NT-ProBNP and Troponin T and Risk of Rapid Kidney Function Decline and Incident CKD in Elderly Adults

Abstract

Background and objectives Elevations in N-terminal pro-B-type natriuretic peptide and high-sensitivity troponin T are associated with poor cardiovascular outcomes. Whether elevations in these cardiac biomarkers are associated with decline in kidney function was evaluated.Design, setting, participants, & measurements N-terminal pro-B-type natriuretic peptide and troponin T were measured at baseline in 3752 participants free of heart failure in the Cardiovascular Health Study. eGFR was determined from the Chronic Kidney Disease Epidemiology Collaboration equation using serum cystatin C. Rapid decline in kidney function was defined as decline in serum cystatin C eGFR$30%, and incident CKD was defined as the onset of serum cystatin C eGFR,60 among those without CKD at baseline (n=2786). Cox regression models were used to examine the associations of each biomarker with kidney function decline adjusting for demographics, baseline serum cystatin C eGFR, diabetes, and other CKD risk factors.Results In total, 503 participants had rapid decline in serum cystatin C eGFR over a mean follow-up time of 6.41 (1.81) years, and 685 participants developed incident CKD over a mean follow-up time of 6.41 (1.74) years. Participants in the highest quartile of N-terminal pro-B-type natriuretic peptide (.237 pg/ml) had an 67% higher risk of rapid decline and 38% higher adjusted risk of incident CKD compared with participants in the lowest quartile (adjusted hazard ratio for serum cystatin C eGFR rapid decline, 1.67; 95% confidence interval, 1.25 to 2.23; hazard ratio for incident CKD, 1.38; 95% confidence interval, 1.08 to 1.76). Participants in the highest category of troponin T (.10.58 pg/ml) had 80% greater risk of rapid decline compared with participants in the lowest category (adjusted hazard ratio, 1.80; 95% confidence interval, 1.35 to 2.40). The association of troponin T with incident CKD was not statistically significant (hazard ratio, 1.17; 95% confidence interval, 0.92 to 1.50).Conclusions Elevated N-terminal pro-B-type natriuretic peptide and troponin T are associated with rapid decline of kidney function and incident CKD. Additional studies are needed to evaluate the mechanisms that may explain this association.

Estimated Glomerular Filtration Rate and Albuminuria Are Associated with Biomarkers of Cardiac Injury in a Population-Based Cohort Study: The Maastricht Study

“…First, owing to the cross-sectional design and the absence of data on hard clinical outcomes, such as incident CVD, we cannot make strong causal inferences and we cannot determine the direction of the associations. In fact, these may be bidirectional (42,43 ). In addition, data on hard clinical outcomes may clarify the clinical relevance of the differences between hs-cTnT and hs-cTnI.…”

Plasma B-type natriuretic peptide concentration is independently associated with kidney function decline in Japanese patients with chronic kidney disease

“…Conversely, elevated concentrations of BNP [22] and N-terminal-proBNP [23,24] were found to be associated with adverse renal outcomes in CKD patients. Higher N-terminal-proBNP levels in a community-based cohort of older adults without clinical heart failure were found to be related to subsequent rapid decline in kidney function and incident CKD [25]. However, studies exploring the effects of BNP and N-terminal-proBNP on renal outcomes [22][23][24][25] have not addressed this relationship, independent of cardiac structure and function.…”

“…Higher N-terminal-proBNP levels in a community-based cohort of older adults without clinical heart failure were found to be related to subsequent rapid decline in kidney function and incident CKD [25]. However, studies exploring the effects of BNP and N-terminal-proBNP on renal outcomes [22][23][24][25] have not addressed this relationship, independent of cardiac structure and function. Therefore, the precise causal relationship between higher BNP levels and poor renal outcomes has not been fully investigated.…”

Can We Save the Kidneys by Protecting the Heart?

“…Therefore, routine assessment of these cardiac biomarkers to guide therapy with the intention to alter the natural history of CKD remains unproven. Regardless of the renal consequences, it is still important to recognize (although beyond the findings of this paper) that detecting elevated cardiac biomarkers represents a valuable opportunity to investigate and intervene on potential underlying cardiac vulnerabilities in patients with CKD, whereas the lack of such biomarker elevations can be prognostically reassuring (8). Second, the key to achieving meaningful use of such clinical biomarkers demands the ability for their levels to indicate a change in therapeutic approaches.…”

“…First, it is important to recognize that the end points used in this study were not hard end points (e.g., incident development of ESRD or mortality associated with renal diseases) but surrogate measures of kidney function decline on the basis of changes in eGFR that were arbitrarily defined (8). Therefore, routine assessment of these cardiac biomarkers to guide therapy with the intention to alter the natural history of CKD remains unproven.…”