A Study of Estimated Glomerular Filtration Rate in Patients Undergoing Diagnostic or Interventional Coronary Contrast Procedures

Introduction

The most important adverse effect of radiocontrast media is contrast-induced acute kidney injury (CI-AKI). The third most common cause of acute kidney injury (AKI) in patients admitted in a healthcare facility is reported to be CI-AKI.[1] The most important risk factor for CI-AKI is preexisting chronic kidney disease (CKD).[2] The risk of CI-AKI increases as the renal function decreases.[3]

The patients with established CKD are at high risk for future cardiovascular events.[4] A coronary intervention invariably requires an intraarterial radiographic contrast, which puts the patient at risk for CI-AKI. The patients known to have CKD who develop an acute coronary syndrome (ACS) have a poor prognosis, with >70% mortality at 2 years.[5] A prospective study has shown that percutaneous coronary intervention (PCI) improved the long-term survival among patients with severe renal dysfunction and ACS.[5] More recent studies have suggested that the risk of AKI due to contrast material is overestimated.^[6–8] Such studies are important, considering that angiographic procedures may be underused in the patients with CKD who present with ACSs, presumably because of the concern about precipitating AKI.[9]

This study aims to study the estimated glomerular filtration rate (eGFR) in patients with preexistent CKD, who undergo coronary angiogram (CAG)/angioplasty (PTCA); eGFR at 1 month and 3 months following the procedures.

Materials and Methods

Results

Total number of subjects included were 282. The mean age of the study population was 66.86 ± 9.08 years with males 79.8% (225). The mean eGFR prior to coronary procedure was 42.91 ± 10.51 mL/min/1.73 m². Other characteristics are expressed in Table 1. Only CAG was done in 174 (61.7%) and PTCA (CAG and PTCA were done in the same sitting) in 108 (38.3%); the details of coronary procedures are expressed in Table 2.

Three patients died in hospital. After discharge, there was no mortality noted within 3 months of coronary procedure. There were no clinically relevant events in 3 months after coronary procedure.

The incidence of CI-AKI (as per KDIGO definition) was 23.4%. AKI stage 1 was in 51 (18.08%) patients, AKI stage 2 in 12 (4.26%) patients, and stage 3 in only 3 patients requiring dialysis. However, in all three, dialysis could be discontinued within 1 month. In patients undergoing PTCA, the incidence of CI-AKI was 38.8%, and those undergoing CAG only was 13.8%. The incidence of CI-AKI increased as the eGFR decreased. The incidence of CI-AKI in the total studied population and respective stage of CKD is expressed in Table 3.

The mean eGFR of the entire study population at 1 month and 3 months after the procedure was 44.6 ± 12.59 and 43.9 ± 13.45 mL/min/1.73 m². The improvement was maximum in PTCA group; however, this change in eGFR was not statistically significant [Figure 1]. The patients who developed CI-AKI were separately analyzed. The mean eGFR did not show a progressive worsening, rather a minor improvement in eGFR at 3 months was observed. However, it was not statistically significant [Figure 2].

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Figure 1

The change in eGFR from baseline to one and three months after coronary procedure in the entire study group

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Figure 2

Variability of eGFR in patients who developed CI-AKI over three months

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Comparison of risk factors between the patients who did not develop AKI and those who developed CI-AKI are shown in Table 4. In our study, type 2 diabetes mellitus, congestive cardiac failure, anemia, pre-procedure eGFR, and albuminuira were found to be significant risk factors for the development of CI-AKI. Among the procedure-related factors, exposure to higher contrast volume was found to be a risk factor.

Discussion

In this prospective observational study, we studied the patients with an eGFR <60 mL/min/1.73 m² who underwent coronary procedures after receiving prophylaxis for CI-AKI as recommended by the KDIGO working group. In-hospital mortality was seen in 1.06% of the study population, and the cause of death was ACS and cardiac arrhythmia. No mortality was noted after discharge within 3 months of study follow up for the entire study group. A recent meta-analysis reported that the in-hospital mortality in patients exposed to contrast material to be 2.4%.[11]

The mean age of the population studied was 66.86 ± 9.0 years and 36 patients (12.77%) of the study population were above the age of 75 yrs. Older age is a known risk factor for CI-AKI.[12]

CI-AKI, as per the KDIGO definition of AKI,[13] was seen in 66 patients (23.4%). Very few studies have been done in patients using the KDIGO definition of AKI, exclusively in patients with eGFR <60 mL/min/1.73 m² undergoing a coronary procedure. In our study, the incidence of AKI stage 1 was 18.08%, AKI stage 2 was 4.26%, and AKI stage 3 was 1.06%. Only three patients in our study required dialysis for a short period (less than 2 weeks). Tsai et al.[14] reported the need for dialysis to be 4.3% and reported that incidence of CI-AKI increased as the baseline preprocedural eGFR decreased. In our study, the incidence of CI-AKI also increased as the stage of CKD progressed. In CKD stage 4, the incidence of CI-AKI was 28.94%. The lower incidence of CI-AKI requiring dialysis in our study group may have been due to rigorous implementation and adherence of CI-AKI prophylaxis with intravenous normal saline and oral N-acetyl cysteine. Other factors contributing to lower severity of CI-AKI in our patients may have been:

1. Exclusion of patients undergoing primary PCI.

2. Higher mean eGFR before the coronary procedure.

3. Lower mean age in our study group.

4. Early referral to nephrologist.

5. More trans-radial route for coronary procedures.

6. More hemodynamically stable patients.

Incidence of CI-AKI was more in the patients undergoing PTCA when compared to the patients undergoing CAG alone. One of the important factors for this difference could be the lower baseline eGFR and higher contrast volume in PTCA group when compared to the CAG group. We could find a direct relationship between volume of contrast used and development of CI-AKI in patients with CKD (P value <0.001).

In our study group, the most used vascular access for coronary contrast procedures was the right radial artery, accounting for 77.7%. A large multicenter study done in 2014, involving 82,225 PCI, demonstrated that the risk for CI-AKI and progression of underlying CKD was lower with trans-radial vascular access compared to transfemoral vascular access.[15]

In our study, we did not find persistent decrease in mean eGFR of the entire study population from baseline to 3 months after coronary procedures. In a recent study, it was reported that only 2% of patients with CKD undergoing coronary procedures develop worsening renal dysfunction over 3 months.[16] In the subgroup analysis of patients who did not develop a CI-AKI, only 0.9% of patients showed lower creatinine clearance compared to baseline.[16] A recent study done in around 21,000 patients undergoing contrast procedures has reported that intravenous contrast material exposure is not an independent risk factor for dialysis or mortality.[7]

In our study, after coronary procedures, we found a mild improvement in the eGFR (3.93%) at 1 month and at 3 months (2.3%). However, the change in eGFR from baseline to 1 month and 3 months after coronary procedures was not statistically significant. Similar findings were also observed in the patients who developed CI-AKI. It is important to highlight that the patients undergoing coronary intervention may have multiple other mechanisms of kidney injury, like hemodynamic instability, neurohormonal activation, venous congestion, inflammation, cardio-renal syndrome, and atheroembolism, which may affect the long-term clinical course.[17] There is a strong possibility that after revascularization there has been a resolution in many of these factors. It is well known that coronary revascularization also leads to sustained improvement in the left ventricular ejection fraction.[18] In our study, patients who benefited the most at 3 months were those who underwent PTCA (Δ eGFR: +1.5 mL/min/1.73 m²) and probable improvement in cardiac function and better perfusion of kidneys may have contributed improvement in eGFR over 3 months, compared to patients who underwent CAG only (Δ eGFR: +0.29 mL/min/1.73 m²).

We are moving towards an era in which intravascular contrast administration is not universally considered to be nephrotoxic. It is known that kidney disease is a risk factor for development of cardiovascular disease.[4] The risk for developing de novo coronary artery disease or death increases significantly even after a minor reduction in GFR; therefore, the patients with CKD are likely to derive greater absolute benefits from invasive approach for ACS.[19] However, the patients with kidney disease suffer from therapeutic nihilism due to risk perception of CI-AKI; a large study showed that fewer patients with CKD than without CKD underwent angiography during their hospital stay (25.2% versus 46.8%; P < 0.0001); they also showed that angiography rates were lower for CKD patients with diabetes than for those without diabetes (23.6% versus 26.3%; P < 0.001).[9] The study also showed that 1 year mortality rate for CKD patients who underwent CAG was 29.8%, PTCA was 25.1%, CABG was 23.4%, and PTCA + CABG was 14.3%, whereas among patients who were considered appropriate to undergo CAG but did not undergo this procedure had a 1 year mortality rate was 47.4%.[9] Renalism (alteration in practice because of an aversion to the risk of radiocontrast-associated nephrotoxicity)[9] must be avoided.

Our study stresses the need to proceed with coronary procedures with recommended prophylaxis for CI-AKI, as the benefits outweigh the risks. A collaborative systematic review has also suggested to consider an early angiographic procedures in CKD as it reduces risk for rehospitalization and reduces risk for death and nonfatal reinfarction.[19]

Conclusion

CI-AKI risk following coronary procedures increases with decline in baseline eGFR. CI-AKI is usually self-limiting.