Study participants were CKD and CCS patients, candidate for diagnostic coronary angiography or PCI, and referred to the CCU. The study participants were subjected to history taking and data collection for age, gender, hypertension, DM, dyslipidemia, smoking, cerebrovascular disease, PVD, acute coronary syndrome (ACS), prior coronary angiography, and prior revascularization procedure. In addition, study participants were subjected to comprehensive clinical examination including measurement of vital signs on admission (systolic and diastolic blood pressure, heart rate, respiratory rate, and body temperature), mean arterial blood pressure, body weight and height, admission and discharge twelve-lead electrocardiograms (ECGs), transthoracic echocardiography (TTE), complete blood count, fasting blood glucose, blood urea, serum creatinine, total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides, creatinine kinase (CK), creatine kinase-MB (CK-MB), and troponin. Normal values for ECG waves and intervals were referenced to the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography) report [
9]. Data documented with ECGs included arrhythmias, new bundle branch block, ST segment elevation, ST segment depression, changes of T wave, or no significant changes. Data documented with TTE included left ventricular ejection fraction (LVEF). The preprocedural CKD was categorized based on the estimated glomerular filtration rate (eGFR) using the simplified Modification of Diet in Renal Disease (MDRD) formula into mild CKD (60–89 ml/min/1.73 m
2), moderate CKD (30–59 ml/min/1.73 m
2), and severe CKD (15–29 ml/min/1.73 m
2), respectively [
10]. Screened participants were enrolled if they had CKD, CCS after previous episode of ACS including ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), or unstable angina (UA), and planned for diagnostic coronary angiography or PCI. Screened participants with normal kidney functions, single functioning kidney, end stage renal disease (ESRD) on regular dialysis, history of kidney transplant, AKI triggered by cocaine, surgery, sepsis, trauma, or cardiogenic shock, pulmonary edema, acute heart failure with LVEF < 30%, systolic blood pressure < 80 mmHg, bronchial asthma, multiple myeloma, pregnancy, allergy to phentolamine or CM, or received barbiturates, antipsychotic agents, phosphodiestrase-5 inhibitors, CM within 7 days of study entry, or α-adrenoreceptor blocker at the time of admission were excluded from the study. Staging of CI-AKI was as per the Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) criteria (Table
1). According to the Kidney Disease Improving Global Outcomes (KDIGO) work group, staging of CI-AKI shouldn’t be different from staging of AKI as per RIFLE criteria or the Acute Kidney Injury Network (AKIN) criteria [
11].
Table 1
Staging of acute kidney injury
Stage 1 | 1.5–1.9 times baseline Or > 0.3 mg/dl (≥ 26.5 μmol/l) increase | < 0.5 ml/kg/hr. for 6–12 hrs |
Stage 2 | 2.0–2.9 times baseline | < 0.5 ml/kg/hr. for ≥12 hrs |
Stage 3 | 3.0 times baseline Or Increase in serum creatinine to ≥4.0 mg/dl (≥ 353.6 μmol/l) Or Initiation of Renal Replacement Therapy Or In patients, < 18 years, decrease in eGFR to < 35 ml/min/1.73 m2 | < 0.3 ml/kg/hr. for ≥24 hrs Or Anuria for ≥12 hrs |