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Proenkephalin A levels predictive of worsening renal status in patients with HF
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Cardiorenal status may be reflected in proenkephalin A levels in patients with acute HF. Proenkephalin A levels may also indicate worsening renal function and were independently predictive of in-hospital mortality and mortality at 1-year follow-up, according to recent findings.
Leong L. Ng, MD, of the department of cardiovascular sciences, University of Leicester, England, and colleagues analyzed the prognostic value of proenkephalin A (PENK) in patients with acute HF. The researchers ascertained levels that may be valuable when making clinical decisions. They also assessed PENK for usefulness in predicting cardiorenal syndrome.
“On the basis of our findings indicating links between PENK and outcomes, there may be potential to use high PENK levels to select patients for intensified therapy settings or low PENK levels to rule out such care,” Ng and colleagues wrote.
In a multicenter study, the researchers measured PENK levels in 1,908 patients with acute HF (1,186 men; mean age, 76 years). The primary endpoint was 1-year all-cause mortality.
During the 1-year follow-up period, 518 patients died, the researchers wrote.
Worsening renal function was independently predicted by PENK levels (OR = 1.58; 95% CI, 1.24-2; model receiver-operating characteristic area, 0.69).
PENK levels were also independently predictive of 1-year mortality (P < .0005), as well as of 1-year death and/or HF (HR = 1.27; 95% CI, 1.1-1.45).
Ng and colleagues determined that PENK levels independently predicted in-hospital mortality, with levels < 133.3 pmol/L defining low-risk patients and > 211.3 pmol/L defining high-risk ones.
“Following acute HF, circulating PENK levels reflect cardiorenal status and provide short-term and long-term prognostic information on both mortality and [CV] morbidity. PENK predicted [worsening renal function] and could be used in conjunction with different clinical risk scores for in-hospital mortality,” Ng and colleagues wrote.
In a related editorial, Roland R.J. van Kimmenade, MD, PhD, of the department of cardiology, Radboud University Medical Center in Nijmegen, the Netherlands, and colleagues wrote “Beyond the introduction of a, thus far, less acknowledged but fascinating (patho)physiological pathway in [HF] mediated by opioid receptors, which we challenge with the oldest element in our present [HF] armamentarium (ie, morphine), Ng et al once again turn our attention to an old complication: [worsening renal function]. Unfortunately, their study was not able (or intended) to distinguish whether enkephalins directly contribute to [worsening renal function] in acute [HF] or are simple markers of underlying risk.” – by Suzanne Reist
Disclosure: Ng reports no relevant financial disclosures. Please see the full study for a list of the other researchers’ relevant financial disclosures. Van Kimmenade reports no relevant financial disclosures. Another editorial author reports receiving research grants from Roche Diagnostics.
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