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A decade ago, controversy surrounded the observa- tion of increased cardiac troponin concentrations in asymptomatic renal disease patients, with one assay claiming better specificity and another better prognos- tic potential. This controversy is largely resolved now, withavailabilityofmoreoutcomedata,improvedlow- end sensitivity of the assays, and a general recognition that renal disease was only one cause, albeit an impor- tant one, of myocardial injury in the absence of an acute coronary syndrome (1). It should come as little surprise,then,thatsoonaftertheintroductionofcom- mercial assays for B-type natriuretic peptide (BNP) 3 and amino-terminal pro-BNP (NT-proBNP) and the publication of seminal studies for their diagnostic ap- plication in patients presenting with dyspnea of uncer- tain etiology, there has been much debate over the in- terpretation and significance of these tests in patients with impaired renal function (2, 3). Chronic kidney disease (CKD), defined as an esti- matedglomerularfiltrationrate(eGFR)60mL/min/ 1.73 m 2 , is a common condition with multiple etiolo- giesthataffectsanestimated8.3millionAmericansand

B-Type Natriuretic Peptide (BNP)/NT-proBNP and Renal Function: Is the Controversy Over?