However it occurs, the kidneys contributed 55–65% of the total clearance of NT-BNP-76 NVP-AUY922 chemical structure in a study measuring the fractional excretion of NT-BNP-76 across a number of organs.91 Other studies in a variety of subjects have demonstrated no difference between BNP-32 and NT-BNP-76 in their fractional excretion across a range of kidney function.91–93 These studies included very few patients with GFR below 30 mL/min. Thus, the kidneys are important to the elimination of both forms of BNP but much remains to be determined about the specific mechanisms

in order to explain why elevations in NT-BNP-76 levels are relatively greater than BNP-32 in patients with ESKD. A reference range specific to the level of kidney function would be very useful, but is yet to be developed. This simplistic question summarizes the dilemma of clinicians when dealing with elevated biomarker levels in patients with ESKD. Should my patient with elevated BNP or troponin be referred to the cardiologist for more extensive cardiac evaluation and treatment? Should I accept that many patients with ESKD have such levels and attribute the result to the fact that they are on dialysis? Clearly, the answers to these questions will depend on careful consideration of the clinical context as well as interpretation

of the biomarker. Troponin and BNP are biochemical markers of specific myocardial pathologies selleck products that are very prevalent in patients with ESKD. Furthermore, the association of these markers with increased mortality in asymptomatic patients undergoing Adenosine dialysis is strong, independent of other factors, and has been consistently demonstrated in many different studies. Reduced kidney function probably does affect the level of these biochemical markers but the precise mechanisms for clearance remain to be determined. Reduced kidney function may amplify the biomarker signal from a myocardium under stress.

While disease of both organs contributes to the biochemical abnormality, the strong association with increased mortality and cardiovascular events in otherwise stable asymptomatic dialysis patients suggests that cardiac pathology is the most important contributor to the biomarker elevations. In the general population, risk stratification can be improved after an acute coronary syndrome by combining assessment of troponin, BNP and C-reactive protein.94 A similar ‘biomarker panel’ in asymptomatic dialysis patients was studied but almost all patients had NT-BNP-76 above the cut-off value. Using cTnI, cTnT and C-reactive protein, the risk of death increased as patients with normal cTnI had increased levels of one, then both of the other markers.43 Such an approach has merit because the biomarkers represent different pathophysiological processes. While the data on the prognostic implications of these biochemical markers in patients on dialysis are strong, the data regarding how to use them to guide therapy are weak (Fig. 1).