A Study of Prevalance of Contrast Induced Nephropathy in Patients of Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention

Dr. Anjali Sharma *¹, Dr Amit Munjal ², Dr Prachi Arun ³, Dr. Naveen Chandra⁴, Dr. Maneera Dhasmana⁵

1. Cardiologist, Anjali Heart Care Centre, Dehradun, Uttarakhand, India.

2. Cardiologist, Munjal Multispeciality Hospital, Fatehabad, Haryana.

3. Associate professor, Dept of pathology, MAMC, AGROHA, Haryana, India.

4. Physician, Anjali Heart Care Centre, Dehradun, Uttarakhand, India.

5. Physician, Max Super Speciality Hospital, Dehradun, Uttarakhand, India.

*Correspondence to: Dr. Anjali Sharma, Cardiologist, Anjali Heart Care Centre, Dehradun, Uttarakhand, India.

              
Copyright.

© 2025 Dr. Anjali Sharma This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: 05 Apr 2025

Published: 19 May 2025

Abbrevations

CIN     -Contrast induced nephropathy

CM      -Contrast media

AKI     - Acute kidney injury

PCI      -Percutaneous coronary intervention

ESRD  -End stage renal disease

CAG    -Coronary angiography

S.Cr     -Serum creatinin

CABG -Coronary artery bypass grafting

CKD    -Chronic kidney disease

IABP   -Intra aortic balloon pump

EF       -Ejection fraction

LOCM -Low osmolar contrast media

HOCM  -High osmolar contrast media

eGFR   - Effective glomerular filtration rate

NO      -Nitric oxide

MDRD -Modified diet in renal disease

BUN    -Blood urea nitrogen

NAC    -N-actyle cystein

CCF -Congestive cardiac failure

ACS  -Acute coronary syndrome

Hb       -Haemoglobin

STEMI            -ST elevation Myocardial infarction NSTEMI -Non ST elevation Myocardial infarction

UA      - Unstable angina

CBC    -Complete blood count

KFT     -Kidney function test

SVD    -Single vessel disease

DVD    `-Double vessel disease

TVD    -Tripple vessel disease

CVA    -Cerebrovuscular accident

PTCA  - Percutaneous coronary angiography

HTN    -Hypertension

DM      -Diabetese mellitus

MACE -Major adverse cardiovascular event

CI-AKI            -contrast induced acute kidney injury

LAD    -Left anterior decending artery

ACEI   -Angiotensin converting enzyme

 

Introduction

Contrast-induced nephropathy (CIN) also known as contrast-induced acute kidney injury is an iatrogenic renal injury that follows intravascular administration of radio-opaque contrast media (CM) in susceptible individuals. CIN was first described during the 1950s in case reports of fatal acute renal failure that had occurred following intravenous pyelography in patients with renal disease arising from multiple myeloma.1, 2

CIN is responsible for a third of all hospital-acquired acute kidney injury (AKI)3, 4 and affects between 1% to 2% of the general population and up to 50% of high-risk subgroups following coronary angiography (CA) or percutaneous coronary intervention (PCI).5

Increase in number of imaging methods and interventional procedures involving use of intravascular CM in both non-cardiac modalities and cardiac modalities has significantly increased the number of patients exposed to CM and thus risk of CIN.

Despite several therapeutic approaches, the rising age and incidence of comorbidity within cardiac patients receiving CM ,CIN remains a significant clinical challenge.6

CIN is a field of ongoing research with focus on pathophysiological mechanisms as well as novel risk assessment, preventative, diagnostic and therapeutic measures.

With growing number of percutaneous procedure in present time there is need to know the current incident of contrast induced nephropathy and its short and long term outcomes as well there is need to know various related risk factor which are predisposing patient for developing contrast induced nephropathy.

CIN represents a significant clinical and health economic problem that may be under- recognised limitations in the currently available biomarkers. Although often a transient injury, CIN may progress to significant persistent renal impairment, ESRF and adverse cardiovascular outcomes. There are a number of recognised risk factors, although the prediction of CIN, particularly prior to contrast administration, remains challenging.

Current interventions are largely centred on the avoidance of dehydration, the withdrawal of nephrotoxic agents and minimisation of contrast load, which has limited efficacy in preventing CIN in vulnerable patients. The unmet clinical need in CIN therefore resides in accurate prediction, effective intervention and rapid detection to prevent adverse cardiorenal outcomes.

Each of these areas, particularly predictive risk scoring systems, innovative pharmacological and mechanical interventions and novel biomarkers are currently the subject of intensive research and development that may lead to the future development effective strategies to mitigate the risk of CIN.

 

Aims and Objectives

Aim of present study is to find the prevalance of contrast induced nephropathy in patients of Acute coronary syndrome undergoing percutaneous intervention and to study short term outcome at 1 month .

 

Specific Objectives :

1. To find out the prevalence of CIN in ACS who undergoing emergency procedure.

2. To find the risk factor of CIN in patient with normal kiney function .

3. To evaluate the short term outcome.

 

Material and Methods:

STUDY PLACE :Department of cardiology, Metro Hospitals and heart institute, Noida

STUDY POPULATION: This is a hospital based prospective observational study, was conducted at Metro Hospitals and Heart Institute including patients with Acute coronary syndrome who had undergone percutaneous coronary intervention in 1 year duration Jan 2017 to Dec 2017, 100 patients were studied fulfilling inclusion and exclusion criteria and had given informed concent .

 

Inclusion criteria

Persons between  25 to 80 years

Patients with acute coronary syndrome undergoing percutaneous coronary intervention.

Exclusion criteria

Patient having pre-existing CKD or GFR <60ml /min Anemic patient (Hb < 9gm%)

Who denied to take part in study . SAMPLE SIZE : 100 .

STUDYPERIOD:        One year (Jan -2017 to Dec- 2017)

STUDY DESIGN: prospective observational study

 

METHODS : We have taken patient who admitted to metro hospitalsand heart institute with acute coronary syndrome and had undergo percutaneous intervention. Patient with acute coronary syndrome include STEMI , NSTEMI and Unstable angina were taken . ACS is defined as (1) onset of symptoms at rest (or with minimal exertion) and lasting longer than 10 minutes unless treated promptly; (2) severe, oppressive pressure or chest discomfort; and (3) an accelerating pattern of symptoms that develop more frequently, occur with greater severity, or awaken the patient from sleep.

 

STEMI is defined by symptoms of myocardial ischemia associated with persistent electocardiographic evidence of ST elevation and subsequent elevation of biologic markers of myocardial necrosis. According to the universal definition of myocardial infarction (MI), ST elevation is defined as new ST elevation of at least 2 mm in men or 1.5 mm in women in at least two contiguous leads. (40)

NSTEMI is defined as Patients with chest pain without persistent (>20 minutes) ST-segment elevation in two or more contiguous leads but with biomarker evidence of myocardial necrosis are classified as having NSTEMI, whereas in patients without biomarkers positive , UA is diagnosed.

History and examination: Patient presented with symptoms suggestive of ACS were included in study detailed history ,general physical and systemic examination was done. 12 lead ECG was done and classified as STEMI if ST elevation of >2mm in two or more contiguous leads . patients with ECG without ST elevation biomarker testing ( Se. troponin T) was done, those with positive biomarker diagnosed as NSTEMI and those with negative results diagnosed as Unstable angina.

Baseline routine blood investigation was done including CBC, ESR, KFT, HbA1C, TropT, eGFR, was calculated using MDRD equaton (modification of diet in renal disease), GFR (mL/min/1.73 m2) = 175 × (Scr)-1.154 × (Age)-0.203 × (0.742 if female), HbA1C was done in diabetics designated (HbA1C < 6.4), uncontrolled diabetics as HbA1C > 6.4.

2-D Echocardiography: 2D echo was done to estimate Ejection fraction : normal LV function EF >50% , LV dysfunction EF <50%.

Percutaneous intervention: Percutaneous intervention was done with standard protocol l. Angiographic findings are reported as having SVD, DVD or TVD. Contrast media used was Omnipaque/Visipaque. Volume of contrast used for procedure will be noted in all patients . At 48 -72 hour again KFT was done and eGFR was calculated using MDRD equation. Patient who had 25% increase in eGFR were diagnosed to have contrast induced nephropathy. Patient were followed at 1 month for any improvement or detioration in kidney function and occurrence of any MACE .

STUDY DURATION: one year( Jan 2017 to Dec 2017 )

STATISTICAL ANALYSIS : All the statistical analysis was performed using SPSS version 20. The clinical profile of patients was analyzed by chi-square test for qualitative variables and student t test for quantitative variables. 5% probability level was considered as statistically significant i.e. p<0.05.

 

ETHICAL CONSIDERATION: The study protocol was approved by the local Ethics Committee and written informed consent was obtained from all the patients.

 

Observations and Results :

Baseline charrecteristics: we have studied total 100 patient who presented with ACS and had undergone emergency percutaneous intervention .Baseline demographic, clinical and angiographic characteristics are as following. Overall the mean age was 60.76 years and sex distribution 17% were females and rest were male. All patient presented with chest pain, 26% patient were Diabetic, Overall 25% were hypertensive, 79% were smoker, past history CVA was present in 2%, on presentation ECG showed STEMI, in 23%,27% had NSTEMI and 49% had unstable angina, Mean LVEF < 42.5% ,baseline mean Hb was 12.3±1.3, Trop T was positive in 51%, mean baseline serum creatinine level was 0.9mg/dl ± 0.1 mg/dl ,the mean baseline eGFR was 87 ± 22.6 ml/min/1. Mean volume of contrast agent administered during PCI was 101.5± Angiographic finding was SVD in 64%, DVD in 24% , TVD in 12 %. IABP was placed in 2%.

Baseline demographic, clinical and angiographic characteristics as well as main procedural data are listed in Tables1.

Please click here to view all tables and figures

Results

In our study of 100 patient we observed 21% patient showed evidence of CIN at 48 hour after percutaneous intervention. Mean age in non CIN group was 59 ± 10yrs and and in CIN group 64 ± 12 yrs (P value = . 09 ). Out of 17% females, 6% develop CIN (P =0 .112) . Mean LVEF < 42.5% in non CIN patient and < 39.5 % in those with CIN( P = 201) . 26% patient were Diabetic, 3% diabetic develop CIN, (P value=.169). Overall 25% were hypertensive, 5% develop CIN (P value = 0.887). 79% were smoker out of which 10% develop CIN, (P = 0.212) . 23% had STEMI, 27% had NSTEMI and 49% had unstable angina, 4% in STEMI, 9% in NSTEMI and 7% in Unstable angina develop CIN (P value=0.190). Trop T was positive in 51%, 14% develop CIN( P value=0.106). On statistical analysis the mean baseline serum creatinine level was 0.9 ± 0.1 mg/dl in non CIN patients and .8 ± 0.2 mg/dl in CIN patients (P = .08). Furthermore, the mean baseline estimated glomerular filtration rate (eGFR) was 87 ± 22.6 ml/min/1.73ml in non CIN patients, while mean GFR in CIN patients was 98 ± 31 ml/min/1.73m2) (P value=.07). At 48- 72 hour mean serum creatinin was 1 ± 0.3 mg/dl in non CIN group, in CIN group it was 1.2±0.0 (P value = .05). eGFR at 48 -72 hr was 78.40 ± 23 ml/min/1.73m2 in non CIN patient, and in CIN patients it was 67.6 ± 29.4 ( P value=.05). on follow up at 1 month Serum cretinin was 1.0 ± .7 mg/dl in non CIN and 1.0 ± .3 in CIN patients ( P=0.9) , eGFR at one month was 78.46 ± 20 in non CIN and in CIN it was 71 ± 24.7 ml/min/1.73m2 (P value= .70). Mean volume of contrast agent administered during PCI in non CIN patients and 107±24 ml in CIN patients (p value=0.14). Baseline Hb was 12.3±1.3 in non CIN patient and 11.4 ± 0.9 in CIN group (p value=.001) . Angiographic finding was SVD in 64%, DVD in 24% , TVD in 12 % in 16% SVD and 5.1% DVD and no one with TVD develop CIN ( Pvalue =.149). Past history CVA was present in 2%, 1% develop CIN( P value=309). IABP was placed in 2% and no one develop CIN (Pvalue =.461).

On logistic regression model Hb is significant { B -1.54, SE=.35, CI for EXP lower limit = .107; upperlimit = .427, (P=.000)}, Logistic regression of eGFR B{=.06, SE=.022, CI of EXP lower limit =1.024; upper limit = 1.116 (P=.002)}. eGFR and Hb emerged as independent predictors of the outcome with a p value <0.05.

 

On basis of above findings and statistical analysis eGFR at 48 – 72hr found significantly related to occurrence of CIN, we also found Hb level to be significantly associated with occurence of CIN in acute coronary syndrome patient. We also found that age ,sex, smoking, diabetes mellitus, Hb , LVEF, IABP, number of vessels involved, past history of CVA, volume of contrast media, ECG finding, and Trop T was not found to be significantly associated with occurrence of CIN in acute coronary syndrome patient with normal renal function as evident by baseline eGFR >60 ml/min/1.73m2 .

We conclude that prevalence of CIN in present study in patient of ACS undergoing emergency percutaneous procedure, with normal baseline renal function is 21%. eGFR is a better predictor of occurrence of CIN after percutaneous intervention then serum creatinine and Hb levels are independent predictor of occurrence of CIN .

Discussion

The reported incidence and clinical significance of CIN varies among studies. This study demonstrates that CIN is a frequent complication in high risk ACS patients undergoing PCI even in patients with normal baseline renal function, and is associated with increased in-hospital morbidity and prolonged hospitalization. Our study is among the first to examine the prevalence of CIN in ACS patients undergoing emergency PCI using eGFR  and follow up at 1 month in tertiary care center in north india. In this study special care was given to assess pre-existing co-morbidities and include patients with near normal baseline renal function. Our study is unique because we have used eGFR as the diagnostic criteria ,secondly we have done follow up these patient at one month to determine the short term outcome of renal function and MACE .

Indeed, accurate assessment of incidence, co-morbidities and risk of CIN, in overburdened cardiology center have not been assessed in the general population and in current practice, due to short time admission and short hospital stay. Several risk factors have been identified for contrast induced nephropathy post PCI.30

In a study by Rehal et al.[31] and based on Mayo clinic PCI registry ,the incidence of PCI in the general population was 3.3%, and dialysis was needed in 0.3% .However, this rate might rise up to 20% or more in selected patient subsets , especially in patients with underlying cardiovascular disease[32] and even to 50% in high risk patients[33-35]. It should be considered ,however ,that renal deterioration after angiography usually occurs transiently, and persistent renal failure requiring dialysis or other clinically severe renal events are rarely reported.[36-39].

Ying Yuan et al. Studied incidence of CI-AKI in patients undergoing emergency PCI was 22.7% which is well correlated with our study, and they found that history of MI, low BSA, LVEF and Hb level, LAD stented, and diuretics use are associated with increased risk of CI-AKI in patients undergoing emergency PCI. In our study we have found Hb level are significantly associated with occurrence of CIN correlating well with the yig yuan findings. 40

 

Mehmet Can Ugur et al. found CIN rate was 22.8% which is again well correlated with our study they found the use of ACEIs and hyperkalemia were found to be associated with the development of CIN (p=0.026 and p<0.001, respectively)41

Thomas T. Tsai et al. found that approximately 7% of patients undergoing PCI experience AKI, which is strongly associated with in-hospital mortality . In a large national cohort study of post-PCI patients, they found that AKI developed in 7.1% of patients, 0.3% of whom required acute dialysis. In risk-adjusted models, clinical factors such as STEMI presentation and baseline CKD markedly increased the risk of the development of AKI or AKI-D. In addition, patients with AKI or AKI-D in the hospital experienced very high rates of in-hospital bleeding, MI, and death. 42

Bartholo-mew et al., identified 8 variables that were associated with contrast induced nephropathy creatinine clearance < 60 ml/min, use of an IABP, urgent coronary procedure, diabetes, chronic heart failure, hypertension, peripheral vascular disease, contrast volume.43 Patients in the highest risk group had a 28% risk of developing contrast nephropathy.44

Mehran and colleagues on top of creatinine clearance <60 ml/min, use of IABP, chronic heart failure, diabetes mellitus and contrast volume identified 3 additional characteristics that were associated with increased risk: older age, the presence of hypotension, and anemia. In their risk score, patients in the highest quartile of risk were associated with an approximately 55% risk for developing contrast induced kidney injury. Also In our study we found low Hb levels are independent risk factor for CIN. 45

 

Because of the high risk of CIN, it is important to evaluate renal function. Biomarkers for renal function include Serum Creatinine, Creatinine clearance calculated using the Cockroft– Gault formula 46, eGFR 47, and Cystatin C 48. Among them, Serum Creatinine is most commonly used to assess renal function in routine clinical practice. However, Serum Creatinine does not provide a reliable measurement of renal function because it depends on muscle mass, age, sex, diet and so on. On the other hand, although Cystatin C is independent of these factors and can reflect even small changes in renal function, it is not practical for use in emergent situations. Therefore, the use of creatinine clearance or eGFR is recommended for the assessment of renal function.49 as in our study we have also used eGFR as assessment tool for CIN, we observed that at 48 hour no significant change in serum creatinine but change in eGFR was significantly related to CIN .

Mechanism or pathogenesis of CIN is not well understood, there is increasing evidence that it occurs as a combination of direct toxicity to the renal tubular epithelium, oxidative stress, ischemic injury, and renal tubular obstruction.50-52 Also, increased intra-tubular pressure secondary to contrast-induced diuresis and increased perivascular hydrostatic pressure may lead to medullary hypoxia through lower medullary blood flow. Renal ischemia may be the result of an imbalance between vasoactive substances (Adenosine and Endothelin) and vasodilators (NO and Prostaglan-dins).53 Significant urine volume is needed to clear the high osmotic load of the contrast medium. Exposure to this high osmotic load results in characteristic histopathological changes of osmotic nephrosis, a morphological pattern with vacuolization and swelling of the renal proximal tubular cells. 54 In a study, this finding was seen in almost a quarter (22%) of patients undergoing renal biopsy within 10 days of contrast exposure.

 

55 All of our patients had a normal renal function before PCI, but a high incidence of CIN might be because of emergency procedure. When creatinine clearance was calculated in our population, a greater number of patients showed reduced baseline renal function (creatinine clearance <60 ml/min). Numerous studies have shown that the volume of contrast medium is a risk factor for contrast induced renal injury. Recent reports suggested the use of more refined indices of contrast volume use as predictors of CIN such as the contrast ratio 56 reflecting body size effect and the volume to creatinine clearance ratio 57. The 250 ml cut-off point was chosen arbitrarily based upon data showing that the average contrast volume used is usually between 250 and 300 ml 56 ,57 but contrast volume used in our study was quiet low ,mean volume of contrast used in patient with CIN was 107 ± 27.6 ml.

Once CIN is established, only supportive care should be given until renal function resolves; infrequently hemodialysis may be required either transiently or permanently but we don’t have observed any patient with persistent renakl failure, all our patients recovered renal function as evaluated by eGFR at one month. Therefore, presently the mainstream approach to overcome this complication is its prevention. This study will allow a pre-procedural identification of high risk patients and implementation of appropriate preventive measures in over burdened Indian hospital setup.

 

Study limitations Our study has some limitations. First, our study included a small population, admitted to a single centre. Furthermore, neither proteinuria nor kidney structure was studied. In our study, 21% developed acute renal failure within 48 h, we cannot exclude the possibility that other factors, such as hemodynamic instability, might have contributed, at least in part, to renal impairment, and influenced the clinical outcome of our patients. This suggests that kidney hypoperfusion, resulting in ischemic renal injury, might play a major role. In addition, our study only reported short term outcomes; thus, no conclusions on long-term mortality and morbidity could be made. These findings should be confirmed in a large multicentre trial and investigated for the long-term effects of CIN.

 

Conclusions

In the era of PCI for CAD patients, CIN is a frequent complication, even in patients with normal renal function, and is associated with a more complicated in-hospital course, though most patient recover spontaneously.

In overburdened Indian hospitals, CIN is frequently underreported because of day care procedures and early discharge.

Since CIN course is mostly benign in normal renal function patients and recovered completely in most of the cases, in some cases it is life threatening. So every attempt should be made to prevent this.

Thus, special care and newer preventive strategies of renal protection during PCI are warranted, particularly in high-risk patients.

Despite uncertainty regarding the degree of nephrotoxi-city produced by various contrast agents, nonionic low-osmolar or iso-osmolar contrast media remains the preferred choice.

Best way to prevent CIN is to identify patients at high risk and provide as low as possible volume administration.

High risk patient must be identified before procedure and risk factors must be addressed to all patients before initiation of procedure.