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. 2025 Sep 25;47(1):2560606. doi: 10.1080/0886022X.2025.2560606

Acute kidney injury among patients aged over 80 years after percutaneous coronary intervention: a multicenter, retrospective cohort study

Xin Liu a,*, Dingyi Wang b,*, Yalin Cheng c,*, Huimin Li d, Yuzhu Lu d, Haiyang Gao c, Jing Ma e,f, Chaozeng Si g, Tingyu Yin g, Guohui Fan b,#,✉, Wenduo Zhang c,✉,#
PMCID: PMC12466182  PMID: 40998584

Abstract

Background

We aimed to investigate the incidence and risk factors of acute kidney injury (AKI) after percutaneous coronary intervention (PCI) in the oldest-old patients (≥80 years), particularly among those with baseline renal insufficiency and peri-operative hydration.

Methods

This retrospective cohort study included patients ≥80 years undergoing PCI at two tertiary hospitals in China (hospitalized between January 2020 and December 2024). Baseline renal dysfunction was defined as eGFR < 60 mL/min/1.73 m2 on admission. The primary endpoint was AKI event after PCI according to KDIGO criteria. Secondary endpoints included in-hospital mortality, renal replacement therapy, and length of hospital stay. Logistic regression was applied to identify AKI risk factors. Restricted cubic splines (RCS, 4 knots) were used to explore the dynamic risk magnitude for AKI as baseline eGFR changes, adjusting for multivariable.

Results

Among the 995 patients included in the final analysis, the incidence of baseline renal insufficiency was 35.9% and that of AKI was 13.8%. Logistic regression showed that STEMI, NSTEMI, acute heart failure, baseline renal insufficiency, a higher neutrophil-to-lymphocyte ratio (NLR), and anemia were independent risk factors for AKI. Among those with baseline renal insufficiency, AKI incidence was 29.7%, and lower baseline eGFR, elevated NLR, and preoperative diuretic use were independent risk factors for AKI. RCS analysis revealed that the AKI risk was significantly increased when eGFR < 67.4 mL/min/1.73 m2, regardless of hydration therapy.

Conclusion

Patients ≥ 80 years old with baseline renal failure confronted higher AKI risk after PCI procedure. Comprehensive strategies beyond hydration may be needed for AKI prevention in this fragile population.

Keywords: Oldest-old, percutaneous coronary intervention, acute kidney injury, renal dysfunction, hydration

Introduction

With the global aging and development in medical techniques, an increasing number of elderly patients with coronary heart disease are undergoing percutaneous coronary intervention (PCI) [1]. Consequently, a common complication of PCI, also known as contrast-induced acute kidney injury (CI-AKI), has been substantially increasing. It has been reported that the incidence of CI-AKI was approximately 7% in all patients undergoing PCI, and was up to 18–20% in patients with acute myocardial infarction (AMI) undergoing PCI [2–4].

Advanced age, together with renal failure, has been considered a strong indicator of AKI [5,6], and the natural decline in renal function after the age of 70s creates a scenario where the coexistence of advanced age and renal failure substantially elevates AKI risk [7]. For the elderly, renal failure was reported as one of the strongest indicators for AKI after PCI in a study of over 40,000 elderly patients, while not identified as risk factor in another study focused on patients over 80 years old [8,9]. Given the controversial evidence and the poor outcome once AKI occurred, current guidelines recommend hydration prophylaxis for most patients with eGFR < 60 mL/min/1.73 m2 before PCI [10]. However, several recent guidelines and reviews have provided a cautious recommendation for hydration in renally impaired patients, given insufficient evidence from some RCTs regarding CI-AKI prevention [11–14]. Existing evidence also showed controversial results [15,16], and no significant CI-AKI prevention nor long-term renal benefits from saline hydration were found [17–19]. Moreover, hydration for elderly patients was also doubtable, as an increased incidence of heart failure occurred with aging, and restrictions on volume intake should be considered. Therefore, whether hydration was effective for the prophylaxis of AKI after PCI in real-world setting remains debatable among the oldest-old population, especially among those with renal failure.

Therefore, it’s reasonable to hypothesize that in the oldest-old population, baseline renal failure might be a strong risk factor, and hydration might have a protective effect for AKI after PCI. We thus conducted this multicenter, retrospective cohort study with the aim of investigating the incidence of AKI, identifying its risk factors, and assessing the impact of peri-procedural hydration on AKI development in patients ≥ 80 years undergoing PCI, with a particular focus on those with baseline renal failure. The findings will yield crucial evidence regarding renal complications and help inform renal protection strategies for this expanding, vulnerable population.

Method

Participants and study design

This was a multicenter, retrospective cohort study. The inclusion criteria were: patients aged ≥ 80 years who underwent PCI and were consecutively recruited from two tertiary hospitals between 1 January 2020 and 30 December 2024. The exclusion criteria included the following: (1) patients with no records of laboratory examinations; (2) patients with only one record of serum creatinine (Scr); (3) patients with end stage renal disease (ESRD) who were already receiving renal replacement therapy. PCI was performed using standard techniques, with the specific approach determined by the operators’ preferences. As this was an observational study, no additional interventions were implemented for the PCI procedure or for the operators. Demographic data, diagnostic findings, medical history, results of physical and laboratory examinations, date of PCI, therapeutic regimens, and clinical outcomes were extracted from medical records.

Throughout the study, a low-osmolar, non-anionic contrast medium was utilized, with a standard volume ranging from 100 to 200 mL per procedure. The study was approved by the Institutional Review Board and Ethics Committee of Beijing Hospital (approval number: 2022BJYYEC-085-01). Informed consent was waived due to the retrospective design.

Outcomes and definitions

The primary outcome was AKI after PCI during hospitalization. AKI was determined if Scr increased by 0.3 mg/dL (26.5 mol/L) within 48 h or increased to ×1.5 times from baseline within the prior 7 days, according to the KDIGO (Kidney Disease: Improving Global Outcomes) consensus guidelines [20]. Baseline Scr levels were measured either at admission or prior to PCI. AKI stages were defined as follows: stage 1, an increase in Scr levels to ≥1.5 times the baseline Scr or an elevation of ≥ 0.3 mg/dL (≥ 26.5 μmol/L); stage 2, an increase of 2.0- to 2.9-fold above baseline Scr; stage 3, an increase of >3.0 times the baseline Scr or an elevation to ≥4.0 mg/dL (≥353.6 μmol/L). Secondary outcomes included in-hospital death, continuous renal replacement therapy (CRRT), and length of hospital stay. Contrast-induced nephropathy (CIN) was defined as an elevation in Scr of more than 25% or ≥0.5 mg/dL (≥44 μmol/L) from baseline within 48 h after PCI [21]. Estimated glomerular filtration rates (eGFR) were calculated according to 2009 CKD Epidemiology Collaboration (CKD-EPI) equation [22]. Subsequently, eGFR values were categorized using a cutoff value of 60/mL/min per 1.73 m2. Hydration was defined as the administration of 1 mL/kg per hour of saline, given up to 12 h before and 6–24 h after PCI [18]. The neutrophil-to-lymphocyte ratio (NLR) was calculated based on baseline peripheral blood cell count results. For patients who had been prescribed metformin or SGLT-2 (Sodium-Glucose Transporter-2) inhibitors prior to PCI, the standard clinical practice at both participating centers was to discontinue these medications 24 h before the procedure.

Coronary heart disease (CHD) was classified based on discharge records, including stable angina, unstable angina, ST-elevated myocardial infarction (STEMI), and non-ST-elevated myocardial infarction (NSTEMI). In addition, the occurrence of acute left heart failure, sudden cardiac death, and the degree of cardiac function as assessed by the New York Heart Association (NYHA) classification were also recorded [23,24].

Statistical analysis

Clinical features were described using frequencies (percentages) or medians (interquartile ranges, IQRs), with group comparisons performed using the χ2 test, Fisher’s exact test, or Mann-Whitney U test where appropriate. Missing data were not imputed in the analysis. Logistic regression models were constructed to identify the risk factors for AKI. Variables with p < 0.05 in univariable analysis, combined with clinically relevant factors, were selected as candidate covariates for multivariable regression; effect sizes were expressed as odds ratios (ORs) with corresponding 95% confidence intervals (CIs). Propensity score matching (PSM) was used to balance baseline characteristics between the hydration groups. Imbalanced variables with p < 0.2 in univariable comparisons—based on clinical relevance and group differences—were included as candidate independent variables. A logistic regression model was constructed to estimate individual propensity scores. Matching was performed at a 1:1 ratio with a caliper of 0.2. The post-matching balance of baseline characteristics was reevaluated.

To further explore the correlation between eGFR and AKI in patients with or without hydration, restricted cubic spline (RCS) analysis with 4 knots was used, adjusted for variables including acute myocardial infarction (AMI), neutrophil-to-lymphocyte ratio (NLR), acute left heart failure, and anemia classification. The RCS curves were then plotted by hydration status, and non-linear relationships were tested separately. The inflection point was defined as the eGFR value corresponding to an OR of 1.

Given that the Berlin Initiative Study (BIS) 1 formula has been recommended for assessing renal function in elderly patients aged >75 years [25,26], we performed sensitivity analyses by replacing CKD-EPI formula with the BIS1 formula, following by analyzing the risk factors for AKI and conducting RCS analysis. Moreover, the BIS2 formula was not applied in our analysis, as cystatin C was not a routine parameter in the two participating centers.

All statistical analyses were conducted using R software (version 4.2.3). A two-sided p-value < 0.05 was considered statistically significant.

Results

Characteristics of all participants

A total of 995 patients aged ≥80 years were included in the final analysis. The study population had a mean age of 83.14 ± 3.1 years, with 592 male participants (59.5%); the overall incidence of AKI was 13.8% (137/995). Among the patients, 648 (65.1%) had an eGFR ≥ 60 mL/min/1.73 m2, and 347 (35.9%) had an eGFR <60 mL/min/1.73 m2 at admission. The incidences of AKI in patients with eGFR ≥ 60 mL/min/1.73 m2 and <60 mL/min/1.73 m2 were 5.3% and 29.7%, respectively, with statistically significant difference (p < 0.001) (Figure 1; Supplementary Table 1).

Figure 1.

Figure 1.

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Study flowchart and AKI incidence in patients with different baseline renal function groups. *eGFR was calculated by CKD-EPI equation. AKI: acute kidney injury; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; eGFR: estimated glomerular filtration rates; PCI: percutaneous coronary intervention.

The comparison of demographic characteristics, clinical presentations, and outcomes between patients with and without AKI who underwent PCI is shown in Table 1. Patients who developed AKI after PCI had higher proportions of STEMI, NSTEMI, and acute heart failure, a higher NYHA class, and a greater burden of comorbidities including underlying heart disease and chronic kidney disease (CKD). The baseline eGFR was significantly lower in AKI group than in non-AKI group (45.8 vs 68.3 mL/min/1.73 m2, p < 0.001), and the NLR was significantly higher in AKI group than in the non-AKI group (4.5 vs 2.63, p < 0.001). The rates of diuretic application and peri-interventional hydration were both significantly higher in the AKI group than that in the non-AKI group (70.7% vs 31.9%, p < 0.001 and 84.7% vs 74.4%, p = 0.009, respectively). For secondary outcomes, patients who developed AKI had significantly higher rates of in-hospital death (11.0% vs 0.4%, p < 0.001) and longer median length of hospitalization (11 vs 6 days, p < 0.001).

Table 1.

Comparisons of characteristics of patients developed AKI or not after PCI.

Parameters Total Non-AKI AKI  
(n = 995) (n = 858) (n = 137) p Value
Age (years) 83.14 ± 3.05 83.08 ± 3.06 83.54 ± 2.94 0.098
 ≤80 170 (17.09%) 151 (17.6%) 19 (13.87%) 0.226
 80–90 809 (81.31%) 695 (81%) 114 (83.21%)
 >90 16 (1.61%) 12 (1.4%) 4 (2.92%)
Male 592 (59.5%) 517 (60.26%) 75 (54.74%) 0.222
BMI (kg/m2) 24.29 ± 3.25 24.26 ± 3.21 24.54 ± 3.55 0.413
 <24 422 (47.15%) 379 (47.73%) 43 (42.57%) 0.205
 24–30 437 (48.83%) 386 (48.61%) 51 (50.5%)
 >30 36 (4.02%) 29 (3.65%) 7 (6.93%)
Type of CHD        
 Stable angina 87 (8.74%) 82 (9.56%) 5 (3.65%) 0.023
 Unstable angina 299 (30.05%) 274 (31.93%) 25 (18.25%) 0.001
 STEMI 62 (6.23%) 39 (4.55%) 23 (16.79%) <0.001
 NSTEMI 214 (21.51%) 162 (18.88%) 52 (37.96%) <0.001
Acute heart failure 76 (7.64%) 47 (5.48%) 29 (21.17%) <0.001
 Sudden cardiac death 2 (0.2%) 1 (0.12%) 1 (0.73%) 0.257
 NYHA classification        
  I 98 (28.49%) 90 (30.41%) 8 (16.67%) <0.001
  II 125 (36.34%) 114 (38.51%) 11 (22.92%)
  III 105 (30.52%) 82 (27.7%) 23 (47.92%)
  IV 16 (4.65%) 10 (3.38%) 6 (12.5%)
Comorbidity        
 Cardiovascular disease 332 (33.37 266 (31%) 66 (48.18%) <0.001
 AMI history 179 (17.99%) 157 (18.3%) 22 (16.06%) 0.526
 Chronic heart failure 79 (7.94%) 55 (6.41%) 24 (17.52%) <0.001
 Atrial fibrillation/atrial flutter 159 (15.98%) 122 (14.22%) 37 (27.01%) <0.001
 Diabetes mellitus 413 (41.51%) 348 (40.56%) 65 (47.45%) 0.129
 Hypertension 822 (82.61%) 702 (81.82%) 120 (87.59%) 0.098
 hyperlipemia 486 (48.84%) 430 (50.12%) 56 (40.88%) 0.045
 Chronic respiratory disease 190 (19.1%) 166 (19.35%) 24 (17.52%) 0.613
 Cancer 98 (9.85%) 84 (9.79%) 14 (10.22%) 0.876
 Chronic kidney disease 175 (17.59%) 110 (12.82%) 65 (47.45%) <0.001
Vital signs on admission        
 Heart rate (beats/min) 74.15 ± 12.64 73.29 ± 11.62 79.46 ± 16.83 <0.001
 Systolic blood pressure (mmHg) 137.82 ± 21.39 138.96 ± 20.85 130.64 ± 23.36 <0.001
 Diastolic blood pressure (mmHg) 70.38 ± 13.19 70.71 ± 13 68.31 ± 14.21 0.058
Respiratory rate (times/min) 18.39 ± 2.74 18.27 ± 2.8 19.09 ± 2.29 0.001
Laboratory examinations on admission      
 Serum creatinine (µmol/L) 81 (68, 102%) 78.8 (68, 96%) 115.1 (89, 161%) <0.001
 eGFR (mL/min/1.73 m2)a 65.21 ± 18.92 68.3 ± 16.28 45.83 ± 22.57 <0.001
 ≥60 648 (65.13%) 614 (71.56%) 34 (24.82%)  
 30–59 295 (29.65%) 227 (26.46%) 68 (49.64%) <0.001
 <30 52 (5.23%) 17 (1.98%) 35 (25.55%)  
 Urea nitrogen (mmol/L) 6.53 (5.24, 8.27) 6.34 (5.12, 7.9) 9.44 (6.53, 13.5) <0.001
 Glucose (mmol/L) 7.05 ± 2.8 6.85 ± 2.69 8.18 ± 3.12 <0.001
 Triglyceride (mmol/L) 1.08 (0.79, 1.51) 1.08 (0.78, 1.49) 1.14 (0.82, 1.66) 0.363
 Total cholesterol (mmol/L) 3.66 ± 0.94 3.65 ± 0.93 3.76 ± 1.03 0.21
 LDL-C (mmol/L) 2.04 ± 0.82 2.02 ± 0.82 2.16 ± 0.8 0.095
 HDL-C (mmol/L) 1.08 ± 0.28 1.09 ± 0.28 1.03 ± 0.29 0.058
 White blood cell (×109/L) 6.66 ± 2.28 6.42 ± 2.01 8.17 ± 3.12 <0.001
 Neutrophil count (×109/L) 4.11 (3.1, 5.2) 3.91 (3.01, 4.97) 5.34 (4.19, 7.35) <0.001
 Lymphocyte count (×109/L) 1.5 ± 0.59 1.53 ± 0.6 1.28 ± 0.49 <0.001
 NLR 2.79 (1.96, 4.14) 2.63 (1.89, 3.83) 4.5 (3.02, 6.97) <0.001
 Haemoglobin (g/L) 121.48 ± 17.03 122.91 ± 16.51 112.5 ± 17.53 <0.001
 RDW (%) 43.58 ± 4.1 43.37 ± 3.36 44.89 ± 7.06 0.015
 PDW (%) 12.74 ± 2.61 12.73 ± 2.6 12.81 ± 2.71 0.735
 Platelet count (×1012/L) 190.62 ± 59.12 190.35 ± 56.53 192.23 ± 72.98 0.756
 Anemia        
  No anemia 666 (67.07%) 609 (71.14%) 57 (41.61%) <0.001
  Mild 282 (28.4%) 216 (25.23%) 66 (48.18%)
  Moderate 41 (4.13%) 27 (3.15%) 14 (10.22%)
  Severe 4 (0.4%) 4 (0.47%) 0 (0%)
 BNP (pg/mL) 191.84 (78.86, 484.37) 158.99 (73.68, 375.69) 672.9 (224.51, 1116.62) <0.001
 NT-proBNP (pg/mL) 710 (239, 2388) 523 (198, 1783) 4088 (1389, 11877) <0.001
 CK-MB (ng/mL) 2.35 (1.44, 6.5) 2.2 (1.4, 4.84) 4.78 (1.9, 33.3) <0.001
 cTnI (ng/mL) 0.17 (0.01, 7.4) 0.1 (0.01, 6) 4.55 (0.08, 21.78) <0.001
 cTnT (ng/mL) 0.03 (0.02, 0.24) 0.03 (0.02, 0.16) 0.39 (0.06, 3.25) <0.001
 Myo (ng/mL) 46.4 (31, 78.94) 43 (30.1, 71.2) 100.6 (54, 298) <0.001
 Cystatin C (mg/L) 1.35 (1.11, 1.77) 1.27 (1.1, 1.61) 1.98 (1.44, 2.68) <0.001
 CRP (mg/L) 2.5 (0.7, 6.1) 2.5 (0.57, 4.5) 3.05 (1.1, 12.71) <0.001
 Uric acid (µmol/L) 355.74 ± 105.23 346.9 ± 97.74 411.04 ± 130.95 <0.001
 Serum albumin (g/L) 38.43 ± 3.57 38.63 ± 3.44 37.31 ± 4.09 <0.001
 Total bilirubin (µmol/L) 10.8 (8.2, 14.38) 10.8 (8.3, 14.2) 11.4 (7.8, 16.95) 0.606
 Fibrinogen (g/L) 3.32 ± 0.92 3.29 ± 0.89 3.5 ± 1.06 0.013
 D-dimer (ng/mL) 91.5 (0.52, 231.5) 85 (0.5, 213) 142 (1.06, 464) <0.001
 FDP (mg/L) 2.23 (2, 3.47) 2.17 (2, 3.3) 2.72 (2, 4.3) 0.01
Medication        
 ACEI/ARB/ARNI 372 (37.39%) 323 (37.65%) 49 (35.77%) 0.673
 β-blocker 529 (53.17%) 443 (51.63%) 86 (62.77%) 0.015
 Statins 649 (65.23%) 561 (65.38%) 88 (64.23%) 0.793
 Diuretics 370 (37.19%) 274 (31.93%) 96 (70.07%) <0.001
 Peri-intervention hydration 754 (75.78%) 638 (74.36%) 116 (84.67%) 0.009
 Insulin treatment 204 (20.5%) 142 (16.55%) 62 (45.26%) <0.001
 Metformin 103 (10.9) 94 (11.6) 9 (6.6) 0.0814
 SGLT-2 38 (4.0) 32 (3.9) 6 (4.4) 0.8086
Outcomes        
 In-hospital death 18 (1.81%) 3 (0.35%) 15 (10.95%) <0.001
 Length of hospital stay (days) 7 (5, 10) 6 (5, 9) 11 (7, 17) <0.001
 CIN 64 (6.74%) 34 (4.19%) 30 (21.9%) <0.001
 CRRT 33 (3.32%) 7 (0.82%) 26 (18.98%) <0.001
 AKI stage – –    
  1     121 (88.32%)  
  2     5 (3.65%)  
  3     11 (8.03%)  
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aeGFR was calculated by CKD-EPI equation. ACEI: Angiotensin-Converting Enzyme Inhibitor; ARB: Angiotensin Receptor Blocker; ARNI: Angiotensin Receptor-Neprilysin Inhibitor; AKI: Acute Kidney Injury; AMI: Acute Myocardial Infarction; BMI: Body Mass Index; BNP: B-type Natriuretic Peptide; CHD: Coronary Heart Disease; CIN: Contrast-Induced Nephropathy; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; CK-MB: Creatine Kinase-Myocardial Band; CRP: C-reactive Protein; CRRT: Continuous Renal Replacement Therapy; FDP: Fibrinogen Degradation Products; HDL-C: High-Density Lipoprotein Cholesterol; LDL-C: Low-Density Lipoprotein Cholesterol; NLR: Neutrophil-to-Lymphocyte Ratio; NT-proBNP: N-terminal pro-B-type Natriuretic Peptide; NSTEMI: Non-ST-Elevation Myocardial Infarction; NYHA: New York Heart Association; PCI: Percutaneous Coronary Intervention; SGLT-2: Sodium-Glucose Transporter 2; STEMI: ST-Elevation Myocardial Infarction; TnI: Troponin I; TnT: Troponin T.

Risk factors for AKI after PCI among oldest-old patients

After adjustment for covariates, STEMI (OR 4.4, 95%CI 2.1–9.2, p < 0.001), NSTEMI (OR 2.3, 95%CI 1.5–3.5, p < 0.001), and acute heart failure (OR 2.4, 95%CI 1.2–4.2, p = 0.01), baseline eGFR of 30–59 mL/min/1.73 m2 (OR 5.2, 95%CI 3.2–8.3, p < 0.001), baseline eGFR < 30 mL/min/1.73 m2 (OR 25.1, 95%CI 11.9–53.1, p < 0.001), NLR (OR 1.1, 95%CI 1.1–1.2, p < 0.001), and anemia (OR 1.5, 95%CI 1.1–2.1, p = 0.025) were independent risk factors for AKI after PCI. Hydration was associated with AKI but not an independent risk factor (Table 2).

Table 2.

Risk factors for AKI after PCI among oldest-old patients.

  Univariable regression
 Multivariable regression
Parameters Odds ratio 95% CI p Value Odds ratio 95% CI p Value
STEMI 4.237 2.441–7.353 <0.001 4.377 2.085–9.188 <0.001
NSTEMI 2.628 1.788–3.863 <0.001 2.338 1.459–3.747 <0.001
Acute heart failure 4.633 2.798–7.673 <0.001 2.245 1.21–4.165 0.01
eGFR (mL/min/1.73 m2)a   <0.001      
 ≥60 Ref     Ref    
 30–59 5.41 3.488–8.391 <0.001 5.153 3.184–8.338 <0.001
 <30 37.18 18.94–72.987 <0.001 25.1 11.861–53.118 <0.001
NLR 1.226 1.159–1.297 <0.001 1.134 1.064–1.21 <0.001
Anemia 2.388 1.821–3.133 <0.001 1.479 1.051–2.083 0.025
Peri-intervention hydration 1.905 1.168–3.107 0.01 1.721 0.963–3.079 0.067
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aeGFR was calculated by CKD-EPI equation. AKI: Acute Kidney Injury; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; NLR: Neutrophil-to-Lymphocyte Ratio; NSTEMI: Non-ST-Elevation Myocardial Infarction; PCI: Percutaneous Coronary Intervention; STEMI: ST-Elevation Myocardial Infarction.

Given that a lower baseline eGFR was strongly associated with AKI after PCI, comparisons of characteristics and outcomes between patients with an eGFR ≥ 60 mL/min/1.73 m2 and those with an eGFR < 60 mL/min/1.73 m2 were performed (Supplementary Table 1). Hydration was more frequently applied in patients with poorer renal function (80.1% in those with an eGFR <60 mL/min/1.73 m2 vs 73.5% in those with an eGFR ≥60 mL/min/1.73 m2, p = 0.019). Comparisons between patients with and without AKI across different eGFR groups are presented in Supplementary Table 1. Among patients with an eGFR ≥ 60 mL/min/1.73 m2, acute heart failure, NLR, anemia, and diuretic use were significantly associated with the development of AKI (Figure 2A). In patients with a baseline eGFR < 60 mL/min/1.73 m2, a lower eGFR (OR 0.9, 95%CI 0.91–0.96, p < 0.001 when eGFR increased 1 mL/min/1.73 m2), NLR (OR 1.2, 95%CI 1.1–1.3, p = 0.001) and diuretic use (OR 2.3, 95%CI 1.2–4.8, p = 0.009) were independent risk factors for AKI after PCI (Figure 2B).

Figure 2.

Figure 2.

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Risk factors for AKI after PCI among patients with different baseline renal functions. (A) baseline eGFR ≥ 60 mL/min/1.73 m2. (B) baseline eGFR ≥ 60 mL/min/1.73 m2. Note: Multivariable logistic regression was conducted by been adjusting for the following factors: age, gender, acute heart failure, chronic heart failure, NLR, anemia, ACEI/ARB application, β-blocker application, diuretics application, diabetes and hydration. eGFR was calculated by CKD-EPI equation. ACEI/ARB: Angiotensin-Converting Enzyme Inhibitor/Angiotensin Receptor Blocker; AKI: acute kidney injury; CI: confidence interval; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; eGFR: estimated glomerular filtration rates; NLR: neutrophil-to-lymphocyte ratio; OR: odds ratio; PCI, percutaneous coronary intervention.

Hydration and AKI after PCI among oldest-old patients

PSM was therefore applied to balance the differences in baseline characteristics between patients who received perioperative hydration and those who did not (Supplementary Tables 2 and 3). The results showed that the incidence of AKI was higher in the non-hydration group than in the hydration group after PSM (14.8% vs 5.9%, p = 0.017, Supplementary Tables 4 and 5).

In a further investigation of the association between baseline eGFR and AKI after PCI in the hydration and non-hydration groups, the RCS curve demonstrated that the risk of AKI increased significantly when baseline eGFR was <67.4 mL/min/1.73 m2, regardless of whether patients received hydration or not (Figure 3). When baseline eGFR was higher than 67.4 mL/min/1.73 m2, patients had a lower risk of AKI after PCI; however, no statistical difference was observed between hydration and non-hydration groups. The RCS also demonstrated that there was no statistical difference between hydration and non-hydration group regarding the eGFR and risk to AKI after PCI, as the confidence interval was nearly completely overlapped.

Figure 3.

Figure 3.

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RCS analysis for the correlation between eGFR and risk of AKI after PCI by hydration groups. eGFR was calculated by CKD-EPI equation. Note: The analysis was adjusted for acute myocardial infarction (AMI), neutrophil-to-lymphocyte ratio (NLR), acute left heart failure, and anemia classification. AKI: acute kidney injury; CKD-EPI: Chronic Kidney Disease Epidemiology Collaboration; eGFR: estimated glomerular filtration rates; OR: odds ratio; RCS: restricted cubic spline.

Sensitivity analysis

The results based on the BIS1 formula for eGFR are presented in Supplementary Tables 6 and 7 and Supplementary Figures 1 and 2. We found that these results were substantially consistent with those derived from the CKD-EPI equation. Although the distribution of patients with an eGFR ≥ or <60 mL/min/1.73 m2 varied with the formula used, a reduced eGFR remained the strongest risk factor for predicting AKI after PCI.

Discussion

Our study identified a high incidence of AKI following PCI in the oldest-old population and recognized the associated risk factors. Baseline renal failure is critical for the development of AKI in this population, underscoring the importance of preventive strategies. Among patients undergoing PCI, AKI is a significant complication after the administration of contrast medium [11]. A meta-analysis involving 1.2 million patients reported a pooled incidence of contrast-associated AKI of 8% following PCI [27], whereas the incidence was substantially higher (15–35%) in patients with STEMI2. The number of studies focusing on the incidence of AKI in elderly patients after PCI is limited, and these studies typically involve small sample sizes: Qiu et, al. reported an incidence of AKI of 13% among 542 STEMI patients aged over 65 years who underwent PCI [28]; Leistner et, al. enrolled 458 patients aged over 80 years who underwent PCI and reported an incidence of 27.3% [8]. The heterogeneity in AKI incidence across studies was most likely attributable to differences in study populations and variations in the diagnostic criteria used to define AKI. In our study, the observed incidence of AKI (13.8%) in the total cohort was consistent with that reported in previous studies. However, through the innovative exploration of AKI incidence among oldest-old patients stratified by renal function, we found that patients with an eGFR < 60 mL/min/1.73 m2 (as calculated by the CKD-EPI formula) had a 5.6-fold higher risk of AKI compared with those with an eGFR ≥60 mL/min/1.73 m2. Our study emphasizes the importance of implementing comprehensive preventive measures against post-PCI AKI through close monitoring of dynamic renal function in the oldest-old population, particularly in those with baseline renal insufficiency.

The inherent characteristics of the aging kidney—characterized by structural and functional deterioration—may increase the susceptibility to AKI following PCI in the oldest-old patients [7]. Furthermore, patients with AMI requiring urgent coronary revascularization have a significantly increased risk of AKI, particularly those with hemodynamic instability or left ventricular dysfunction [29]. PCI itself introduces unique risk determinants beyond general contrast exposure, thereby rendering this population exceptionally vulnerable to AKI with substantial clinical implications. Most of the existing evidence indicates that reduced baseline eGFR and advanced age are independent risk factors for post-PCI AKI, with renal dysfunction showing the strongest association [13]. Notably, baseline renal impairment has been emphasized as the predominant risk factor for contrast-associated AKI. In our oldest-old cohort, the independent risk factors for post-PCI AKI were largely consistent with previous studies. Additionally, we found that the NLR, as a marker of inflammatory status, exhibited a positive association with the risk of post-PCI AKI in this oldest-old population. This observation may be explained in terms of the interaction between systemic inflammation and the pathogenesis of AKI. The NLR has been validated as an indicator of inflammation-associated physiological stress in previous studies [30]. Recent studies have also correlated elevated NLR with the incidence of AKI and mortality in patients undergoing cardiac surgery, gastrointestinal procedures, abdominal aortic repair, and major trauma [31–33]. Another inflammatory marker, CRP, was also observed to be elevated in patients with AKI, which is consistent with the hypothesis regarding the association between inflammation and the risk of post-PCI AKI [34]. However, further research into this hypothesis is warranted, particularly considering the evidence that contrast agents may modulate complement activation and that patients with AKI are predisposed to infectious complications. The inconsistency of risk factor identification between our study and previous evidence also indicates the presence of distinct mechanisms in this specific population.

Contrast-induced (CI)-nephropathy is the primary cause of AKI following PCI. Although the pathogenesis of CI-AKI remains incompletely elucidated, current evidence suggested that the underlying mechanisms involve nephrotoxicity, inflammatory activation, oxidative stress, reactive oxygen species production, and renal medullary ischemia [3,5]. To prevent CI-AKI, hydration remains the cornerstone with its beneficial effects widely recognized and strongly recommended in clinical guidelines [13,35]. Hydration prophylaxis is recommended for most patients with an eGFR < 60 mL/min/1.73 m2 [10]; however, controversy persists [11–16], and no significant benefits of saline hydration in preventing CI-AKI or improving long-term renal outcomes have been identified [17–19]. In our study, hydration prophylaxis also showed no beneficial effect on post-PCI AKI. Therefore, aggressive hydration regimens may paradoxically increase the risk of CI-AKI and post-PCI mortality in renal insufficiency (eGFR < 90 mL/min/1.73 m2) [36]. On the other hand, alternative hydration protocols hold promise, with sodium bicarbonate demonstrating superior efficacy compared with sodium chloride in stable patients with Scr >1.1 mg/dL [37]. Notably, critical gaps remain regarding hydration protocols—including type, timing, and dosage—in renally impaired individuals, particularly among the oldest-old [38].

The occurrence of post-PCI AKI is associated with long-term renal impairment, the need for renal replacement therapy, and subsequent all-cause mortality [21,39], rendering it a critical prognostic factor that demands heightened vigilance in the elderly. However, a significant evidence gap exists regarding the incidence of AKI and its associated factors in patients over 80 years old undergoing PCI, particularly when stratified by baseline renal function status. In the sensitivity analysis, we found that the results derived from BIS1 formula were substantially consistent with those based on CKD-EPI equation. Although the distribution of patients with an eGFR ≥ or <60 mL/min/1.73 m2 varied with different formulas, a declined eGFR remained the strongest risk factor for predicting post-PCI AKI. These results indicate heterogeneity in the estimation of renal function using different formulas.

The strengths of our study include the following: our investigation represents the largest cohort study to date evaluating post-PCI AKI in the oldest-old population. Prior studies in this population have primarily focused on incidence rates and conventional risk factors. Our analysis not only confirms severe renal impairment as a robust risk predictor but also identifies novel independent risk factors, including anemia and elevated NLR. Moreover, we found that conventional hydration prophylaxis exhibited limited clinical efficacy in this high-risk population. This necessitates the exploration of alternative protective strategies, including precision-guided hydration protocols utilizing real-time hemodynamic monitoring [40], as well as ultra-low contrast angiography or ‘zero-contrast’ PCI techniques [38].

Our study has the following limitations. Firstly, variable AKI definitions (RIFLE, AKIN, KDIGO) and inconsistent timing of post-PCI Scr assessment (24 h vs 72 h) directly contribute to substantial variation in reported AKI incidence, inconsistent evaluation of prophylactic interventions across studies, and potential underdiagnosis due to delayed elevation of creatinine [41]. Secondly, only in-hospital outcomes were recorded, and evaluations of AKI progression or recovery trajectories were not available. Thirdly, the exact dosage for each individual patient could not be obtained from the database, and thus the multivariable risk model may be potentially biased. Additionally, the wide confidence intervals of the RCS curves indicate potential uncertainty in the results. Our study found that in the oldest-old population with renal insufficiency, the incidence of AKI approaches one-third, signifying an extremely high risk; however, there is currently a lack of clear consensus or evidence addressing this clinical scenario. With the progression of population aging and the growing burden of cardiovascular and metabolic diseases, an increasing number of elderly individuals are undergoing PCI. Preventing PCI-related complications in this population will emerge as a critical clinical challenge, necessitating in-depth research into both mechanisms and clinical aspects to prevent complications such as AKI and improve prognosis.

Conclusion

Patients ≥80 years old with baseline renal failure confronted higher risk of AKI following PCI, and comprehensive strategies beyond hydration may be required for AKI prevention in this fragile population.

Supplementary Material

PCIsupplementary2025730R1.docx
IRNF_A_2560606_SM6621.docx (313.6KB, docx)

Acknowledgments

We acknowledge all healthcare personnel who contributed to this study. XL, WDZ, GHF and DYW conceived and designed the study, had full access to all study data, and take responsibility for the integrity of the data and the accuracy of the data analysis. YLC, HML, YZL and HYG collected the data. XL and DYW drafted the manuscript. YLC and JM performed the analysis. GHF and WDZ revised the manuscript, and all authors critically revised the manuscript for important intellectual content and gave final approval for the version to be published. All authors agree to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. No part of the material has been published or is under consideration elsewhere, including the Internet.

Funding Statement

This work has been supported by grants from Chinese Society of Cardiology’s Foundation (CSCF2024B01); Beijing Hospital Clinical Research 121 Project (BJ-2019-197); National High Level Hospital Clinical Research Funding (BJ-2023-086); National High Level Hospital Clinical Research Funding; Elite Medical Professionals. Project of China-Japan Friendship Hospital (NO. ZRJY2023-QM20), Professionals Initiative of China-Japan Friendship Hospital（NO.ZRJY2025-GG03) ; Chinese Academy of Medical Sciences (CAMS) Innovation Fund for Medical Sciences (CIFMS) (2021- I2M-1-001); CAMS Institute of Respiratory Medicine Grant for Young Scholars (2023- ZF-8).

Disclosure statement

The authors declare no conflicts of interest or financial relationships to disclose. No payment was provided to any individual for the production of this manuscript.

Data availability statement

Readers may access the data by contacting the corresponding authors to obtain permission.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

PCIsupplementary2025730R1.docx
IRNF_A_2560606_SM6621.docx (313.6KB, docx)

Data Availability Statement

Readers may access the data by contacting the corresponding authors to obtain permission.

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