| 1. |
|
|
| 2. |
- Tolomeo, P., et al.
(författare)
-
Importance of cystatin C in estimating glomerular filtration rate: the PARADIGM-HF trial
- 2023
-
Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 44:24, s. 2202-2212
-
Tidskriftsartikel (refereegranskat)abstract
- Aims The 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation combining creatinine and cystatin C provides a better estimation of glomerular filtration rate (GFR) compared to the creatinine-only equation.Methods and results CKD-EPI creatinine-cystatin C equation (creatinine-cystatin) was compared to creatinine-only (creatinine) equation in a subpopulation of Prospective comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure (PARADIGM-HF). Patients were categorized according to difference in eGFR using the two equations: Group 1 (<-10 mL/min/1.73 m(2), i.e. creatinine-cystatin more than 10 mL/min lower than creatinine), Group 2 (>-10 and <10 mL/min/1.73 m(2)), and Group 3 (>10 mL/min/1.73 m(2), i.e. creatinine-cystatin more than 10 mL/min higher than creatinine). Cystatin C and creatinine were available in 1966 patients at randomization. Median (interquartile range) eGFR difference was -0.7 (-6.4-4.8) mL/min/1.73 m(2). Compared to creatinine, creatinine-cystatin led to a substantial reclassification of chronic kidney disease stages. Overall, 212 (11%) and 355 (18%) patients were reallocated to a better and worse eGFR category, respectively. Compared to patients in Group 2, those in Group 1 (lower eGFR with creatinine-cystatin) had higher mortality and those in Group 3 (higher eGFR with creatinine-cystatin) had lower mortality. Increasing difference in eGFR (due to lower eGFR with creatinine-cystatin compared to creatinine) was associated with increasing elevation of biomarkers (including N-terminal pro-B-type natriuretic peptide and troponin) and worsening Kansas City Cardiomyopathy Questionnaire clinical summary score. The reason why the equations diverged with increasing severity of heart failure was that creatinine did not rise as steeply as cystatin C.Conclusion The CKD-EPI creatinine-only equation may overestimate GFR in sicker patients.
|
|
| 3. |
- Tolomeo, Paolo, et al.
(författare)
-
Independent prognostic importance of blood urea nitrogen to creatinine ratio in heart failure
- 2024
-
Ingår i: EUROPEAN JOURNAL OF HEART FAILURE. - 1388-9842 .- 1879-0844.
-
Tidskriftsartikel (refereegranskat)abstract
- Aim Blood urea nitrogen (BUN) to creatinine ratio is associated with worse outcomes in acute heart failure (HF) but little is known about its importance in chronic HF.Methods and results We combined individual patient data from clinical trials (HF with reduced ejection fraction [HFrEF]: PARADIGM-HF, ATMOSPHERE and DAPA-HF, and HF with preserved ejection fraction [HFpEF]: PARAGON-HF and I-PRESERVE). The primary outcome examined was a composite time to first HF hospitalization or cardiovascular death; its components and all-cause death were also examined. Each HF phenotype was categorized according to median BUN/creatinine ratio, generating four groups that is, HFpEF <= and >median BUN/creatinine ratio and HFrEF <= and >median BUN/creatinine ratio. The association between BUN/creatinine ratio and outcomes was evaluated using the Kaplan-Meier estimator and Cox proportional hazard models. Overall, 28 820 patients were analysed. The median (IQR) BUN/creatinine ratio was 20.1 (Q1-Q3 16.7-24.7) in HFpEF and 18.7 (15.2-22.8) in HFrEF. In both HFpEF and HFrEF, higher BUN/creatinine ratio was associated with older age, female sex, and diabetes, but similar estimated glomerular filtration rate (eGFR). The risk of each outcome examined was significantly higher in patients with BUN/creatinine ratio >= median, compared toConclusion Higher BUN/creatinine ratio was associated with worse outcomes in patients with chronic HF across the spectrum of left ventricular ejection fraction, independently of eGFR and NT-proBNP. BUN/creatinine ratio may reflect neurohumoral activation (especially increased arginine vasopressin), altered renal blood flow or other pathophysiologic mechanisms not incorporated in conventional prognostic variables.
|
|
