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% confi- dence interval, 0.92 to 1.50). Conclusions ElevatedN-terminal pro–B-type natriuretic peptide and troponin T are associatedwith rapid decline of kidney function and incident CKD. Additional studies are needed to evaluate the mechanisms that may explain this association.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 205-214 |
| Number of pages | 10 |
| Journal | Clinical Journal of the American Society of Nephrology |
| Volume | 10 |
| Issue number | 2 |
| DOIs | |
| State | Published - 2015 |
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ASJC Scopus subject areas
- Nephrology
- Transplantation
- Epidemiology
- Critical Care and Intensive Care Medicine
Cite this
NT-ProBNP and troponin T and risk of rapid kidney function decline and incident CKD in elderly adults. / Bansal, Nisha; Katz, Ronit; Dalrymple, Lorien; De Boer, Ian; Defilippi, Christopher; Kestenbaum, Bryan; Park, Meyeon; Sarnak, Mark; Seliger, Stephen; Shlipak, Michael; Shlipak, Michael; Shlipak, Michael; Shlipak, Michael.
In: Clinical Journal of the American Society of Nephrology, Vol. 10, No. 2, 2015, p. 205-214.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - NT-ProBNP and troponin T and risk of rapid kidney function decline and incident CKD in elderly adults
AU - Bansal, Nisha
AU - Katz, Ronit
AU - Dalrymple, Lorien
AU - De Boer, Ian
AU - Defilippi, Christopher
AU - Kestenbaum, Bryan
AU - Park, Meyeon
AU - Sarnak, Mark
AU - Seliger, Stephen
AU - Shlipak, Michael
AU - Shlipak, Michael
AU - Shlipak, Michael
AU - Shlipak, Michael
PY - 2015
Y1 - 2015
N2 - 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% confi- dence interval, 0.92 to 1.50). Conclusions ElevatedN-terminal pro–B-type natriuretic peptide and troponin T are associatedwith rapid decline of kidney function and incident CKD. Additional studies are needed to evaluate the mechanisms that may explain this association.
AB - 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% confi- dence interval, 0.92 to 1.50). Conclusions ElevatedN-terminal pro–B-type natriuretic peptide and troponin T are associatedwith rapid decline of kidney function and incident CKD. Additional studies are needed to evaluate the mechanisms that may explain this association.
UR - http://www.scopus.com/inward/record.url?scp=84923794931&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84923794931&partnerID=8YFLogxK
U2 - 10.2215/CJN.04910514
DO - 10.2215/CJN.04910514
M3 - Article
C2 - 25605700
AN - SCOPUS:84923794931
VL - 10
SP - 205
EP - 214
JO - Clinical Journal of the American Society of Nephrology
JF - Clinical Journal of the American Society of Nephrology
SN - 1555-9041
IS - 2
ER -