Key result
Simultaneous BNP and hs-cTnI elevations are linked to ~780% greater risk of dialysis-dependent kidney failure.
Why the study?
Are elevated levels of BNP and hs-cTnI associated with adverse outcomes in stable kidney transplant recipients?
Cohort (n=1,131)
Are elevated levels of BNP and hs-cTnI associated with adverse outcomes in stable kidney transplant recipients?
Hazard Ratio: 8.8 (95% CI 3.4–23.1)
Elevated BNP and hs-cTnI are strongly associated with mortality, cardiovascular, and kidney outcomes in stable kidney transplant recipients, identifying candidates for targeted risk reduction.
May support risk stratification in stable kidney transplant recipients; leaves open whether biomarker-guided interventions improve outcomes.
BACKGROUND: Approximately 200 000 kidney transplant recipients are living in the United States; they are at increased risk for cardiovascular and other adverse outcomes. Biomarkers predicting these outcomes are needed. Using specimens collected during the Folic Acid for Vascular Outcome Reduction in Transplantation trial, we determined whether plasma levels of B-type natriuretic peptide (BNP) and cardiac troponin I are associated with adverse outcomes in stable kidney transplant recipients. METHODS: Five hundred ten subjects were selected randomly from the 4110 Folic Acid for Vascular Outcome Reduction in Transplantation participants. This cohort was then enriched for all additional subjects with adverse outcomes (death, dialysis-dependent kidney failure (DDKF), and cardiovascular outcomes) for a total of 1131 participants studied. Quartiles of BNP and high-sensitivity cardiac troponin I (hs-cTnI) were included in adjusted models. Combinations of normal and elevated hs-cTnI (>26.2 ng/L) and BNP (>100 pg/mL) were also studied. RESULTS: Median concentrations (interquartile ranges) were 5.6 (3.3-10.5) ng/L for hs-cTnI and 39 (15, 94) pg/mL for BNP. Hazard ratios for each adverse outcome were higher with higher quartiles of BNP after adjustment and remained statistically significant after adding hs-cTnI to the model. The highest quartile hazard ratio for DDKF was 2.47 (95% confidence interval [95% CI], 1.21-5.05). Simultaneous elevations of BNP and hs-cTnI over clinical cutoffs were strongly associated with adverse outcomes with hazard ratios 8.8 (95% CI, 3.4-23.1) for DDKF and 6.3 (95% CI, 2.7-15.0) for cardiovascular outcomes. CONCLUSIONS: Higher BNP is associated with mortality and cardiovascular and kidney outcomes in stable kidney transplant recipients. Elevated BNP and hs-cTnI identify candidates for targeted risk reduction.
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Jarolı́m et al. (2016) conducted a cohort in Stable kidney transplant recipients (n=1,131). Simultaneous elevations of BNP (>100 pg/mL) and hs-cTnI (>26.2 ng/L) vs. Normal levels of BNP and hs-cTnI was evaluated on Dialysis-dependent kidney failure (DDKF) (HR 8.8, 95% CI 3.4-23.1). Simultaneous elevations of BNP and hs-cTnI were strongly associated with dialysis-dependent kidney failure (HR 8.8; 95% CI 3.4-23.1) and cardiovascular outcomes (HR 6.3; 95% CI 2.7-15.0).
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