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Predictors of Heart Failure in Pediatric Patients with End-Stage Kidney Disease Secondary to Nephrotic Syndrome
Meng Wei1, Huiping Huang2, Yajun Shen1
1Ministry of Education Key Laboratory of Women and Children's Diseases and Birth Defects, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610000, China.
Insights
Heart failure (HF) is a significant risk factor for poor outcomes in pediatric end-stage kidney disease (ESKD) patients. Early detection of HF using cardiac biomarkers and echocardiography can improve survival rates.
Area of Science:
- Pediatric Nephrology
- Cardiology
- Renal Disease
Background:
- Steroid-resistant nephrotic syndrome (SRNS) is a leading cause of pediatric end-stage kidney disease (ESKD).
- Heart failure (HF) development and its prognostic implications in pediatric ESKD secondary to SRNS are not well-defined.
Purpose of the Study:
- To investigate prognostic risk factors for HF development in pediatric ESKD patients with SRNS.
- To determine the incidence, clinical characteristics, and predictors of HF in this population.
Main Methods:
- Retrospective cohort study of 172 pediatric patients with ESKD secondary to NS (2014-2020).
- Stratification based on clinical outcomes and HF occurrence.
- Multivariate logistic regression to identify risk factors for early HF and adverse prognosis.
Main Results:
- HF developed in 15.7% within the first year and 26.2% by five years post-ESKD diagnosis.
- Elevated cardiac troponin I, cardiac arrhythmias, left heart enlargement, and valvular regurgitation were independent risk factors for HF.
- Early HF onset significantly reduced five-year survival.
Conclusions:
- HF is a major predictor of reduced survival in pediatric ESKD.
- Left heart enlargement and elevated cardiac troponin I are robust early predictors of HF.
- Systematic baseline echocardiographic and biomarker screening at ESKD onset is recommended for early intervention.
Abstract:
Background and Objectives: To investigate prognostic risk factors and determine the incidence, clinical characteristics, and predictors of heart failure (HF) development in pediatric patients with end-stage kidney disease (ESKD) secondary to steroid-resistant nephrotic syndrome (SRNS). Materials and Methods: We conducted a retrospective cohort study of pediatric patients diagnosed with ESKD secondary to nephrotic syndrome (NS) between 2014 and 2020. Patients were stratified based on clinical outcomes and the occurrence of HF during follow-up. Comparative analyses of clinical characteristics, laboratory parameters, and cardiac assessments were performed across groups. Multivariate logistic regression was used to identify independent risk factors for HF development within the first year and for adverse prognosis at five years. Results: The cohort comprised 172 children with ESKD secondary to NS. Multivariate logistic regression identified HF as an independent risk factor for adverse long-term outcomes in pediatric patients with ESKD. During follow-up, HF developed in 27 patients (15.7%) within the first year after ESKD diagnosis, and in 45 patients (26.2%) by the end of five years. Early HF onset (within the first year) was associated with a significantly reduced five-year survival rate. Independent risk factors for HF development included elevated cardiac troponin I levels (OR = 6.786, 95% CI: 2.326-19.799), a history of cardiac arrhythmias (OR = 2.951, 95% CI: 1.260-6.912), and the presence of left heart enlargement (OR = 23.669, 95% CI: 2.876-194.827), and valvular regurgitation at the initial post-ESKD diagnosis evaluation. Conclusions: HF is associated with markedly reduced survival. Crucially, our findings demonstrate that pre-existing cardiovascular structural abnormalities-specifically left heart enlargement-and elevated cTnI are robust, early predictors of HF. These findings necessitate a paradigm shift in pediatric ESKD management, we advocate for the implementation of systematic baseline echocardiographic and biomarker screening at the immediate onset of ESKD. Identifying these subclinical, yet modifiable, structural changes provide a critical therapeutic window for targeted anti-remodeling interventions to significantly improve long-term prognosis.
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