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Published on: February 4, 2015
[Post-hemolytic renal failure in children with glucose-6-phosphate dehydrogenase deficiency at the University
B Balaka1, D Agbèrè, P Bonkoungou
1Service de Pédiatrie, Centre hospitalier universitaire de Lomé, Togo. bbalaka@favo.net
Insights
In children with glucose-6-phosphate dehydrogenase deficiency (G6PD), multiple infections and drug combinations are key factors leading to acute hemolysis and severe kidney failure. Early identification and management are crucial for better outcomes.
Area of Science:
- Pediatric Nephrology
- Hematology
- Clinical Pharmacology
Context:
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common genetic disorder, particularly prevalent in tropical regions.
- Hemolysis and subsequent renal failure pose significant health risks in affected children.
- Identifying triggers for these complications is vital for effective clinical management.
Purpose:
- To determine predisposing factors for acute hemolysis and post-hemolytic renal failure in children with G6PD deficiency.
- To evaluate the role of hemolytic agents, infections, and drug associations in precipitating these adverse events.
- To assess the outcomes and management strategies for hemolysis and renal failure in this pediatric population.
Summary:
- G6PD deficiency was identified in 32.1% of children with hemoglobinuria.
- Anuric renal failure occurred in 35.1% of G6PD-deficient patients, often linked to infections and drug combinations.
- Multiple-germ infections and drug associations were identified as primary risk factors for renal failure, with an 80.7% reversibility rate.
Impact:
- Highlights the critical role of infections and drug interactions in G6PD-related hemolysis and renal failure.
- Suggests that local endemic infections in tropical areas may contribute significantly to these complications.
- Informs clinical practice regarding the avoidance of specific triggers and the importance of prompt management in G6PD-deficient children.
Abstract:
The purpose of the study was to identify predisposing factors for acute hemolysis and post-hemolytic renal failure in children with glucose-6-phosphate dehydrogenase deficiency (G6PD). Any child presenting hemoglobinuria during the study period was prospectively evaluated. Evaluation included detection of the presence of hemolytic agents, laboratory tests to measure hemolysis, G6PD activity, infection and renal failure, and assessment of outcome and management of hemolysis and renal failure. G6PD deficiency was documented in 32.1% of the 230 children admitted with hemoglobinuria. Anuric renal failure occurred during the hemolysis episode in 35.1% of patients with G6PD deficiency (21 boys and 5 girls between 30 months to 13 years old). Acute hemolysis associated with infection occurred before any treatment in 53.8% of cases and after beginning treatment in 46.1%. In 84.6% of cases, occurrence of acute hemolysis involved association of drugs considered as nonhemolytic either with themselves or with other drugs. Anuric renal failure occurred after beginning treatment in all cases and was most severe in patients with of multiple-germ infection (30.7%) and drug association (84.6%). Renal failure was reversible in 80.7% and fatal in 19.2%. Multiple-germ infection and drug association appeared as the main predisposing factors for post hemolytic anuric renal failure in patients with G6PD deficiency. The high frequency of these factors in tropical areas suggests implication of local endemic infections.
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