Test May Detect STEMI Patients at Risk for Contrast Nephropathy After PCI


Measuring serum B-type natriuretic peptide (BNP) levels at hospital admission may help identify patients with ST-segment elevation myocardial infarction (STEMI) who are at risk for developing contrast-induced acute kidney injury (AKI) following percutaneous coronary intervention (PCI). The findings were published online November 22, 2012, ahead of print in Circulation: Cardiovascular Interventions.

Researchers led by Roxana Mehran, MD, of Mount Sinai School of Medicine (New York, NY), looked at 979 STEMI patients from the HORIZONS-AMI trial whose BNP levels were measured in the emergency room prior to primary PCI. Contrast-induced AKI, defined as a relative increase of over 25% or an absolute increase of ≥ 0.5 mg/dL in creatinine within 48 hours of index angiography, developed in 131 (13%) patients. Median BNP levels were markedly increased in patients who did vs. did not develop the condition (151.0 pg/mL vs. 62.6 pg/mL; P < 0.0001). In addition, risk of contrast-induced AKI rose with each quartile of BNP (table 1).

Table 1. Risk of Contrast-Induced AKI by Quartile of BNP

 

Quartile 1
BNP ≤ 30 pg/mL
(n = 301)

Quartile 2
BNP > 30,
≤ 71 pg/mL
(n = 200)

Quartile 3
BNP > 71,
≤ 263 pg/mL
(n = 254)

Quartile 4
BNP > 263 pg/mL
(n = 224)

P Value for Trend

Contrast-Induced AKI

5.6%

12.5%

16.9%

20.5%

< 0.0001


On multivariable analysis, BNP was an independent predictor of contrast-induced AKI (OR 1.29; 95% CI 1.10-1.51; P = 0.0015). The results were consistent across multiple subgroups. In addition, adding BNP measurements improved both the current clinical risk prediction model based on angiographic, clinical, and lab-based variables (P < 0.001) and the Mehran Risk Score (P = 0.015) for contrast-induced AKI.

The researchers note that current risk stratification tools for contrast-induced AKI are designed to predict the condition after planned coronary procedures, and not at the time of admission in patients with STEMI. However, “point-of-care tests are available in which BNP concentrations are available within 20 minutes, making it a potentially useful candidate for early prognostication,” they say.

Mechanism Behind Marker Unclear

The exact mechanism tying BNP to contrast-induced AKI, though, is not clear, the researchers note. BNP may, for instance, exert a direct effect in precipitating the condition since it is a potent natriuretic, diuretic and vasodilator with negative inotropic effects on the myocardium. However, elevated BNP concentrations are also associated with other risk factors that are more closely associated with development of contrast-induced AKI, such as older age and diabetes. In fact, patients in the study who developed contrast induced AKI were older (66.7 years vs. 60.4 years; P < 0.001) and more frequently had diabetes (28% vs. 16%; P < 0.001) as well as preexisting kidney disease (9% vs. 3%; P = 0.002) than patients without the condition.

“In conclusion, measurement of serum BNP at hospital admission may help identify patients who are at risk for developing [contrast induced] AKI after primary PCI in STEMI,” Dr. Mehran and colleagues write. “Randomized trials are warranted to determine whether this knowledge prior to contrast administration might facilitate application of therapeutic measures to prevent [the condition].”

An Interesting Predicament

In an e-mail communication with TCTMD, Peter A. McCullough, MD, MPH, of St. John Providence Health System (Warren, MI), noted that BNP “may be the first bona fide marker that predicts risk before the procedure in addition to serum creatinine and other renal markers of chronic filtration function.”

He explained that “as the kidney begins to become resistant to BNP, the heart produces more of the hormone, reflecting the kidneys being in a state of vulnerability to injury and in some cases failure.”

However, how to respond to high BNP levels in STEMI patients is less clear, he cautioned, since extra hydration, one of the few proven methods of protecting against contrast-induced AKI, may be contraindicated. “It’s an interesting predicament, high BNP usually means heart failure or risk for heart failure with fluid [intake],” Dr. McCullough noted.

Note: Dr. Mehran and several other coauthors of the study are faculty members of the Cardiovascular Research Foundation, which owns and operates TCTMD.

 


Source:
Jarai R, Dangas G, Huber K, et al. B-type natriuretic peptide and risk of contrast-induced acute kidney injury in acute ST-segment elevation myocardial infarction. A substudy from the HORIZONS-AMI trial. Circ Cardiovasc Interv. 2012;Epub ahead of print.

 

 

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Disclosures
  • The trial was sponsored by the Cardiovascular Research Foundation with unrestricted grant support from Boston Scientific and The Medicines Company.
  • Dr. Mehran reports receiving a research grant from Bristol Myers Squibb/Sanofi and The Medicines Company, and serving as a consultant to Abbott Vascular, Janssen, and Regado Biosciences.
  • Dr. McCullough reports no relevant conflicts of interest.

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