Acute Kidney Injury Following Percutaneous Coronary Intervention for Acute Coronary Syndrome: Incidence,Aetiology,Risk Factors and Outcomes

Abstract

We investigated the predictors, aetiology and long-term outcomes of acute kidney injury (AKI) following urgent percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). Acute kidney injury occurred in 198 (7.2%) of 2917 patients: 14.1% of AKI cases were attributed to cardiogenic shock and 5.1% were classified as atheroembolic renal disease (AERD). Significant risk factors for AKI included age (odds ratio [OR] 1.05, 95% confidence limits [CI] 1.03-1.06), diabetes (OR 1.73, 95% CI 1.20-2.47), hypertension (OR 1.43, 95% CI 1.03-2.00), heart failure (OR 3.01, 95% CI 1.58-5.57), femoral access (OR 1.50, 95% CI 1.03-2.15), cardiogenic shock (OR 2.03, 95% CI 1.19-3.37) and ST-elevation myocardial infarction (STEMI) (OR 3.89, 95% CI 2.80-5.47). One-year mortality after AERD was 44.4% and renal replacement therapy (RRT) requirement 22.2% (compared with mortality 33.3% and RRT requirement 7.4%, respectively, in all other AKI patients). Mortality at 1 year was associated with AKI (OR 4.33, 95% CI 2.89-6.43), age (OR 1.08, 95% CI 1.06-1.09), heart failure (OR 1.92, 95% CI 1.05-3.44), femoral access (OR 2.05, 95% CI 1.41-2.95) and cardiogenic shock (OR 3.63, 95% CI 2.26-5.77). Acute kidney injury after urgent PCI is strongly associated with worse outcomes. Atheroembolic renal disease has a poor outcome and a high likelihood of long-term RRT requirement.

Keywords

acute kidney injury percutaneous coronary intervention embolism contrast media

Introduction

Acute kidney injury (AKI) following percutaneous coronary intervention (PCI) is common, ranging in occurrence between 3.3% and 14.5% of patients.^1-3 Acute kidney injury as a complication of PCI has been found to be a risk factor for increased mortality after PCI,⁴ as well as after myocardial infarction with,⁵ or without,⁶ cardiogenic shock.

Given the use of intravenous contrast media, AKI may be due to contrast-induced nephropathy (CIN), defined as a 25% relative increase, or a 44 μmol/L absolute increase, in serum creatinine within 72 hour of contrast exposure, in the absence of an alternative explanation.⁷ Kidney injury may also occur following haemodynamic instability due to cardiogenic shock, or from cholesterol embolization, termed atheroembolic renal disease (AERD), which typically occurs of an iatrogenic nature likely due to inadvertent vascular trauma with angiographic catheters.

This study investigated the incidence and aetiology of AKI after urgent PCI, as well as the risk factors predisposing to developing AKI. Analysis was also carried out into the risk factors associated with mortality in patients after PCI, and the risk factors for mortality in patients who develop AKI.

Materials and Methods

Patient Selection and Demographics

This was a single centre, retrospective cohort study of patients with acute coronary syndrome (ACS) referred to a regional cardiac centre. Consecutive patients (n = 2917) undergoing urgent in-patient PCI for ACS were retrospectively enrolled over a 3-year period (2012-2015). Using National Health Service numbers as a unique patient identifier, demographic data were collected along with serum creatinine level (n = 74,776), eosinophil count (n = 45,348) and erythrocyte sedimentation rate (ESR) (n = 546) which were obtained from local and national databases.

Individual baseline creatinine values were calculated as the mean of all serum creatinine values preceding the date of intervention (DOI). Where available this was used to identify patients who had an AKI at DOI (baseline ≥ 1.5 times that of DOI). If DOI creatinine values were not available for a patient, the baseline value was used as a comparator. Those patients who had AKI pre-intervention (n = 13) were undergoing renal replacement therapy (RRT) at the time of intervention (n = 13) or had no DOI creatinine value or baseline creatinine available (n = 149) were excluded from the dataset (Figure 1).

Incidence of Acute Kidney Injury

Comparison was made between creatinine values at DOI and available blood tests over the subsequent 14-day period for the 2742 patients who met the inclusion criteria. Acute kidney injury was identified as per National Institute for Health and Care Excellence (NICE) guidelines⁸; either as an increase in serum creatinine by ≥26 μmol/L within 48 h or an increase in serum creatinine ≥1.5 times that of DOI creatinine.

Identification of Aetiologies of AKI

After collecting the total number of AKI patients, the data was further analysed to identify the aetiology of AKI. Those presenting with cardiogenic shock were classified as a hypo-perfusion cause of kidney injury. Atheroembolic renal disease was identified if eosinophilia (>0.4 × 10⁹/L)^9,10 and/or elevated ESR (>30 mm/h)¹¹ was noted concurrently with the change in creatinine. To confirm the eosinophilia or elevated ESR was not related to other pathology, the medical history of patients was obtained, and eosinophil and ESR values prior to DOI were explored. In those patients not meeting the above criteria, the cause of AKI was determined to be contrast nephropathy.

Risk Factors for AKI

Demographic and cardiovascular risk factors were recorded including age, gender, body mass index (BMI), smoking status, hypertension and hypercholesterolaemia as well as past medical history (diabetes mellitus, previous stroke, previous renal transplant, heart failure [defined as left ventricular ejection fraction ≤30%], previous myocardial infarction [MI] and previous coronary artery bypass graft [CABG]). A comparison of the prevalence of these risk factors was made between the 2544 patients without AKI, and the 198 patients with AKI. We also investigated the potential effect of arterial access for the PCI (radial or femoral artery), whether cardiogenic shock had been present on arrival (defined as cool, clammy with pulse rate >100 beats/min, systolic blood pressure <100 mmHg, or inotropic support or intra-aortic balloon pump required), and volume of contrast given.

Survival After PCI for ACS With and Without AKI

The predictive value of identified risk factors (above) as well as the incidence of AKI was compared for 2 separate groups – those alive at 1 year after PCI and those who had died. The date of death of all patients was recorded to create survival curves after comparing patients that developed AKI after PCI with those that did not. The 198 patients diagnosed with AKI were further divided into 1-year survival and 1-year mortality subgroups to evaluate risk factors within the AKI group that might predict 1-year mortality, including presumed aetiology of AKI.

Statistical Analysis

Statistical analysis was performed using Prism 9, GraphPad (GraphPad Software, San Diego, United States). The unpaired Student’s “t” test was used to compare continuous variables (age and volume of contrast given) and the chi-square test was used to compare proportions of categorical variables in univariate analysis, with a 2-sided P < .05 deemed significant for all statistical tests. Multivariate analysis was carried out using multiple logistic regression, and differences in data were expressed as an odds ratio (OR) with 95% confidence limits (CI). Differences in 1-year survival were assessed using Cox regression described in terms of hazard ratios (HRs) and 95% CI and median time-to-events. Difference between survival curves was calculated using the log-rank approach.

Results

Baseline Characteristics

Baseline characteristics for the 2742 patients undergoing PCI for ACS after exclusion criteria between 2012 and 2015 are summarized in Table 1. Of the 2742 patients, 1582 (57.7%) had a recorded volume of contrast given.

Table 1.

Baseline Demographic Data (Prior to Exclusion).

	n	%
Total patients	2742	—
Age (years)	65.4 ± 12.4	—
Mean ± standard deviation
>75 Years	626	22.8
Male sex	1966	71.7
Diabetic	465	17.0
Hypertension	1489	54.3
High cholesterol	1378	50.3
Previous stroke	28	1.0
Renal transplant	115	4.2
Heart failure^a	73	2.7
Ex-/current smoker	1786	65.1
Previous MI	382	13.9
Previous CABG	129	4.7
Femoral access	428	15.6
Cardiogenic shock (on arrival^b)	118	4.3
STEMI presentation	1221	44.5
NSTEMI or UA presentation	1521	55.5
Volume of contrast given (ml)	183.7 ± 226.3	—
Mean ±standard deviation

MI, myocardial infarction; CABG, coronary artery bypass graft; STEMI, ST-elevation myocardial infarction; NSTEMI, non-ST-elevation myocardial infarction; UA, unstable angina.

^aDefined as left ventricular ejection fraction ≤30% on transthoracic echocardiogram.

^bCardiogenic shock defined as pulse >100 bpm, systolic BP <100 mmHg, cool, clammy or need for inotropic support/intra-aortic balloon pump.

Incidence and Aetiologies of Renal Injury

Acute kidney injury developed in 198 patients following PCI for ACS; 167 were identified as having AKI by the measure of a serum creatinine rise of ≥26 μmol/l within 48 hour, while 122 were identified as having AKI based on an increase in serum creatinine ≥1.5 times that of DOI creatinine. Therefore, 198 (7.2%) out of the total 2742 patients investigated satisfied 1, or both, of these criteria. Further analysis of the 198 patients with AKI showed that 28 (14.1%) had presented upon arrival in cardiogenic shock. Ten of the 198 patients with AKI were identified to have an eosinophilia and/or elevated ESR and were hence diagnosed as AERD, equal to 5.1% of all patients with AKI, and .4% of patients undergoing the procedure. One of the identified AERD also presented in cardiogenic shock.

There were 161 patients remaining with an AKI without cardiogenic shock, and without eosinophilia and/or raised ESR, and thus diagnosed as CIN. The frequency of each different aetiology of renal injury is shown in Table 2.

Table 2.

Number of Patients from AKI with Eosinophilia and/or Raised ESR, Cardiogenic Shock or Other Aetiology of AKI.

	n	% Total patients (n = 2742)	% Identified AKI (n = 198)
All AKI	198	7.2	100.0
CIN	161	5.9	81.3
Cardiogenic shock alone	27	1.0	13.6
AERD alone	9	0.3	4.5
Cardiogenic shock and AERD	1	.01	0.5
All cardiogenic shock	28	1.0	14.1
All AERD	10	0.4	5.1

AKI, acute kidney injury; AERD, atheroembolic renal disease; CIN, contrast-induced nephropathy; ESR, erythrocyte sedimentation rate.

Risk Factors for Developing AKI

Comparison of risk factors with multivariate analysis (Table 3) demonstrated that compared with non-AKI patients, the AKI group had a statistically significant higher mean age (OR 1.05, 95% CI 1.03-1.06, P < .0001), a higher prevalence of diabetes (OR 1.73, 95% CI 1.20-2.47, P = .0029), a higher prevalence of hypertension (OR 1.43, 95% CI 1.03-2.00, P = .0334) and a higher prevalence of heart failure (OR 3.01, 95% CI 1.58-5.57, P = .0006). Acute kidney injury was also more common in patients having PCI via femoral access (OR 1.50, 95% CI 1.03-2.15, P = .0318), patients in cardiogenic shock on arrival (OR 2.03, 95% CI 1.19-3.37, P = .0080) and patients presenting with ST-elevation myocardial infarction (STEMI) (OR 3.89, 95% CI 2.80-5.47, P < .0001). There was no significant difference between the 2 groups for volume of contrast given (Student’s t test: P = .8331).

Table 3.

Comparison of Demographic and Cardiovascular Risk Factors for Patients With, and Without, AKI After PCI.

	Non-AKI	%	AKI	%	Univ	Multiv
Total patients	2544	92.8	198	7.2		—
Age (years)	64.9 ± 12.3	—	71.7 ± 12.2	—	t 7.48*	1.05*
Mean ± standard deviation
Male sex	1829	71.9	136	68.7	.86
Diabetic	413	16.2	52	26.3	1.84*	1.73*
Hypertension	1364	53.6	125	63.1	1.48*	1.43*
High cholesterol	1283	50.4	95	48.0	.91
Previous stroke	26	1.0	2	1.0	.99
Renal transplant	110	4.3	5	2.5	.57
Heart failure	54	2.1	19	9.6	4.89*	3.01*
Ex-/current smoker	1673	65.8	113	57.1	.69*	.85
Previous MI	349	13.7	33	16.7	1.26
Previous CABG	118	4.6	11	5.6	1.21
Femoral access	372	14.6	56	28.3	2.30*	1.50*
Cardiogenic shock (on arrival)	90	3.5	28	14.1	4.49*	2.03*
STEMI presentation	1080	42.5	141	71.2	3.35*	3.89*
Volume of contrast given (ml)	183.9 ± 234.9	—	182.6 ± 77.1	—	t .21
Mean ±standard deviation

MI, myocardial infarction; CABG, coronary artery bypass graft; STEMI, ST-elevation myocardial infarction; PCI, percutaneous coronary intervention.

All data for univariate (Univ) and multivariate (Multiv) analysis are odds ratio unless stated t-test values.

*Statistically significant.

1-Year Survival Outcome

After multivariate analysis (Table 4), there was a significant difference in mortality in patients with an AKI (OR 4.33, 95% CI 2.89-6.43, P < .0001), a higher average age (OR 1.08, 95% CI 1.06-1.09, P < .0001), patients with heart failure (OR 1.92, 95% CI 1.05-3.44, P = .032), undergoing PCI via femoral access (OR 2.05, 95% CI 1.42-2.95, P = .0001) and presenting with cardiogenic shock (OR 3.63, 95% CI 2.26-5.77, P < .0001).

Table 4.

Comparison of Demographic and Cardiovascular Risk Factors Between 1-Year Survival and 1-Year Mortality After Non-elective PCI.

	1-year Survival	%	1-year Mortality	%	Univ	Multiv
Total patients	2548	92.9	194	7.1
AKI	131	5.1	67	34.5	9.73*	4.33*
Age (years)	64.7 ± 12.2	—	75.2 ± 11.4	—	t 12.27*	1.08*
Mean ± standard deviation
Male sex	1847	72.5	119	61.3	.60*	.93
Diabetic	414	16.2	43	22.2	1.47*	1.25
Hypertension	1366	53.6	115	59.3	1.26
High cholesterol	1285	50.4	104	53.6	1.14
Previous stroke	26	1.0	3	1.5	1.52
Renal transplant	110	4.3	4	2.1	.47
Heart failure	56	2.2	28	14.4	7.51*	1.92*
Ex-/current smoker	1675	65.7	111	57.2	.70*	1.04
Previous MI	351	13.8	40	20.6	1.63*	1.11
Previous CABG	118	4.6	12	6.2	1.36
Femoral access	361	14.2	76	39.2	3.90*	2.05*
Cardiogenic shock (on arrival)	104	4.1	53	27.3	7.17*	3.63*

AKI, acute kidney injury; MI, myocardial infarction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention.

All data for univariate (Univ) and multivariate (Multiv) analysis are odds ratio unless stated T-test values.

*Statistically significant.

Comparison of Survival Between AKI and Non-AKI

The median follow-up period for the patients was 2555 days (7.00 years), with interquartile range of 2291 days (6.27 years) to 2805 days (7.68 years). Analysis of survival between non-AKI and AKI groups demonstrated that AKI increased the risk of mortality with a HR of 4.23 (95% CI 3.00-5.98, P < .0001) and a median time of survival of 3.96 years (median time of survival was not reached in the non-AKI group, as the percentage survival was >50% during the follow-up period of 7.02 years for this group) (Figure 2). There was an assumption of proportional hazards and there was no evidence that the assumption was violated, P > .05.

1-Year Survival Outcome for AKI Patients

After multivariate analysis of the significant risk factors of 1-year mortality, mortality in patients with an AKI after 1 year was only significantly associated with increased age (OR 1.04, 95% CI 1.01-1.07, P = .01) and presenting with cardiogenic shock (OR 4.05, 95% CI 1.56-10.90, P = .004).

Discussion

In this study, we found that 7.2% of patients undergoing PCI for ACS developed AKI, which was in keeping with previous studies investigating incidence of AKI in PCI.^1-3 Results from the National Cardiovascular Data Registry (NCDR) Cath-PCI Registry³ demonstrate that after PCI, for any indication, the factors most strongly associated with development of AKI included STEMI, severe chronic kidney disease and cardiogenic shock. In our series of patients presenting with ACS, multivariate analysis revealed, age, diabetes mellitus, hypertension, heart failure, femoral access, STEMI presentation and cardiogenic shock as significant risk factors for the development of AKI after PCI. Importantly, we did not find any association between the volume of contrast given and AKI.

Although there is a demonstrated association between contrast medium volume and CIN,^12-15 there are also a number of studies that have demonstrated no significant link.^16,17 Where volume of contrast has been shown to be a risk factor for developing CIN, much higher average volumes of contrast were used than those recorded in our study (378 ± 200 vs 183 ± 77 mL).¹⁴ This, may explain our finding that contrast volume was not a risk factor for the development of AKI.

The risk of developing CIN in particular has also been widely studied, with a systematic review of 16 scoring systems being published.¹⁸ This demonstrated the models with “good discriminative ability included measures of chronic kidney disease, age, diabetes mellitus, heart failure or impaired ejection fraction and hypotension or shock.

While the pathophysiology of AKI in ACS after PCI can be multifactorial, its presence is associated with worse mortality irrespective of the cause.¹⁹ Our investigation of the risk factors for 1-year mortality demonstrated a significant higher probability of mortality in patients with AKI who were older, had femoral rather than radial access for performing PCI and presented with cardiogenic shock. Radial arterial access has been previously associated with less AKI after PCI for ACS than femoral.²⁰ This may be due to a number of factors such as reduced access site bleeding or less AERD. In any case, given the paucity of treatment options for AERD, it is a strong reason to favour radial over femoral arterial access when possible.

Atheroembolic renal disease is a significant but commonly overlooked diagnosis, despite being associated with a poor prognosis. The condition stems from diffuse atherosclerosis of the aorta, disruption of which can lead to emboli to other organs.²¹ Embolization of cholesterol crystals²² to the kidneys leads to an inflammatory reaction and thrombus formation causing arterial obstruction.²³ Renal biopsy is regarded as the definitive method for diagnosis and is able to detect emboli in 75% of cases,²⁴ although due to clinical instability, biopsy of skin lesions may be preferred, with high diagnostic sensitivity.²⁵

Given the risk of renal biopsy, if the classical triad of precipitating factor, acute/subacute renal failure and cutaneous signs of cholesterol embolization is present, then biopsy is not required for diagnosis.²⁶ Regarding laboratory tests for diagnosis, eosinophilia (defined as the equivalent of >0.5 × 10⁹/L) has been demonstrated in 71% of iatrogenic cases of AERD in one study,⁹ and 80% of AERD of all causes in a separate study.¹⁰ Erythrocyte sedimentation rate (>30 mm/h) was elevated in 97% of patients with histologically proven AERD in which ESR was reported.¹¹ Differing data exist for the reliability of hypocomplementemia in the diagnosis of AERD.^27-29 The treatment for AERD is mostly supportive, although there is some evidence that statin use, either prior to, or after, AERD diagnosis, may benefit prognosis.⁹

All patients with eosinophilia >0.5 × 10⁹/L and concurrent AKI had a rise in eosinophils from a baseline value <0.5 × 10⁹/L, except for 1 patient with a baseline of 0.5 × 10⁹/L. In this case, there was a further rise in eosinophil count from this baseline value after intervention. Only 1 patient had a diagnosis of AERD made on the basis of an ESR rise. In this same patient, there was also an increase in eosinophil count from a baseline normal eosinophil count prior to intervention. Investigation of past medical history of each of the cases of AERD for common causes of eosinophilia (neoplasia, parasitic infection, allergic disorders and connective tissue diseases)³⁰ and elevated ESR (infections, neoplasia, renal disease and inflammatory disorders)³¹ showed 1 patient with pre-existing prostatic malignancy, and another one with rheumatoid arthritis. Both of these patients had a normal eosinophil count prior to emergency PCI, which then increased after intervention, and neither had an ESR reported after intervention.

We found eosinophilia and/or raised ESR was present in 5.1% of the patients with AKI, in keeping with a diagnosis of AERD.^9,10 These patients with AERD AKI had a 1-year mortality rate of 44.4% and a 1-year RRT requirement of 22.2%. This was compared with a 1-year mortality rate of 33.3% in AKI patients of other etiologies, and a RRT requirement of 7.4%. We found a 1-year mortality of 5.0% in the non-AKI group, and a RRT requirement of .3%. This was in keeping with other papers for survival and renal replacement requirement in AERD. In a prospective study of 95 patients with AERD, the mortality rate was 37.9%, and end stage renal disease had developed in 24%²⁷ over a mean follow-up period of 61.5 months (5.13 years). Similar findings were noted in another study, where 354 patients with AERD followed up for 2 years had a mortality rate of 28.8% and a RRT requirement of 32.7%.⁹ In both these studies, iatrogenic AERD was diagnosed in the presence of: (1) renal function deterioration in atherosclerotic patients; (2) simultaneous ischaemic changes to the lower abdomen and/or extremities and (3) presence of 1 or more precipitating factors, including arterial angiography, while spontaneous AERD was diagnosed when tissue biopsy demonstrated cholesterol clefts, or fundoscopic examination disclosed retinal emboli.

Coronary angiography via the femoral artery is the most common procedure causing AERD,⁹ and – although the exact incidence is not known – between 1.1% and 4.25% of patients are thought to develop AERD after coronary intervention, diagnosed by tissue biopsy.³²

Regarding all patients undergoing PCI in our study, we found .4% of patients who subsequently developed an AKI with an eosinophilia and/or ESR, which is lower than that in previous studies (1.1-4.25%),³² and this may be because serum analysis alone may miss some cases of AERD. It is also likely that our institute incidence of AERD may be lower than previously reported due to high levels of radial artery access for all patients (84.4%). We found that the rate of femoral access in patients developing AERD (33.3%) was twice that of patients who had undergone PCI and did not then develop an AKI (14.6%).

This study has some limitations. Firstly, this was a retrospective analysis and contrast volumes and BMI were not available for all patients. Of the 2742 patients included, 2323 (84.7%) had their BMI documented, 1582 (57.7%) had the volume of contrast administered documented and 1405 (51.2%) had values for both BMI and contrast volume recorded. We found no significant difference between contrast volumes given to patients who subsequently developed an AKI, compared with the group that did not on univariate analysis, with a high number of patients studied (n = 1582). This finding was also the case when contrast volume per body surface area was analysed, for a high number of patients studied (n = 1405).

Secondly, we found STEMI presentation was an independent risk factor for developing AKI. However, door to balloon times were not included in the analysis. Patients with NSTEMI will have longer in-hospital time before PCI than patients with STEMI and as such may be less volume depleted and more likely to receive adequate pre-hydration. Although patients with pre-existing AKI immediately prior to angiography were excluded, this still may have affected the result of the analysis if any of the STEMI patients were relatively dehydrated.

Thirdly, medications taken by patients undergoing urgent PCI were not included in the analysis so potential nephrotoxic medications that patients were taking prior to intervention, or were started after intervention, were not recorded.

Finally, we used biochemical parameters alone to define AERD. While this is a less definitive diagnosis than the gold standard of histological confirmation, it has been used previously when diagnosing iatrogenic AERD with a clear precipitating event.⁹

Conclusion

Acute kidney injury is a common complication post-PCI associated with poor outcomes and is more likely with STEMI presentation and cardiogenic shock. Importantly, femoral access is independently associated with increased risk of AKI and 1-year mortality. In patients with AKI post-PCI, a diagnosis of CIN is often, but potentially wrongly, made. Acute kidney injury in a patient with recent vascular insult, multiple cardiovascular risk factors, signs of peripheral embolization and/or an eosinophilia, should prompt the clinician to consider a unifying diagnosis of AERD. Given the often-emergent nature of PCI in patients following ACS, strategies to limit AERD are limited but consideration should be given to using radial arterial access whenever possible.

Footnotes

Author Contribution

All authors contributed to: (1) substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data; (2) drafting the article or revising it critically for important intellectual content and (3) final approval of the version to be published.

Declaration of Conflicting Interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Elliott J Carande

Nicholas Maskell

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