Abstract

The role of brain natriuretic peptide (BNP) in the prevention of contrast-induced nephropathy (CIN) is unknown. This study aimed to investigate BNP's effect on CIN in chronic kidney disease (CKD) patients undergoing elective percutaneous coronary intervention (PCI) or coronary angiography (CAG). The patients were randomized to BNP (0.005 μg/kg/min before contrast media (CM) exposure and saline hydration, n = 106) or saline hydration alone (n = 103). Cystatin C, serum creatinine (SCr) levels, and estimated glomerular filtration rates (eGFR) were assessed at several time points. The primary endpoint was CIN incidence; secondary endpoint included changes in cystatin C, SCr, and eGFR. CIN incidence was significantly lower in the BNP group compared to controls (6.6% versus 16.5%, P = 0.025). In addition, a more significant deterioration of eGFR, cystatin C, and SCr from 48 h to 1 week (P < 0.05) was observed in controls compared to the BNP group. Although eGFR gradually deteriorated in both groups, a faster recovery was achieved in the BNP group. Multivariate logistic regression revealed that using >100 mL of CM (odds ratio: 4.36, P = 0.004) and BNP administration (odds ratio: 0.21, P = 0.006) were independently associated with CIN. Combined with hydration, exogenous BNP administration before CM effectively decreases CIN incidence in CKD patients.

Highlights

  • Contrast-induced nephropathy (CIN) is a prevalent but underdiagnosed complication of percutaneous coronary intervention (PCI) and is associated with prolonged hospitalization and high mortality [1]

  • We found that exogenous brain natriuretic peptide (BNP) administration before contrast media (CM) exposure significantly decreases CIN incidence in patients with chronic kidney disease (CKD)

  • One patient suffered from hypotension; two patients had heart dysfunction; one patient suffered from refractory angina and needed early invasive therapy before the study; one patient had end-stage renal failure; and four patients were lost to follow-up after the procedure

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Summary

Introduction

Contrast-induced nephropathy (CIN) is a prevalent but underdiagnosed complication of percutaneous coronary intervention (PCI) and is associated with prolonged hospitalization and high mortality [1]. The exact pathogenesis of CIN is still incompletely understood, multiple factors, including renal vasoconstriction, direct cytotoxic effects of contrast media (CM), oxidative stress, inflammation, and tubular obstruction, are likely involved [2, 3]. Many risk factors are associated with CIN including the preexistence of renal dysfunction, hypotension, heart failure, diabetes mellitus, older age, anemia, and CM amount and type [4,5,6]. Baseline renal dysfunction is arguably the most important risk factor [6]. Several prevention strategies have been proposed in recent years such as low dose of low osmolar or isotonic CM, hydration, and nephroprotective drugs (N-acetyl-cysteine, vasoactive drugs, and statins), BioMed Research International but no optimal strategy for preventing CIN has yet been established

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