Diabetes Mellitus and the Increased Risk of Acute Kidney Injury Following Acute Coronary Syndrome
1
Cardiorenal Team, Diabetes, Metabolism, & Inflammation, Joseph Bank Laboratories, University of Lincoln, Lincoln LN6 7DQ, UK
2
Lincoln Heart Centre, Lincoln County Hospital, United Lincolnshire Hospitals NHS Trust, Greetwell Road, Lincoln LN2 5QY, UK
3
Cardiology Department, Hull University Teaching Hospitals, Hull HU16 5JQ, UK
*
Author to whom correspondence should be addressed.
Diabetology 2025, 6(12), 148; https://doi.org/10.3390/diabetology6120148
Submission received: 15 September 2025
/
Revised: 18 October 2025
/
Accepted: 20 November 2025
/
Published: 1 December 2025
Abstract
Background/objectives: Diabetes mellitus (DM) increases susceptibility to both cardiovascular and renal complications. Acute kidney injury (AKI) in the setting of acute coronary syndrome (ACS) is a frequent manifestation of acute cardiorenal syndrome (type 1); however, the impact of diabetes on the condition remains incompletely characterised. This study aimed to evaluate the real-world incidence, severity, and recurrence of AKI in individuals with ACS, focusing on the additional risk conferred by DM, and to assess the adequacy of post-discharge renal monitoring. Methods: We conducted a single-centre, retrospective observational study of 990 ACS admissions between July 2020 and June 2021 at the United Lincolnshire Hospitals NHS Trust. Acute kidney injury was defined using Kidney Disease Improving Global Outcomes criteria and stratified by severity. Outcome measures included incidence of AKI during admission, recurrence of AKI, and renal function monitoring within 12 months post-discharge. Results: Of 990 individuals recruited, 315 (31.8%) had DM. Overall, 14.2% individuals developed AKI during admission, being more frequently observed in those with DM (20.0% vs. 11.6%; RR 1.7, p < 0.001). Severe AKI (stage 3) was higher in those with diabetes (2.9% vs. 0.7%, p = 0.017). Recurrent AKI within 12 months occurred in 9.7%, with a higher incidence in those with DM (15.8% vs. 6.9%, p < 0.001). Post-discharge renal follow-up was performed in 88.7% of persons with AKI and similar in those with and without DM. Conclusions: Acute kidney injury is a common and serious complication of ACS, with DM substantially increasing the risk and severity of the condition during acute events and post-discharge. Despite this, individuals with DM receive similar monitoring in the post-discharge period. Improved systems for post-discharge renal monitoring and early initiation of protective therapies are required to mitigate long-term risk.
1. Introduction
Diabetes mellitus (DM) remains a global healthcare concern, affecting more than 463 million people worldwide [1]. It is a well-established risk factor for both chronic kidney disease (CKD) and acute kidney injury (AKI) [2]. A significant proportion of individuals with DM may already have underlying kidney disease as a consequence of microvascular and macrovascular dysfunction, with their risk of developing AKI up to five times higher than in those without the condition [2].
Acute cardiorenal syndrome (CRS: type 1) is defined as the development of AKI secondary to an acute cardiovascular condition [3,4]. Among such cardiovascular insults, acute coronary syndrome (ACS) represents a key precipitant, with 12.7-to-29.9% of individuals developing AKI in this context [3,4,5,6,7]. However, real-world incidence may vary depending on population characteristics, risk factors, and local practice patterns. Key risk factors include CKD, high volumes of intravenous contrast, haemodynamic instability, left ventricular systolic dysfunction (LVSD), reduced renal perfusion, bleeding, coronary interventions, and the use of nephrotoxic medications [5,7,8]. The condition may be worsened by the inflammatory cascade initiated in response to myocardial ischaemia and injury [7]. Therefore, AKI in the context of ACS represents a relatively frequent and complex dynamic in high-risk individuals.
The development of AKI in the context of ACS carries significant implications with individuals experiencing higher in-hospital and greater long-term morbidity and mortality [1,3,4,6,7,9], with the risk of death being 3.5-to-17 times higher than in those without AKI [3,4,6]. They are also more likely to have extended hospital and intensive care unit stays, with the duration correlating directly with the severity of AKI [3]. Long-term renal consequences are also well documented [2]. Even milder episodes may accelerate a decline in renal function, accelerating the progression to end-stage renal disease (ESRD), particularly when the injury is prolonged or severe [7].
Given that DM independently increases the likelihood of AKI, and that ACS already represents a high-risk setting for CRS, the combination of these factors places individuals with DM and ACS at particular high risk for adverse renal and cardiovascular outcomes. This study was therefore undertaken to provide a more comprehensive evaluation of the burden of AKI in individuals with ACS, with a particular emphasis on the additional risk conferred by DM across all types. In contrast to previous studies that have largely focused on in-hospital incidence and severity, this work also examines recurrence of AKI and the adequacy of post-discharge renal follow-up in a real-world setting, thereby offering new insights into long-term renal risk in this vulnerable population.
2. Methods
2.1. Study Design and Setting
A single-centre, retrospective, observational study was conducted at the Heart Centre, United Lincolnshire Hospitals NHS Trust (ULHT). Individuals presenting with ACS between July 2020 and June 2021 were identified from the local Myocardial Infarction National Audit Project (MINAP) registry and considered for inclusion.
2.2. Population and Data Collection
All individuals with a confirmed diagnosis of ACS were included in the primary analysis. Individuals with alternative diagnoses at the index admission, such as myocarditis, were excluded. Individuals with and without DM were identified and included irrespective of type of diabetes. Baseline data were collected from review of clinical notes, while blood test results were accessed via the local WebV IT system, which is integrated across the trust, care boards, and GP practices. Post-discharge blood tests were also reviewed through this system for up to 12 months to determine whether repeat renal function tests had been conducted and to identify any recurrent AKI episodes. For secondary objectives concerning post-discharge events and monitoring, individuals were included if they had at least 12 months of follow-up or had appropriate renal testing prior to death. Those who died during the index admission or before follow-up renal testing or were lost to follow-up within the 12-month period were censored from the analysis. The project was registered locally as a clinical audit and service improvement project (registration number L-0994).
2.3. Definitions
ACS included myocardial infarction (MI) and unstable angina. MI was defined according to the 4th Universal Definition, requiring typical clinical, electrocardiographic, or imaging evidence of ischaemia, along with a rise or fall in cardiac troponin levels, with at least one value above the 99th percentile of the upper reference limit [10]. Unstable angina was defined by the presence of typical symptoms without a significant troponin rise. AKI was defined biochemically as a rapid increase in creatinine to more than 1.5 times the baseline with a corresponding drop in estimated glomerular filtration rate (eGFR), known or presumed to have occurred within the previous 7 days, or an increase of 26 micromol/L or more within 48 h, as per Kidney Disease: Improving Global Outcomes (KDIGO) criteria [11,12]. Further categorisation was based on severity: AKI1 represented a 1.5-to-2 times increase in creatinine from baseline, AKI2 represented a 2-to-3 times increase, and AKI3 represented a ≥3 times increase [13]. As this was a retrospective, non-intensive care study, urine output criteria were not used; only biochemical criteria were applied. DM was defined according to World Health Organization criteria, requiring typical symptoms such as polyuria, polydipsia, and weight loss, along with an elevated biochemical result (glycated haemoglobin (HbA1c) ≥ 48 mmol/mol or fasting plasma glucose ≥ 7.0 mmol/L), or two elevated values in the absence of symptoms [14]. Satisfactory renal function follow-up was defined as at least one outpatient serum creatinine/eGFR function test within 12 months of discharge. Left ventricular systolic function was assessed using Simpson’s Biplane method or, where this was not feasible, by estimation and recorded as ‘preserved’ (ejection fraction greater than or equal to 45%), ‘moderately impaired’ (36–44%) or ‘severely impaired’ (less than 36%).
2.4. Outcomes
The primary outcome of this study was to evaluate the incidence and severity of AKI during admission for ACS in individuals with DM compared with those without it. Secondary outcomes included recurrence of AKI within 12 months post-discharge and adequacy of post-discharge renal monitoring within the same period.
2.5. Statistical Analysis
Categorical data were presented as numbers with percentages, and continuous data were recorded as medians with interquartile ranges. Overall results were followed by descriptive and unadjusted intergroup comparisons based on the presence or absence of AKI and DM. Statistical significance was assessed using Pearson’s Chi-square, Wilcoxon rank-sum, and Fisher’s exact test where applicable, with p < 0.05 considered significant. Data were recorded in Excel and analysed using R 4.4.1.
3. Results
3.1. Patient Characteristics
Of the 1012 individuals listed in the registry, 22 were excluded due to missing data or having a diagnosis other than ACS, leaving 990 who met the inclusion criteria. Overall, 315 individuals (31.8%) had DM. People with AKI were older (median 74.0 vs. 67.0 years, p < 0.001), more likely to have DM (44.7% vs. 29.7%, p < 0.001), and had higher rates of severe LVSD (42.0% vs. 11.5%, p < 0.001). Additional characteristics including peak troponin, serum creatinine, presence of pulmonary oedema and cardiogenic shock, and discharge therapies are summarized in Table 1.
3.2. AKI Incidence and Severity
During admission, 14.2% (141/990) of individuals developed AKI. The majority had stage 1 AKI (12.2% [121/990]), while stage 2 and stage 3 AKI were less common (0.6% [6/990] and 1.4% [14/990], respectively). Individuals with DM were more likely to develop AKI during admission (20.0% [63/315] vs. 11.6% [78/675], relative risk [RR] 1.7, p < 0.001), particularly the most severe form, stage 3 (2.9% [9/315] vs. 0.7% [5/675], RR 4.1, p = 0.017, Table 2).
3.3. Clinical Outcomes
Individuals who developed AKI had significantly longer hospital stays (median 7.5 days, interquartile range [IQR] 3.2–14.3) compared to those who did not (median 3.0 days, IQR 1.5–5.8; p < 0.001). The presence of DM was also associated with prolonged admissions (4.5 days, IQR 1.9-to-8.6 vs. 2.9 days, IQR 1.5-to-5.7; RR 1.6, p < 0.001). In-hospital mortality was significantly higher among those with AKI (22.0% [31/141]) compared to those without (2.8% [24/849]; p < 0.001), which increased with the severity of AKI: 16.5% (20/121) for stage 1, 50.0% (3/6) for stage 2, and 57.1% (8/14) for stage 3. Despite individuals with DM being almost twice as likely to have developed severe LVSD during admission, they were less likely to have received key therapies, including beta-blockers (64.7% vs. 83.1%, p < 0.001), angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) (55.3% vs. 83.1%, p < 0.001), at the time of discharge, or undergo coronary revascularisation (76.3% vs. 84.9%, p = 0.018; Table 1).
3.4. Post Discharge Mortality and Recurrence of AKI
Of the 935 individuals successfully discharged, 4 were excluded due to missing data. Among the remaining 931 individuals, 8.1% (75/931) died from any cause within 12 months. Mortality was significantly higher in those who had developed AKI during admission (19.3% vs. 6.6%, p < 0.001). Most of these deaths occurred in people who had stage 1 AKI during their index admission (91.7%). Among those discharged, 40 individuals died prior to the 12 months required follow-up and before any assessments could be performed and were excluded, along with 4 individuals who were lost to follow-up. Of the remaining 891 individuals, 9.7% (86/891) developed a further episode of AKI within 12 months. This was significantly more frequent among those who had AKI at the index event (22.7% vs. 8.1%, p < 0.001) and those who had DM (15.8% [44/279] vs. 6.9% [42/612], p < 0.001).
3.5. Renal Follow Up
Among the 97 people with AKI at admission who survived to discharge and had follow-up data, 88.7% (86/97; p < 0.001) underwent appropriate renal function monitoring within the same 12-month period. Follow-up rates were similar between those with and without DM (93.0% vs. 85.2%, p = 0.337).
4. Discussion
This study demonstrates that DM substantially increases both the incidence and severity of AKI in individuals with ACS. Approximately one in five people with DM developed AKI during hospitalisation, nearly double the rate in those without DM. Acute kidney injury was also associated with longer hospital stays, reduced use of evidence-based discharge therapies, and higher mortality. Those who experienced AKI during the index admission continued to experience elevated risk extended beyond discharge with nearly one-fifth of individuals suffering a terminal event, and approximately one-quarter experiencing a recurrent episode of AKI within 12 months. Despite this heightened risk, fewer than 90% of individuals underwent follow-up renal function assessment, indicating missed opportunities for improved patient care and optimisation of modifiable risk factors.
The incidence and severity of AKI are strongly influenced by underlying comorbidities, and DM is a key driver. Previous work has shown variable AKI rates across various conditions, occurring in 8.6-to-9.8% of individuals with community-acquired pneumonia [8,15] and in 11-to-23% of hospitalised patients overall, with higher rates in intensive care and cardiac surgery cohorts [16]. In ACS, registry and trial data have reported incidences ranging from 12.1-to-16.5% [9,17,18,19], with extremes of 35.7-to-59% among patients undergoing percutaneous coronary intervention (PCI) or thrombolysis, and 31.9% after coronary artery bypass graft (CABG) [11]. A meta-analysis of over 100,000 individuals estimated an incidence of 15.8% for ACS-related AKI [6]. Our observed rate of 14.2% therefore aligns closely with prior reports. In people with DM specifically, the incidence of AKI is higher. One long-term study in individuals with stable DM reported a 30% incidence in AKI over 69 months [20]. In our cohort, DM nearly doubled the risk of AKI during ACS, consistent with this broader evidence. Regarding severity, Monseu et al. reported 80% stage 1, 14% stage 2, and 6% stage 3 AKI [20], similar to Liao et al. [19]. We found a comparable distribution, with 85.9% stage 1, though a higher proportion had stage 3 (9.9%) compared to stage 2 (4.3%). This may reflect sample size or population risk profile.
Our findings reinforce the well-established link between AKI and poor clinical outcomes. Previous studies have reported hospital stays of 5-to-8 days for individuals with AKI, versus 3 days for those without [9]. Acute kidney injury is associated with significant short- and long-term morbidity and mortality [11]. Affected individuals have both longer hospital stays and an elevated risk of future events, even up to 3 years post-discharge [9,11]. In-hospital mortality ranges from 6.6% in mild AKI to 31.8% in severe cases [17] and up to 39.6% overall competed to 2.1-to-7.5% without AKI [17,19]. Post-discharge, the excess risk persists, with one-year mortality reported between 27% and 44% [9]. In individuals undergoing PCI, one-year mortality was 9.8% vs. 2.9% in those with and without AKI [18], while a meta-analysis reported early mortality of 15% vs. 2% [6]. Our findings echo these trends. We observed prolonged hospital stays in those with AKI (7.5 vs. 3.0 days and increased mortality at all stages, with rates even higher than those reported by Fox et al. (stage 1: 16.5% vs. 6.6%, stage 2: 50% vs. 14.2%, stage 3: 57.1% vs. 31.8%) [17], highlighting the significant burden on healthcare systems associated with the condition.
The presence of DM continues to play an important role in the management of such individuals [17] as diabetes is shown to amplify peri-procedural AKI risk [21], increase dialysis requirement fivefold [22] and worsen outcomes after myocardial infarction [20]. Interestingly, individuals with diabetes were less likely to present with STEMI but demonstrated lower rates of PCI and higher rates of surgical revascularisation compared with those without diabetes. This likely reflects a higher prevalence of complex and diffuse multi-vessel coronary artery disease among people with diabetes, rendering them less suitable for PCI and more frequently directed toward CABG or conservative management. Although individuals with DM were more likely to have severe LV systolic dysfunction and AKI during admission, they were less likely to have received key cardioprotective therapies at discharge, including beta-blockers and ACE inhibitors. One plausible explanation for this observation is the higher incidence of AKI among those with DM, leading clinicians to defer initiation of such therapies until after discharge, as some of these agents may exacerbate renal dysfunction in the acute setting. Furthermore, even though serum potassium data were not systematically collected in this study, individuals with diabetes had higher serum creatinine levels during admission, suggesting a greater degree of renal impairment. This may have influenced clinicians to defer the initiation of potassium-retaining or nephrotoxic therapies such as ACE inhibitors or ARBs until after discharge, in order to minimise the risk of hyperkalaemia or further renal injury in the acute setting. As our dataset only captured medication initiation at the point of discharge, further information on post-discharge prescribing would have been valuable to better understand local management practices.
Recurrent AKI is increasingly recognised as a key driver of long-term kidney disease progression, particularly in individuals with DM [1]. Our study is among the few to report recurrence rates in the context of ACS, with 22.7% of those with index AKI experiencing another episode within 12 months, compared to 8.1% of those without. This cumulative burden of injury increases the risk of ESRD and cardiovascular events. Current National Institute for Health and Care Excellence (NICE) guidance recommends monitoring of eGFR after AKI, continuing for at least 3 years, and nephrology referral if eGFR falls below 30 mL/min/1.73 m2 [23]. In our cohort, 88.7% of individuals with AKI had follow-up renal testing within 12 months, but this still falls short of universal coverage, particularly given the high-risk nature of this population.
In addition, when individuals present with ACS and AKI, there is an opportunity to optimise therapies with proven cardiovascular and renal benefit. Sodium/glucose co-transporter 2 inhibitors (SGLT2is), including dapagliflozin and empagliflozin, have demonstrated substantial reductions in CKD progression in high-risk populations [24,25]. Similarly, glucagon-like peptide-1 receptor agonists (GLP-1RAs) also have efficacy in terms of reduced renal risk [26]. Incorporating these therapies into the care of individuals with diabetes after ACS and AKI could mitigate long-term risk, complement guideline-directed cardiac therapies, and maximise the benefits of systematic renal monitoring. Embedding renal and metabolic optimisation into post-ACS pathways represents a tangible opportunity to improve outcomes in this high-risk population.
It is important to recognise that this study has limitations. Firstly, the follow-up period was limited to 12 months, precluding assessment of longer-term renal and cardiovascular outcomes. A longer duration would provide further insight into the long-term risks associated with AKI in individuals with ACS. Nevertheless, the findings effectively highlight the increased short- and medium-term risks linked to the condition in our region. Second, analysis was conducted at a single centre, which may limit the generalisability of the results, as outcomes could vary depending on regional factors, patient demographics, and comorbidities. Despite this, the study offers valuable insight into the local burden of disease and risk profile, which can inform more effective allocation of healthcare resources. Third, the study did not differentiate between type 2 diabetes mellitus (T2DM) and other forms of diabetes, limiting the ability to assess risk by diabetes subtype. However, given that that approximately 90% of the population with diabetes comprises individuals with T2DM [27], the overall risk profile is likely to reflect type 2 as the predominant group. Finally, residual confounding cannot be excluded, as we did not adjust for baseline renal function, contrast load, or medication use. Despite these limitations, the study adds valuable real-world evidence by quantifying the incidence, severity, recurrence, and monitoring of AKI in ACS, and highlights the particular vulnerability of those with DM.
5. Conclusions
Diabetes mellitus markedly increases the risk, severity, and recurrence of AKI in patients with ACS, leading to longer hospital stays, and higher in-hospital and long-term mortality. Despite this, post-discharge renal surveillance remains inconsistent. These findings highlight the need for structured post-discharge monitoring and proactive optimisation of modifiable risk factors to improve outcomes in people with DM following ACS.
Author Contributions
M.U.S. and K.L. contributed to the conception or design of the work. M.U.S. contributed to data acquisition while M.U.S. and K.L. contributed to analysis and M.U.S., P.E.S., C.E.H., and K.L. contributed to interpretation of data for the work. M.U.S. and K.L. drafted the manuscript and P.E.S. and C.E.H. critically revised the manuscript. All gave final approval and agreed to be accountable for all aspects of work ensuring integrity and accuracy. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
The project was registered locally as a clinical audit and service improvement project (registration number L-0994).
Informed Consent Statement
Data was collected retrospectively after the above approvals and therefore formal informed consent was not applicable.
Data Availability Statement
The data underlying this article will be shared on reasonable request to the corresponding author.
Conflicts of Interest
M.U.S. received honoraria, travel and educational grant from Boehringer Ingelheim. None declared for any of the other authors.
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Table 1.
Baseline demographics and characteristics of individuals with and without AKI. ACEi: Angiotensin converting enzyme inhibitors, AKI: Acute kidney injury, ARBs: Angiotensin receptor blockers, BMI: Body mass index, BP: Blood pressure, CABG: Coronary artery bypass grafting.
Table 1.
Baseline demographics and characteristics of individuals with and without AKI. ACEi: Angiotensin converting enzyme inhibitors, AKI: Acute kidney injury, ARBs: Angiotensin receptor blockers, BMI: Body mass index, BP: Blood pressure, CABG: Coronary artery bypass grafting.
| Characteristic | Overall N = 990 1 | Without AKI N = 849 1 | With AKI N = 141 1 | p-Value 2 |
|---|---|---|---|---|
| Sex | 0.998 | |||
| Male | 688/990 (69.5%) | 590/849 (69.5%) | 98/141 (69.5%) | |
| Female | 302/990 (30.5%) | 259/849 (30.5%) | 43/141 (30.5%) | |
| Age At Admission (years) | 68.0 (58.0–77.0) | 67.0 (58.0–76.0) | 74.0 (65.0–79.0) | <0.001 |
| Smoking Status | 0.598 | |||
| Never smoked | 321/873 (36.8%) | 278/757 (36.7%) | 43/116 (37.1%) | |
| Ex-smoker | 310/873 (35.5%) | 265/757 (35.0%) | 45/116 (38.8%) | |
| Current smoker | 242/873 (27.7%) | 214/757 (28.3%) | 28/116 (24.1%) | |
| Unknown | 117 | 92 | 25 | |
| Systolic BP (mmHg) | 141.0 (124.0–160.0) | 141.0 (125.0–161.0) | 140.0 (115.0–158.0) | 0.038 |
| Unknown | 8 | 4 | 4 | |
| Heart Rate on Admission (beats/min) | 77.0 (66.0–90.0) | 76.0 (66.0–89.0) | 83.0 (68.0–100.0) | 0.008 |
| Unknown | 10 | 6 | 4 | |
| Admission Glucose (mmol/L) | 7.2 (6.2–9.6) | 7.0 (6.1–9.2) | 8.8 (6.8–13.5) | <0.001 |
| Unknown | 38 | 36 | 2 | |
| BMI (kg/m2) | 28.1 (24.9–31.6) | 28.3 (24.9–31.8) | 27.4 (24.5–30.6) | 0.136 |
| Unknown | 15 | 8 | 7 | |
| Left ventricular systolic function | <0.001 | |||
| Preserved | 391/789 (49.6%) | 359/670 (53.6%) | 32/119 (26.9%) | |
| Moderately impaired | 271/789 (34.3%) | 234/670 (34.9%) | 37/119 (31.1%) | |
| Severely impaired | 127/789 (16.1%) | 77/670 (11.5%) | 50/119 (42.0%) | |
| Not assessed | 201 | 179 | 22 | |
| Creatinine (µm/L) | 84.0 (70.0–103.0) | 83.0 (69.0–99.0) | 104.0 (80.0–146.0) | <0.001 |
| Unknown | 9 | 9 | 0 | |
| Killip class | <0.001 | |||
| No evidence of heart failure | 818/909 (90.0%) | 734/786 (93.4%) | 84/123 (68.3%) | |
| Pulmonary oedema | 54/909 (5.9%) | 30/786 (3.8%) | 24/123 (19.5%) | |
| Cardiogenic shock | 37/909 (4.1%) | 22/786 (2.8%) | 15/123 (12.2%) | |
| Unknown | 81 | 63 | 18 | |
| Length of stay (days) | 3.3 (1.6–6.6) | 3.0 (1.5–5.8) | 7.5 (3.2–14.3) | <0.001 |
| Peak Troponin (ng/L) | 218.0 (74.0–800.0) | 186.0 (69.0–660.0) | 562.0 (152.0–2128.0) | <0.001 |
| Unknown | 26 | 22 | 4 | |
| Discharge Diagnosis | 0.034 | |||
| ST elevation Myocardial infarction | 439/990 (44.3%) | 365/849 (43.0%) | 74/141 (52.5%) | |
| Non-ST elevation Myocardial infarction | 549/990 (55.5%) | 483/849 (56.9%) | 66/141 (46.8%) | |
| Unstable angina | 2/990 (0.2%) | 1/849 (0.1%) | 1/141 (0.7%) | |
| In-hospital mortality | 55/990 (5.6%) | 24/849 (2.8%) | 31/141 (22.0%) | <0.001 |
| Beta-blockers | 795/987 (80.5%) | 705/848 (83.1%) | 90/139 (64.7%) | <0.001 |
| Unknown | 3 | 1 | 2 | |
| ACEi/ARBs | 811/989 (82.0%) | 733/848 (86.4%) | 78/141 (55.3%) | <0.001 |
| Unknown | 1 | 1 | 0 | |
| Statins | 845/989 (85.4%) | 746/848 (88.0%) | 99/141 (70.2%) | <0.001 |
| Unknown | 1 | 1 | 0 | |
| Aspirin | 779/989 (78.8%) | 695/848 (82.0%) | 84/141 (59.6%) | <0.001 |
| Unknown | 1 | 1 | 0 | |
| Coronary Angiography during admission | 894/984 (90.9%) | 781/845 (92.4%) | 113/139 (81.3%) | <0.001 |
| Coronary revascularisation | 0.018 | |||
| Percutaneous coronary intervention | 774/982 (78.8%) | 677/843 (80.3%) | 97/139 (69.8%) | |
| CABG | 48/982 (4.9%) | 39/843 (4.6%) | 9/139 (6.5%) | |
| Medical Management | 160/982 (16.3%) | 127/843 (15.1%) | 33/139 (23.7%) | |
| Unknown | 8 | 6 | 2 | |
| Thienopyridine | 149/989 (15.1%) | 125/848 (14.7%) | 24/141 (17.0%) | 0.483 |
| Unknown | 1 | 1 | 0 | |
| Ticagrelor | 711/989 (71.9%) | 637/848 (75.1%) | 74/141 (52.5%) | <0.001 |
| Unknown | 1 | 1 | 0 | |
| MRA | 106/989 (10.7%) | 82/848 (9.7%) | 24/141 (17.0%) | 0.009 |
| Unknown | 1 | 1 | 0 | |
| Diabetes status | <0.001 | |||
| Diabetic | 315/990 (31.8%) | 252/849 (29.7%) | 63/141 (44.7%) | |
| Non Diabetic | 675/990 (68.2%) | 597/849 (70.3%) | 78/141 (55.3%) | |
| Further AKI within 12 months post discharge | 86/990 (8.7%) | 64/849 (7.5%) | 22/141 (15.6%) | 0.002 |
1 n/N (%); Median (Q1–Q3). 2 Pearson’s Chi-squared test; Wilcoxon rank sum test; Fisher’s exact test. MRA = Mineralocorticoid receptor antagonist.
Table 2.
Intergroup analysis based on presence or absence of DM. AKI: Acute kidney injury, BMI: Body mass index, CABG: Coronary artery bypass graft.
Table 2.
Intergroup analysis based on presence or absence of DM. AKI: Acute kidney injury, BMI: Body mass index, CABG: Coronary artery bypass graft.
| Characteristic | Overall N = 990 1 | With DM N = 315 1 | Without DM N = 675 1 | p-Value 2 |
|---|---|---|---|---|
| Age At Admission | 68.0 (58.0–77.0) | 70.0 (61.0–78.0) | 67.0 (57.0–76.0) | <0.001 |
| Admission Glucose (mmol/L) | 7.2 (6.2–9.6) | 10.1 (7.7–14.5) | 6.7 (5.9–7.9) | <0.001 |
| Unknown | 38 | 12 | 26 | |
| BMI (kg/m2) | 28.1 (24.9–31.6) | 29.1 (25.8–32.8) | 27.7 (24.4–31.3) | <0.001 |
| Unknown | 15 | 5 | 10 | |
| Left ventricular systolic function | 0.002 | |||
| Preserved | 391/789 (49.6%) | 122/243 (50.2%) | 269/546 (49.3%) | |
| Moderately impaired | 271/789 (34.3%) | 67/243 (27.6%) | 204/546 (37.4%) | |
| Severely impaired | 127/789 (16.1%) | 54/243 (22.2%) | 73/546 (13.4%) | |
| Not assessed | 201 | 72 | 129 | |
| Creatinine (µm/L) | 84.0 (70.0–103.0) | 88.5 (70.0–114.0) | 84.0 (70.0–99.0) | 0.007 |
| Unknown | 9 | 1 | 8 | |
| Killip class | <0.001 | |||
| No evidence of heart failure | 818/909 (90.0%) | 243/285 (85.3%) | 575/624 (92.1%) | |
| Pulmonary oedema | 54/909 (5.9%) | 30/285 (10.5%) | 24/624 (3.8%) | |
| Cardiogenic shock | 37/909 (4.1%) | 12/285 (4.2%) | 25/624 (4.0%) | |
| Unknown | 81 | 30 | 51 | |
| Length of stay (days) | 3.3 (1.6–6.6) | 4.5 (1.9–8.6) | 2.9 (1.5–5.7) | <0.001 |
| Discharge Diagnosis | <0.001 | |||
| ST elevation Myocardial infarction | 439/990 (44.3%) | 102/315 (32.4%) | 337/675 (49.9%) | |
| Non-ST elevation Myocardial infarction | 549/990 (55.5%) | 211/315 (67.0%) | 338/675 (50.1%) | |
| Unstable angina | 2/990 (0.2%) | 2/315 (0.6%) | 0/675 (0.0%) | |
| In-hospital mortality | 55/990 (5.6%) | 21/315 (6.7%) | 34/675 (5.0%) | 0.297 |
| Beta-blockers | 795/987 (80.5%) | 231/313 (73.8%) | 564/674 (83.7%) | <0.001 |
| Unknown | 3 | 2 | 1 | |
| ACEi/ARBs | 811/989 (82.0%) | 234/314 (74.5%) | 577/675 (85.5%) | <0.001 |
| Unknown | 1 | 1 | 0 | |
| Coronary Angiography during admission | 894/984 (90.9%) | 275/314 (87.6%) | 619/670 (92.4%) | 0.013 |
| Coronary revascularisation | <0.001 | |||
| Percutaneous coronary intervention | 774/982 (78.8%) | 222/312 (71.2%) | 552/670 (82.4%) | |
| CABG | 48/982 (4.9%) | 29/312 (9.3%) | 19/670 (2.8%) | |
| Medical Management | 160/982 (16.3%) | 61/312 (19.6%) | 99/670 (14.8%) | |
| Unknown | 8 | 3 | 5 | |
| AKI at Admission | 141/990 (14.2%) | 63/315 (20.0%) | 78/675 (11.6%) | <0.001 |
| Stages of AKI at Admission | <0.001 | |||
| 1 | 121/990 (12.2%) | 53/315 (16.8%) | 68/675 (10.1%) | |
| 2 | 6/990 (0.6%) | 1/315 (0.3%) | 5/675 (0.7%) | |
| 3 | 14/990 (1.4%) | 9/315 (2.9%) | 5/675 (0.7%) |
1 n/N (%); Median (Q1–Q3). 2 Pearson’s Chi-squared test; Wilcoxon rank sum test; Fisher’s exact test. ACEi/ARBs = Angiotensin Converting Enzyme inhibitors/Angiotensin receptor blockers.
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Shah, M.U.; Squires, P.E.; Hills, C.E.; Lee, K. Diabetes Mellitus and the Increased Risk of Acute Kidney Injury Following Acute Coronary Syndrome. Diabetology 2025, 6, 148. https://doi.org/10.3390/diabetology6120148
AMA Style
Shah MU, Squires PE, Hills CE, Lee K. Diabetes Mellitus and the Increased Risk of Acute Kidney Injury Following Acute Coronary Syndrome. Diabetology. 2025; 6(12):148. https://doi.org/10.3390/diabetology6120148
Chicago/Turabian StyleShah, Muhammad Usman, Paul Edward Squires, Claire Elizabeth Hills, and Kelvin Lee. 2025. "Diabetes Mellitus and the Increased Risk of Acute Kidney Injury Following Acute Coronary Syndrome" Diabetology 6, no. 12: 148. https://doi.org/10.3390/diabetology6120148
APA StyleShah, M. U., Squires, P. E., Hills, C. E., & Lee, K. (2025). Diabetes Mellitus and the Increased Risk of Acute Kidney Injury Following Acute Coronary Syndrome. Diabetology, 6(12), 148. https://doi.org/10.3390/diabetology6120148
