Mamta Padhy1, Smita Kaushik1, M P Girish2, Sudhesna Mohapatra1, Seema Shah1, Bidhan Chandra Koner3. 1. Department of Biochemistry, Maulana Azad Medical College, New Delhi 110002, India. 2. Department of Cardiology, GB Pant Hospital, New Delhi 110002, India. 3. Department of Biochemistry, Maulana Azad Medical College, New Delhi 110002, India. Electronic address: bckoner@hotmail.com.
Abstract
BACKGROUND: Contrast-induced acute kidney injury (AKI) is diagnosed by estimating serum creatinine at 48-72h after diagnostic or interventional coronary angiography. It is too late for an early intervention. Neutrophil gelatinase associated lipocalin (NGAL) and cystatin C are novel markers of AKI. We determined the optimum cut-off level of NGAL and cystatin C in early diagnosis and prediction of AKI in patients undergoing coronary angiography followed by angioplasty. METHODS: In a nested case control study, serum NGAL, cystatin C by ELISA and serum creatinine by Jaffe's kinetic method were estimated at 0, 4, 24 and 48h of coronary angiography followed by angioplasty in 30 cases who developed contrast-induced AKI and 30 subjects who did not develop AKI. eGFR was estimated for both cases and controls by the MDRD equation. ROC was used to determine the optimum cut-off. RESULTS: Serum NGAL increased sharply at 4h after the procedure and then gradually declined to near normal level at 48h in AKI cases. The rise in cystatin C peaked at 24h and then declined but remained high till 48h. In controls, they remained static. The optimum cut-off of serum NGAL and cystatin C was 155.2ng/ml and 0.517mg/l respectively at 4h and 89.5ng/ml and 0.99mg/l respectively at 24h of angiography. Odds ratio for hypertensives to develop AKI was 3.57 (CI: 1.2-11.1, p=0.03). CONCLUSION: Serum NGAL and cystatin C may act as early markers of contrast-induced AKI in patients undergoing percutaneous coronary intervention. Patients with hypertension are susceptible to develop contrast-induced AKI.
BACKGROUND: Contrast-induced acute kidney injury (AKI) is diagnosed by estimating serum creatinine at 48-72h after diagnostic or interventional coronary angiography. It is too late for an early intervention. Neutrophil gelatinase associated lipocalin (NGAL) and cystatin C are novel markers of AKI. We determined the optimum cut-off level of NGAL and cystatin C in early diagnosis and prediction of AKI in patients undergoing coronary angiography followed by angioplasty. METHODS: In a nested case control study, serum NGAL, cystatin C by ELISA and serum creatinine by Jaffe's kinetic method were estimated at 0, 4, 24 and 48h of coronary angiography followed by angioplasty in 30 cases who developed contrast-induced AKI and 30 subjects who did not develop AKI. eGFR was estimated for both cases and controls by the MDRD equation. ROC was used to determine the optimum cut-off. RESULTS: Serum NGAL increased sharply at 4h after the procedure and then gradually declined to near normal level at 48h in AKI cases. The rise in cystatin C peaked at 24h and then declined but remained high till 48h. In controls, they remained static. The optimum cut-off of serum NGAL and cystatin C was 155.2ng/ml and 0.517mg/l respectively at 4h and 89.5ng/ml and 0.99mg/l respectively at 24h of angiography. Odds ratio for hypertensives to develop AKI was 3.57 (CI: 1.2-11.1, p=0.03). CONCLUSION: Serum NGAL and cystatin C may act as early markers of contrast-induced AKI in patients undergoing percutaneous coronary intervention. Patients with hypertension are susceptible to develop contrast-induced AKI.