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Increased D-glucaric acid excretion in children with renal disease
Insights
Urinary D-glucaric acid excretion, a marker for microsomal enzyme activity, significantly increases in infants and children with early-stage renal disease, particularly tubulopathy and pyelonephritis.
Area of Science:
- Biochemistry
- Pediatric Nephrology
- Pharmacology
Background:
- Microsomal enzyme activity is crucial for drug metabolism.
- Assessing enzyme activity in pediatric renal disease is clinically important.
- Urinary D-glucaric acid is a known biomarker for enzyme induction.
Purpose of the Study:
- To assess non-specific microsomal enzyme activity in infants and children with renal disease.
- To investigate the correlation between renal disease severity and D-glucaric acid excretion.
- To explore the implications of altered enzyme activity in pediatric nephropathies.
Main Methods:
- Measured urinary D-glucaric acid excretion in 85 infants and children.
- Compared excretion levels between patients with various renal diseases and healthy controls.
- Analyzed data considering the influence of enzyme-inducing drugs.
Main Results:
- Significantly elevated urinary D-glucaric acid excretion was observed in early stages of renal disease.
- The increase was most pronounced in patients with tubulopathy and pyelonephritis.
- Elevated excretion was noted even in patients receiving enzyme-inducing drugs, suggesting disease-specific alterations.
Conclusions:
- Early-stage renal disease in children is associated with increased microsomal enzyme activity.
- Urinary D-glucaric acid is a sensitive indicator of renal disease in pediatric populations.
- Findings suggest potential therapeutic strategies targeting drug metabolism in pediatric renal patients.
Abstract:
In 85 infants and children, non-specific microsomal enzyme activity was assessed by measuring the urinary D-glucaric acid excretion. In patients with renal disease of various etiology, a highly significant increase in the D-glucaric acid excretion was observed at any early stage of the illness. This change was most marked in patients suffering from tubulopthy and pyelonephritis. Excretion of D-glucaric acid was significantly more pronounced in patients with renal disease than in controls, even in those groups of infants and children who were given enzyme-inducing drugs. As an explanation for the elevation of urinary D-glucaric acid levels in patients with mild renal disease, the possibility and biochemical mechanism of an induction of drug metabolizing enzymes are discussed and some therapeutic conclusions are drawn.
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