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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2017  |  Volume : 28  |  Issue : 2  |  Page : 318-324
Risk factors for contrast-induced nephropathy after coronary angiography

1 Department of Medicine, Armed Forces Medical College, Pune, Maharashtra, India
2 Department of Nephrology, Army Hospital (R&R), New Delhi, India
3 Department of Cardiology, Army Hospital (R&R), New Delhi, India
4 Department of Endocrinology, Army Hospital (R&R), New Delhi, India

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Date of Web Publication23-Mar-2017


Contrast-induced nephropathy (CIN) is of concern after the use of radiocontrast media for coronary angiography (CAG) and percutaneous coronary intervention (PCI). We studied the incidence of CIN and its risk factors in patients undergoing CAG. In this prospective study, we included all patients with normal renal parameters undergoing CAG with nonionic radiocontrast media. We excluded patients with known chronic kidney disease, baseline creatinine more than 1.5 mg/dL, significant hypotension, anemia, and patients with acute myocardial infarction undergoing emergency PCI. Serum creatinine was done at baseline and serially for seven days after the procedure. Appropriate statistical tests were used to analyze the results and P <0.05 was considered statistically significant. The study population (n = 500, 348 males and 152 females) had a mean age of 56.6 ± 12.5 years. Twelve patients (2.4%) developed CIN and were equally distributed irrespective of the age, diabetes, or PCI procedure. CIN was observed to be more common in patients with hypertension than in those without hypertension (P = 0.0158). The total volume of contrast administered to CIN group (175 ± 59.3) was not significant as compared to that of non-CIN (159.1 ± 56) group (P = 0.334). None of the patients in our study required renal replacement therapy, and there was no mortality. CIN is observed in 2.4% of patients undergoing CAG and had a self-limiting course. Hypertension is the only observed risk factor, and further large-scale studies are necessary to delineate the novel risk factors for CIN in the general population with normal kidney function.

How to cite this article:
Kumar S, Nair RK, Aggarwal N, Abbot A K, Muthukrishnan J, Kumar KH. Risk factors for contrast-induced nephropathy after coronary angiography. Saudi J Kidney Dis Transpl 2017;28:318-24

How to cite this URL:
Kumar S, Nair RK, Aggarwal N, Abbot A K, Muthukrishnan J, Kumar KH. Risk factors for contrast-induced nephropathy after coronary angiography. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2022 Dec 4];28:318-24. Available from: https://www.sjkdt.org/text.asp?2017/28/2/318/202758

   Introduction Top

The use of iodinated radiocontrast agents to delineate normal structures for diagnostic or therapeutic purposes represents a major advancement in the field of medical imaging. The use of intravascular contrast media (CM) has been increasing steadily over the past few years with different types each claiming to minimize the side effects.[1] Contrast-induced nephropathy (CIN) is one of the common and serious adverse effects of the procedures using CM.[2] Various studies have reported the incidence of CIN to be between 2% and 50%, depending on the definition of CIN.[3],[4],[5] CIN is the third most common cause of “in-hospital” acute kidney injury (AKI), after hypotension and surgery. CIN is a preventable cause of AKI, and hence it is imperative to ensure the judicious use of CM in patients to prevent the associated complications.

Coronary angiography (CAG) for diagnostic or therapeutic purposes such as percutaneous coronary intervention (PCI) is one of the common procedures which require the use of intravenous CM. The reported incidence of CIN in high-risk patients following CAG varies from 10% to 20%.[6] The high rate of CIN in post-PCI patients could be related either to the patient (advanced age, previous CKD, diabetes, dehydration, and concomitant use of other nephrotoxic drugs) or procedure related (intra-arterial route of administration, use of high osmolar CM, repeated exposure to contrast within 48 h, volume of contrast used, etc.).[7] The prevention of CIN is of paramount importance, with an ever increasing number of CAGs and PCIs being done on an outpatient basis.[8] We conducted this study to detect the incidence of CIN in patients undergoing CAG with an aim to identify the subset of patients who are at high risk for CIN after cardiac catheterization and PCI.

   Materials and Methods Top

This was a prospective study carried out at a tertiary care center located in northern part of India on 500 Indian patients who underwent CAG between March 2014 and June 2015. The flow diagram of the study participants is given in [Figure 1]. We included all patients with normal renal parameters undergoing CAG with nonionic radiocontrast media. We excluded patients with known chronic kidney disease, baseline creatinine more than 1.5 mg/dL, significant hypotension, anemia, and patients with acute myocardial infarction undergoing emergency PCI. Patients were screened for CIN by evaluating their serum creatinine procedure and on day 3, 4, 5, and 7 after the procedure. The study population (n = 500) was divided into two groups: Group 1 (patients who developed CIN, n = 12) and Group 2 (patients without CIN, n = 488). CIN was defined as a relative (≥25%) or an absolute increase (≥0.5 mg/dL) in serum creatinine at 48 h from the patient’s baseline value following the exp9 osure to CM in the absence of any other cause.[9]
Figure 1: Flow diagram of the study.

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At the time of admission, blood samples were tested for hematological and biochemistry panel. Urinalysis was carried out in all patients, and ultrasonography of kidneys, ureters, and bladder was done. Nephrotoxic drugs if any, being used, and metformin was stopped 24 h before the procedure. Each patient’s hydration status was assessed by clinical bedside tests such as skin turgor, mucous membrane hydration, pulse, and blood pressure. Oral hydration was used to correct the hydration status of any patient found to be inadequately hydrated. Diabetic patients were only taken up once their glycemic control was adequate (fasting glucose <130 mg/dL and postprandial glucose <180 mg/dL).

CAG was performed in the Cardiac Catheterization Laboratory by Cardiologist using the Philips biplane equipment. PCI, when indicated, was also done for all patients during the procedure. Tri-iodinated nonionic monomeric water-soluble radiocontrast (Omnipaque™ manufactured by GE Healthcare, which contains iohexol) was used as the CM. Its iodine content is 350 mg/L, osmolality is 780 mOsm/ kg H2O, and viscosity at 37°C is 10.6 mPa. The volume of contrast used was dictated by the procedure being carried out on each patient and at the discretion of the cardiologists based on standard guidelines. The volume of contrast given to each patient was <5 × [body weight (in kg)/serum creatinine (in mg/dL)] as has been described as the upper safe limit previously.[10]

All intraprocedural events were recorded with special reference to hypotension. Postprocedure, every patient remained hospitalized for at least 72 h during which time, they were managed as per the standard postcardiac catheterization protocol of the hospital with strict immobilization of the limb and regular monitoring of vital parameters. All patients were hydrated adequately as per the standard protocol, and no nephrotoxic drugs were used in them postcontrast exposure.[11] Any patient, who developed CIN, was monitored in-hospital with serial kidney function tests and urine output record, besides ensuring adequate hy-dration and preventing the use of any nephrotoxic drugs among them, until they recovered renal function.

Data are presented as a mean and standard deviation or numbers with percentages. Comparison between the groups was done using Mann-Whitney test, and Fisher’s exact test was used for the frequency estimation. A twotailed P <0.05 is considered statistically significant for all the tests. The statistical analysis and graph generation were done using GraphPad Prism Software version 6 (GraphPad Software, San Diego, California, USA).

   Results Top

We evaluated a total of 683 patients out of which 500 were included in the study. Of the total, 348 (69.6%) were males and 152 (30.4%) were females. Mean age of patients was 56.6 ± 12.5 years. The baseline characteristics of the patients are shown in [Table 1]. Twelve patients (2.4%) developed CIN in the entire study population. [Table 1] also provides the detailed differentiating features between the patients with and without CIN. Briefly, the incidence of CIN was equally distributed among the various strata of BMI, patients who underwent PCI during the angiography procedure, and in patients with comorbid ailments such as diabetes. CIN was observed to be more common in patients with hypertension than in those without hypertension (P = 0.0158). Elderly patients were also not observed to have an increased incidence of CIN compared to rest of the population.
Table 1: Baseline parameters and comparison between patients with and without CIN.

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Descriptive analysis of the volume of contrast was also done to determine the role of volume of CM in the genesis of CIN. The mean volume of contrast given to patients in this study was 159.5 ± 56.1 mL. Patients who underwent intervention were given a significantly higher volume of CM (187.8 ± 23.2 mL) compared to those who did not undergo intervention (66.9 ± 22.2 mL; P <0.001). However, the difference in volume of contrast administered to CIN group (175 ± 59.3) was not significant as compared to that of non-CIN (159.1 ± 56) group (P = 0.334). None of the patients in our study required renal replacement therapy, and there was no mortality. Serial monitoring of creatinine in the CIN group showed that all the patients had normal kidney function by the end of day 7 as shown in [Figure 2].
Figure 2: Trendline of serum creatinine.

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   Discussion Top

Our study showed 2.4% incidence of CIN in patients undergoing CAG, which is similar to that of previous studies.[12],[13],[14] Rihal et al found an overall incidence of 3.3% in their series of 7586 patients who underwent cardiac catheterization.[15] The risk of CIN in their patients with normal renal function was 2.4%. Few authors have shown a significantly higher incidence of CIN in patients undergoing contrast-related procedures ranging from 5% to 15%.[6] The stringent exclusion criteria employed in our study could have contributed to the low incidence of CIN in comparison to other studies.[6],[16] We excluded patients with preexisting CKD and a baseline creatinine more than 1.5 mg/dL, whereas other authors have included these patients in their study.[6],[16],[17] Moreover, the mean volume of contrast used in our study (160 mL) was significantly lower than that in the studies mentioned above (240–290 mL).

Another important observation of our study is the self-limiting course of the CIN in all patients without the requirement of renal replacement therapy. A similar observation was noted by Lautin et al,[18] but this is in contrast to many previous studies of CIN.[18],[19],[20] Multiple factors could explain this observation including careful patient selection, minimal use of CM, avoidance of nephrotoxic drugs, and ensuring proper hydration in the postprocedure period. Advanced age has been demonstrated to be a risk factor for the occurrence of CIN.[7] However, despite the incidence of CIN in the elderly being higher than that in the younger individuals in our study (4.9% vs. 2.4%), it did not achieve statistical significance (P = 0.10) due to above-mentioned factors. Previous studies did not show ethnicity as an independent risk factor for the occurrence of CIN.[21],[22] Our study population consists of Indians only, and the data may be applicable to other South Asians for the genetic and metabolic similarities between them.[23]

Our study is also consistent with that of many studies, who found the presence of hypertension to be a significant risk factor for the occurrence of CIN.[24],[25] The role of hypertension in predisposing to CIN can be associated with advanced atherosclerosis of the aorta and suggests that atheroembolization to the kidney during CAG may also be an important cause of AKI.[26] Hypertension-induced endothelial injury could be one of the predisposing factors for the CIN, which is being studied further in animal models.[27] Our study showed no difference in the incidence of CIN in patients who had undergone prior CAG or PCI similar to the earlier studies. Further studies with larger sample size are required to confirm any association between the CIN and prior CAG or PCI.

In this study, apart from hypertension, none of the other conventional risk factors such as advanced age, diabetes, and volume of contrast were found to have a significant association with incidence of CIN. This could be due to a small number of patients (12 out of 500) having CIN in our study. Parfrey et al showed that diabetes patients with preserved renal function had a comparable rate of CIN to that of a healthy population.[28] We included patients with good glycemic control and ensured adequate hydration which are the best measures for prevention of CIN associated with diabetes. Patients with PCI did not have a higher incidence of CIN despite receiving a higher CM dose due to the smaller volume of CM used than in other studies.[29] This observation emphasizes that preexisting renal compromise and comorbid ailments play an important role in the development of CIN other than the type and quantity of CM.

The current definition of the CIN is based on the absolute or relative increase in the serum creatinine.[30] The creatinine may not actually reflect the underlying kidney function and give an accurate prediction of the glomerular filtration rate (GFR). Cystatin C is considered as a more robust marker for the estimation of GFR and may be useful in monitoring for the CIN.[31] The strengths of our study include careful selection of patients, judicious use of CM, documented follow-up in a tertiary level multidisciplinary care setup, and highlighting the simple measures such as adequate hydration, withdrawal of nephrotoxic agents, and careful monitoring of the patients. The limitations of our study include small sample size, data derived from a single hospital may not be applicable to other centers, and a small number of CIN patients in the sample. Our data being derived from Indian patients may not be applicable to patients of other race and ethnicity.

   Conclusion Top

To conclude, CIN is a potential risk factor for all patients undergoing diagnostic or therapeutic procedures with radiocontrast media. Our study demonstrates that the incidence of CIN could be reduced by proper prescreening, prevention of hypotension, good glycemic control, and adequate hydration. The genetic makeup of the patients in the study could also contribute to the risk potential which requires further research. The goal of the clinician is to prevent CIN justifying the old idiom of “prevention is better than cure.” Simple measures such as adequate hydration and proper monitoring are enough in most of the cases with only a few patients of CIN requiring the renal replacement therapy.

Conflict of interest:

None declared.

   References Top

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Correspondence Address:
K.V. S. Hari Kumar
Department of Endocrinology, Army Hospital (R&R), New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.202758

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