initiation (chronic dialysis, kidney transplantation). Secondary outcomes were also assessed in time‐to‐event analyses for individual components of the composite kidney outcome. Due to the outcome of interest relying on valid serum creatinine (SCr) levels, the analysis excluded patients who lacked SCr measurements at baseline or during follow‐up, as well as those already undergoing KRT (Figure 1).

The Kidney Disease Improving Global Outcomes (KDIGO) stage defined AKI as an increase in SCr by ≥ 0.3 mg/dL within 48 h or an increase to at least 1.5 times the baseline value within 7 days after the index date [20]. AKD was defined as the occurrence of AKI or an eGFR < 60 mL/min/1.73 m² or a decrease in eGFR by ≥ 35% within the period spanning 8 days and 3 months after the index date [21]. Kidney function deterioration was defined as a decline of ≥ 30% eGFR from baseline sustained for at least 3 months after the index date [22].

The eGFR was calculated using the Taiwan version of the abbreviated Modification of Diet in Renal Disease equation (eGFR = 175 × SCr^−1.154 × age^−0.203 × 0.742 [if woman]) [23]. To determine eGFR changes over time (from baseline to the end of follow‐up), multiple readings were averaged within a 3‐month interval, thereby helping to standardize the data across patients. All participants were followed from the index date until the outcome event occurred or censoring (due to in‐hospital death, the last recorded encounter, or the end of the dataset on December 31, 2018), whichever came first.

2.4. Statistical Analysis

Baseline patient characteristics, including demographic characteristics, laboratory results, comorbid conditions, and previous prescription use were identified within 1 year of the index date. Baseline comorbid conditions were identified using at least two claims of ICD‐9/10‐CM codes and a minimum interval of 28 days from the last outpatient visit or at least one claim of hospitalization (Table S1). Previous medication use for ≥ 28 days was identified in the outpatient setting.

To account for baseline differences between patients who did and did not receive SGLT2i, we conducted 1:2 propensity score (PS) matching to reduce selection bias and create comparable groups. An individual PS was estimated for each patient using a multivariate logistic regression model (PROC LOGISTIC) including all baseline demographic and clinical characteristics listed in Table 1.

TABLE 1.

Patient Characteristics before and after propensity score matching.

	Before matching						After matching
	No of patients	SGLT2i (n = 346)		Non‐SGLT2i (n = 688)		SMD	No of patients	SGLT2i (n = 344)		Non‐SGLT2i (n = 688)		SMD
		n	(%)	n	(%)			n	(%)	n	(%)
Age group, year						0.160						0.012
< 65	23,679	195	(56.36)	23,484	(64.18)		583	193	(56.10)	390	(56.69)
65+	13,256	151	(43.64)	13,105	(35.82)		449	151	(43.90)	298	(43.31)
Male sex	20,327	220	(63.58)	20,107	(54.95)	0.176	638	218	(63.37)	420	(61.05)	0.048
Baseline laboratory results
eGFR, ml/min/1.73m2						0.331						0.078
≥ 90	16,753	122	(35.26)	16,631	(45.45)		377	121	(35.17)	256	(37.21)
60–89.9	13,836	142	(41.04)	13,694	(37.43)		422	141	(40.99)	281	(40.84)
45–59.9	3505	56	(16.18)	3449	(9.43)		165	56	(16.28)	109	(15.84)
30–44.9	1769	12	(3.47)	1757	(4.80)		28	12	(3.49)	16	(2.33)
15–29.9	688	14	(4.05)	674	(1.84)		40	14	(4.07)	26	(3.78)
< 15	384	0	(0.00)	384	(1.05)
HbA1C						2.452						0.039
≤ 7.0	8960	81	(23.41)	8879	(24.27)		251	81	(23.55)	170	(24.71)
> 7.0	3049	261	(75.43)	2788	(7.62)		771	259	(75.29)	512	(74.42)
Missing	24,926	4	(1.16)	24,922	(68.11)		10	4	(1.16)	6	(0.87)
Baseline comorbidity
Individual Charlson comorbid condition
Acute myocardial infarction	319	20	(5.78)	299	(0.82)	0.281	52	20	(5.81)	32	(4.65)	0.052
Congestive heart failure	870	34	(9.83)	836	(2.28)	0.320	100	34	(9.88)	66	(9.59)	0.010
Peripheral vascular diseases	418	7	(2.02)	411	(1.12)	0.072	16	7	(2.03)	9	(1.31)	0.057
Cerebral vascular accident	3267	61	(17.63)	3206	(8.76)	0.264	185	61	(17.73)	124	(18.02)	0.008
Dementia	395	5	(1.45)	390	(1.07)	0.034	19	5	(1.45)	14	(2.03)	0.044
Pulmonary disease	2530	32	(9.25)	2498	(6.83)	0.089	92	32	(9.30)	60	(8.72)	0.020
Connective tissue disorder	425	1	(0.29)	424	(1.16)	0.103	4	1	(0.29)	3	(0.44)	0.024
Peptic ulcer	4527	70	(20.23)	4457	(12.18)	0.220	200	70	(20.35)	130	(18.90)	0.037
Liver diseases	4834	72	(20.81)	4762	(13.01)	0.209	201	70	(20.35)	131	(19.04)	0.033
Diabetes	5586	265	(76.59)	5321	(14.54)	1.593	796	264	(76.74)	532	(77.33)	0.014
Diabetes complications	1770	129	(37.28)	1641	(4.48)	0.882	373	128	(37.21)	245	(35.61)	0.033
Renal disease	2514	35	(10.12)	2479	(6.78)	0.120	95	35	(10.17)	60	(8.72)	0.050
Cancer	13,451	92	(26.59)	13,359	(36.51)	0.215	276	92	(26.74)	184	(26.74)	0.000
Metastatic cancer	3165	8	(2.31)	3157	(8.63)	0.280	25	8	(2.33)	17	(2.47)	0.010
Hypertension	10,694	249	(71.97)	10,445	(28.55)	0.964	738	247	(71.80)	491	(71.37)	0.010
Hyperlipidemia	6650	242	(69.94)	6408	(17.51)	1.245	713	240	(69.77)	473	(68.75)	0.022
Prior medication
Antidiabetic agents	4636	341	(98.55)	4295	(11.74)	3.576	1017	339	(98.55)	678	(98.55)	0.000
Lipid‐lowering agents	5648	266	(76.88)	5382	(14.71)	1.597	796	264	(76.74)	532	(77.33)	0.014
Anti‐hypertensive medication	9929	263	(76.01)	9666	(26.42)	1.143	784	261	(75.87)	523	(76.02)	0.003
NSAID	5318	50	(14.45)	5268	(14.40)	0.002	151	50	(14.53)	101	(14.68)	0.004
Anti‐platelet	4488	165	(47.69)	4323	(11.82)	0.853	477	163	(47.38)	314	(45.64)	0.035

Abbreviations: CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; NSAID, nonsteroidal anti‐inflammatory drugs; SMD, standardized mean difference, SMD < 0.1 was considered no significant difference.

A greedy algorithm (OneToManyMTCH macro) [24] was applied hierarchically, beginning with exact 8‐digit matches and proceeding to progressively fewer digits, prioritizing the closest matches. Matching was performed without replacement, such that each non‐SGLT2i patient was matched only once. The balance of baseline covariates was assessed using standardized mean difference (SMD), with values < 0.1 indicating adequate balance [25]. PS distributions were also examined visually to confirm sufficient overlap and the common support assumption (Figure S1). The hazard ratios (HR) with 95% confidence interval (CI) for adverse kidney outcomes associated with SGLT2 inhibitor use were estimated using Cox proportional hazards models (PROC PHREG). Robust variance estimator accounting for the PS–matched pairs was obtained with the COVSANDWICH option.

Stratified analyses were conducted by pre‐specified variables (age, sex, baseline eGFR, diabetes status) to evaluate the potential effect of modification on kidney function deterioration. To assess the robustness of the observed association to unmeasured confounding, the E‐value was calculated based on the HR and 95% CI for the kidney function deterioration outcome [26]. The cumulative incidence of kidney function deterioration was also estimated using the Kaplan–Meier method and compared with the log‐rank test.

A linear mixed‐effects model for repeated measurements was used to assess changes in eGFR from baseline over time between the SGLT2i and non‐SGLT2i groups. The mean difference in the change from baseline eGFR between the groups was obtained in the model, which included terms for the treatment group, follow‐up time (months), and interaction between follow‐up time and treatment group. Statistical significance was set at a two‐sided p‐value < 0.05 for all statistical analyses. SAS version 9.4 (SAS Institute, Cary, NC, USA) was used for the data processing and analysis.

3. Results

3.1. Patient Characteristics

In the PS‐matched cohort, there were 344 patients with SGLT2i and 688 patients in the control group (Table 1). Overall, 61.82% were men, 43.5% were aged ≥ 65 years, 22.58% had eGFR < 60 mL/min/1.73 m², and 75.44% had HbA1C > 7.0. The baseline demographic and clinical characteristics and medication use showed a good balance between the comparison groups (Table 1) (SMD < 0.1) (Figure S1). Most patients who received SGLT2i therapy remained on SGLT2i (72.09%), and a higher proportion of these patients were also on ACEI/ARB (45.64%) during the follow‐up period compared to the 38.08% observed in the control group (Table S2).

3.2. Adverse Kidney Outcome

Over the 2‐year follow‐up period, the overall incidence of composite adverse kidney outcome was 32.8%. This rate was higher in the control group (34.3%) than in the SGLT2i group (29.94%). Regarding the individual component of the composite outcome, the incident rate was highest for AKD (25.87%), followed by kidney function deterioration (10.66%), AKI (2.03%), and KRT (0.68%) (Table 2).

TABLE 2.

Incidence of adverse kidney event in SGLT2i and non‐SGLT2i groups.

Outcome	No of events	SGLT2i (n = 344)		non‐SGLT2i (n = 688)		p	Relative risk
		n	(%)	n	(%)
Composite kidney event	339	103	(29.94)	236	(34.30)	0.1597	0.87
AKD	267	86	(25.00)	181	(26.31)	0.6510	0.95
Kidney function deterioration	110	17	(4.94)	93	(13.52)	0.0001	0.37
AKI	21	8	(2.33)	13	(1.89)	0.6400	1.23
Stage 1	15	7	(2.03)	8	(1.16)	0.5510	1.75
Stage 2	5	1	(0.29)	4	(0.58)		0.5
Stage 3 (KRT not included)	1	0		1	(0.15)		—
KRT	7	1	(0.29)	6	(0.87)	0.2834	0.33

Note: Composite kidney event: AKI, AKD, KRT, or kidney function deterioration. Kidney function deterioration defined as an eGFR reduction ≥ 30% for at least 3 months in the follow‐up period.

Abbreviations: AKD, acute kidney disease; AKI, acute kidney injury; KRT, kidney replacement therapy included kidney transplant and chronic dialysis initiation; SGLT2i, Sodium‐glucose transport protein 2 inhibitors.

For the primary composite outcome, there was no significant difference between the SGLT2i and control groups (HR, 0.95; 95% CI, 0.75–1.20) (Table 3). Similarly, SGLT2i use was not associated with a reduced risk of AKI (HR, 1.23; 95% CI, 0.51–2.96) or AKD (HR, 0.98; 95% CI, 0.75–1.26). In contrast, SGLT2i use was associated with a lower risk of kidney function deterioration compared with no use (HR, 0.48; 95% CI, 0.29–0.81) (Figure S2, p = 0.0049). The corresponding E‐value for the point estimate was 3.59 and 1.77 for the upper limit (0.81) of 95% CI. These results suggest that only an unmeasured confounder associated with both treatment assignment and outcome by a hazard ratio of at least 3.6‐fold each could fully explain away the observed protective association. Even a more moderate confounder with associations of about 1.8‐fold each could shift the confidence interval to include the null.

TABLE 3.

Hazard ratios for adverse kidney outcome: SGLT2i users compared to non‐users.

Outcome	Hazard ratio	(95% CI)	p
Composite kidney event	0.95	(0.75−1.20)	0.6712
AKI	1.23	(0.51−2.96)	0.6427
AKD	0.98	(0.76−1.26)	0.8495
Kidney function deterioration	0.48	(0.29−0.81)	0.0056
KRT	0.43	(0.05−3.59)	0.4362

Note: Composite kidney event: AKI, AKD, KRT, or kidney function deterioration. Kidney function deterioration defined as an eGFR reduction ≥ 30% for at least 3 months during the follow‐up.

Abbreviations: AKD, acute kidney disease; AKI, acute kidney injury; KRT, kidney replacement therapy.

The exploratory stratified analyses consistently demonstrated an association between SGLT2i use and a reduced hazard of kidney function deterioration across patients aged < 65 years (HR, 0.35; 95% CI, 0.16–0.78), men (HR, 0.45; 95% CI, 0.22–0.89), patients with baseline eGFR < 60 mL/min/1.73m² (HR, 0.43; 95% CI, 0.22–0.84), and patients with diabetes (HR, 0.50; 95% CI, 0.29–0.86) (Table S3).

3.3. The Change From Baseline in eGFR

During the first 3 months, the eGFR declined more steeply in the SGLT2i group than in the non‐SGLT2i group. Thereafter, from baseline to 24 months, the median eGFR slope was −2.01 [−14.42, 4.49] and −2.43 [−11.28, 3.74] mL/min/1.73m² per year for the SGLT2i and non‐SGLT2i groups, respectively. This resulted in a between‐group difference of 0.29 (95% CI, 0.16–0.42) mL/min/1.73m² per year (Figure 2A).

FIGURE 2.

Change from baseline in eGFR. (A) Overall patients; (B) with CKD; (C) without CKD. The absolute mean change from baseline in eGFR between SGLT2i (red) and non‐SGLT2i (blue) groups. The mean eGFR at baseline was 81.77 (±29.35) mL/min/1.73m² in the SGLT2i group and 82.64 (±31.47) mL/min/1.73m² in the non‐SGLT2i group. CKD, chronic kidney disease defined by baseline eGFR < 60 mL/min/1.73m².

In patients with baseline eGFR < 60 mL/min/1.73 m², the annual median eGFR slopes were −2.26 [−16.07, 4.49] with SGLT2i and −2.27 [−11.23, 3.68] with non‐SGLT2i. This yielded a between‐group difference of 0.35 (95% CI, 0.19–0.50; p < 0.001) mL/min/1.732 m² per year (Figure 2B).

Among those with baseline eGFR ≥ 60 mL/min/1.73 m², the annual median eGFR change was −1.28 [−12.87, 4.41] for SGLT2i and −2.70 [−11.90, 4.19] for non‐SGLT2i, resulting in a statistically insignificant between‐group difference of 0.2 mL/min/1.73 m² per year (95% CI, −0.04–0.43; p = 0.1019) (Figure 2C) (Table S4).

4. Discussion

SGLT2i showed no immediate effect on AKI or AKD after contrast media administration. However, SGLT2 was associated with better long‐term kidney outcomes (after 3 months). While sensitivity analysis suggests this reno‐protective effect is robust, the E‐value indicates that modest unmeasured confounding could still weaken the effect slightly.

Previous studies have suggested that PC‐AKI mainly occurs through two mechanisms: hypoxic damage to the renal parenchyma, especially the medulla, and the cytotoxic effects of contrast media on renal capillaries and tubules [27]. Hypoxia and subsequent ischemia–reperfusion injury result in the production of ROS and oxidative stress [28]. SGLT2 inhibitors are strong anti‐oxidant and anti‐hypoxic agents that were proposed to be beneficial in PC‐AKI. Recently, Liu et al. demonstrated that dapagliflozin use was associated with a lower risk of PC‐AKI in patients with DM and CKD undergoing elective percutaneous coronary intervention (PCI) [29]. A retrospective, single‐center, case–control study showed that PC‐AKI risk was lower in the SGLT2i‐user group (OR, 0.86; 95% CI, 0.76–0.98; p = 0.028) in ST elevation MI patients undergoing primary PCI [30]. Since most patients in our study had a high average eGFR (82 mL/min/1.73 m²) and included both PCI and non‐PCI groups (with non‐PCI typically involving lower contrast volume), the incidence of post‐contrast AKI or AKD was relatively low. This low event rate may have diluted the SGLT2i protective effect, leading to a statistically insignificant finding.

Contrast media exposure causes AKI may lead to the long‐term deterioration of kidney function. Repeated use of contrast media, often necessary in these patients, compounds the long‐term risk to kidney function [1]. The presence of a higher percentage of underlying comorbidities, such as cardiovascular disease or diabetes, make these patients particularly vulnerable. In our study cohort, the median annual eGFR ranged from −2.01 to −2.43 mL/min/1.73 m², which remained greater than that observed in the general population (approximately −1 mL/min/1.73 m² per year) [31].

Subgroup analysis revealed that men, patients under 65 years of age, those with eGFR < 60 mL/min/1.73 m² (CKD), those with diabetes benefited more from SGLT2i use. Both CKD and DM are established risk factors for contrast‐induced nephropathy [6]. Previous clinical trials have shown that canagliflozin [12], empagliflozin [32], and dapagliflozin [33] improve kidney outcomes and are associated with a slower progression of kidney disease in patients with diabetes. Large‐scale trials, including EMPA‐KIDNEY [34] and DAPA‐CKD [35], have further confirmed that SGLT2i provide reno‐protective effects in CKD patients, regardless of whether they have diabetes. Furthermore, recent data from the SGLT2‐I AMI PROTECT registry, which involves patients with AMI undergoing PCI, demonstrated that SGLT2i use is linked to better long‐term cardiovascular outcomes, including reduced cardiovascular mortality and hospitalization for heart failure [36]. Therefore, despite the lack of significant immediate benefits in preventing PC‐AKI, the long‐term use of SGLT2i remains a rational approach for cardiovascular and renal protection in high‐risk patients.

The findings of the current study must be interpreted considering several limitations. First, this is an observational study in a moderately sized cohort of Taiwanese patients. Although the CGRD integrates data from multiple CGMHs across Taiwan, the generalizability of treatment patterns, healthcare access, and follow‐up protocols beyond Taiwan's national health insurance systems may be limited. Differences in healthcare infrastructure, reimbursement policies, and clinical practice in other countries could affect the applicability of these results to broader populations. Second, unmeasured confounders, such as volume status and major surgeries associated with AKI risk, were not captured in the assessment of AKI outcomes. Third, excluding patients without baseline or follow‐up creatinine values may have introduced selection bias and further limited generalizability.

In conclusion, SGLT2i showed no effect on composite adverse kidney outcomes among patients receiving contrast media exposure, partly due to the equal risk of short‐term kidney events (AKI and AKD). Conversely, the lower risk of kidney function deterioration observed in patients treated with SGLT2i than in those not treated with SGLT2i plays an important role in preventing long‐term kidney complications. These findings may improve the current understanding of SGLT2i effects among patients receiving contrast media in clinical practice. Patients not using SGLT2i during contrast media administration should be considered at high risk of kidney function deterioration, requiring close monitoring and regular follow‐up.

Author Contributions

L.‐C.L. and C.‐N.H. wrote the manuscript. L.‐C.L. and C.‐N.H. designed the research. L.‐C.L., Y.‐L.T., and S.‐J.C. performed the research. H.‐C.K. and C.‐N.H. analyzed the data.

Funding

This work was funded by Kaohsiung Chang‐Gung Memorial Hospital, Kaohsiung, Taiwan (CORPG8M0361 and CRRPG8N0021 to L.‐C. Li).

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Appendix S1: cts70405‐sup‐0001‐supinfo.docx.

Li L.‐C., Tain Y.‐L., Chien S.‐J., Kuo H.‐C., and Hsu C.‐N., “Sodium‐Glucose Cotransporter 2 Inhibitors Use and Adverse Kidney Outcomes in Patients Receiving Contrast Media,” Clinical and Translational Science 18, no. 12 (2025): e70405, 10.1111/cts.70405.