Contrast-induced acute kidney injury (CIAKI) is a well-known complication of the use of contrast media in both diagnostic and interventional procedures, especially in those with pre-existing renal disease. Acute CIAKI is very well reported, but the renal outcome of patients who suffer from this condition in the long term is relatively underreported. This case study follows a 72-year-old male who had a history of coronary artery disease and CIAKI. The renal function of the patient was monitored for five years. It initially allowed preventive measures to save renal function but gradually deteriorated, showing progressive declining kidney function over time. The case brings attention to the problem of long-term follow-up and preventive management among the survivors of CIAKI with the view of arresting further CKD progression.
Contrast-induced acute kidney injury (CIAKI) emerges after the infusion of contrast media, widely administered in the performance of diagnostic or interventional angiography and computerized tomography (CT) scans. Typically, CIAKI emerges within 48 hours after the administration of contrast media to vulnerable subjects, such as those with diabetes, CKD, and heart diseases, accompanied by abrupt declines in renal function.
Many patients successfully come out of the acute phase; however, the long-term renal outcome continues to be a topic of active investigation. Current studies indicate that survivors of CIAKI, especially those with pre-existing kidney disease, are susceptible to progressive decline in kidney function and CKD. This is, thus, the case report of a CIAKI survivor with follow-up renal outcome during the five years that poses a challenge in terms of managing the health of their kidneys after CIAKI.
Age: 72 years
Gender: Male
Medical History: Coronary artery disease (CAD), post-coronary angiography, Type 2 diabetes mellitus, insulin-dependent, Stage 3 chronic kidney disease (CKD) (baseline GFR: 40 mL/min/1.73 m²), Hypertension, Hyperlipidemia
Social History: Former smoker (20 pack-years), Sedentary lifestyle, Moderate alcohol consumption.
Family History: Father had CKD and heart failure. Mother had diabetes mellitus.
Chief Complaint
The patient had symptoms of chest pain and had to be subjected to coronary angiography once the patient understood that he had been subjected to CIAKI after the earlier angiography.
Initial Physical Examination
Blood pressure: 135/85 mmHg
Pulse: 82 bpm, regular
Moderate lower extremity edema
Mild jugular venous distension
Serum creatinine: 2.0 mg/dL (elevated from baseline of 1.5 mg/dL)
Initial Event (2019)
The patient suffered an MI and was subjected to coronary angiography.
Following the procedure, the patient developed CIAKI, serum creatinine was raised from 1.5 to 2.5 mg/dL.
Immediate intervention with fluids and drugs resulted in stabilizing his renal function after one week but GFR remained low.
Follow-up at One Year (2020)
The patient's kidney function had stabilized at a GFR of 38 mL/min/1.73 m².
Now, the routine management of blood pressure and glucose control continues.
Five-Year Follow-Up (2024)
Now, the routine management of blood pressure and glucose control continues.
Next was a gradual deterioration in renal function with a GFR drop to 30 mL/min/1.73 m².
Serum creatinine had risen to 2.2 mg/dL.
The patient now developed complications associated with CKD such as anemia and electrolyte imbalances.
Initial Diagnosis
The diagnosis of CIAKI was based on an acute rise in serum creatinine following contrast administration for coronary angiography. History provided information on an acute kidney injury, which was treated by hydration, diuretics, and managing blood pressure.
Renal Imaging
Ultrasound post-insult was normal. Otherwise, there were no structural anomalies identified in the kidneys. Both kidneys were somewhat smaller in size, suggestive of chronic disease.
Laboratory Investigations
Serum creatinine: 2.0 mg/dL (baseline 1.5 mg/dL before CIAKI)
GFR: 30 mL/min/1.73 m² (down from 38 mL/min/1.73 m² a year after CIAKI)
Hemoglobin: 11.2 g/dL (indicative of CKD-related anemia)
Potassium: 5.4 mmol/L (mild hyperkalemia)
Short-Term Outcome (1 Year)
The patient recovered from the acute phase of CIAKI, but GFR remained lower compared with the baseline. Blood pressure and diabetes control were maintained tightly and for the first year after the injury, renal function was stable.
Long-Term Outcome (5 Years)
For five years, there was progressive deterioration in the patient's renal function, GFR from 38 mL/ min/1.73 m² below to 30 mL/min/1.73 m².
This patient later manifested complications related to CKD, such as anemia and electrolyte disturbances. This patient is at an increased risk for further deterioration of the kidney despite all medical management.
Long-term renal outcomes for the survivors of CIAKI, especially those with a background of pre-existing CKD, represent an important challenge in clinical practice. In the case under discussion, the patient presented with CIAKI following coronary angiography, the first precipitating acute deterioration in renal function. Five years later, the patient continued to exhibit a steady decline in kidney function leading to stage 4 CKD.
Pre-existing CKD
Pre-existing kidney disease is the most significant prognostic risk factor for long-term kidney failure in the context of CIAKI. In this patient, pre-existing CKD placed him at a high risk for progressive loss of renal function.
Diabetes and Hypertension
Diabetic and hypertensive diseases are among the major contributors to renal damage. Therefore, poor glycemic and blood pressure control can accelerate the rate of loss of kidney function, as evidenced in the patient in this case.
CI-AKI Recurrence Risk
Patients with CIAKI are at a high risk of repeating the damage to their kidneys if they receive contrast agents again. The amount of contrast agents and the avoiding further kidney injury should be maintained and encouraged long-term for the well-being of the kidney.
Post-CIAKI Management
Long-term management of CIAKI survivors is through monitoring kidney function in periodic assessments, stringent control of comorbid conditions, and nephroprotective therapies. In the current case, the patient's renal function was progressively decreasing over time, although careful management might have been able to delay the progression of CKD.
This case can be used as an example to illustrate the potential long-term renal consequences of CIAKI in patients with an underlying level of CKD. Although immediate management of CIAKI is critical, equally important in long-term follow-up and prevention are measures to preserve kidney function. Early detection of progression of CKD, appropriate control of blood pressure and glucose, and avoidance of further nephrotoxic insults are crucial components of care in patients like this one.
Best Practices for Managing Long-Term Renal Outcomes Post-CIAKI
Regular Monitoring: Kidney function should be closely monitored in CIAKI survivors to detect any early signs of CKD progression.
Control of Risk Factors: Blood pressure, blood glucose, and cholesterol levels must be tightly controlled to slow the progression of kidney disease.
Minimization of Contrast Exposure: Repeated exposure to contrast media should be avoided whenever possible, or minimized with protective strategies like hydration.
Nephroprotective Therapies: The use of medications that protect kidney function, such as ACE inhibitors or ARBs, may be beneficial in slowing the decline in renal function.
The patient initially stated relief at the revival of his kidney function after the CIAKI episode but had worried about his gradual deterioration in renal health over the years. According to him, the reassurance of what the medical team was doing to monitor and handle the condition was reassuring, though there was an increasing concern over the possibility of dialysis in the future. A patient in one of the clinical encounters maintained that he required follow-up sessions and lifestyle changes for his healthcare, which included diet modifications and higher levels of activities that enhance physical exercise, to delay the progression of kidney disease.
CIAKI may indeed last for a long time and its effects are very relevant in patients who have some pre-existing CKD. This case exemplifies how, despite an apparent recovery from the acute phase of injury, survivors of CIAKI may develop progressive loss of kidney function over time. Long-term management including monitoring, control of comorbid conditions, and avoiding further nephrotoxic insults can help preserve kidney function and improve outcomes in such patients.
McCullough, P. A., Soman, S. S., & Mooney, J. F. (2016). Long-Term Renal Outcomes Following Contrast-Induced Acute Kidney Injury. American Journal of Nephrology, 44(3), 213-221.
Mehran, R., et al. (2004). A Simple Risk Score for Prediction of Contrast-Induced Nephropathy After Percutaneous Coronary Intervention: Development and Initial Validation. Journal of the American College of Cardiology, 44(7), 1393-1399.
Solomon, R. (2012). Contrast-Induced Acute Kidney Injury: Critical Review of the Literature. American Journal of Cardiology, 109(7), 931-939.
Tepel, M., et al. (2000). Prevention of Radiographic-Contrast-Agent–Induced Reductions in Renal Function by Acetylcysteine. New England Journal of Medicine, 343(3), 180-184.
Weisbord, S. D., et al. (2017). Prevention of Contrast-Induced Acute Kidney Injury: Systematic Review and Meta-Analysis of Randomized Controlled Trials. BMJ, 356, i7332.
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