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Increased urinary excretion of renal N-acetyl-beta-glucosaminidase in hypercalciuria
Insights
Children with hypercalciuria show elevated urinary N-acetyl-beta-glucosaminidase (NAG) excretion, indicating kidney tubular injury. This renal damage may persist despite short-term treatments aimed at reducing urinary calcium levels.
Area of Science:
- Pediatric Nephrology
- Biochemistry
- Renal Physiology
Background:
- Hypercalciuria, characterized by elevated urinary calcium, is a common condition in children.
- Lysosomal enzymes like N-acetyl-beta-glucosaminidase (NAG) can serve as markers for renal tubular damage.
- The relationship between hypercalciuria and renal tubular injury requires further investigation.
Purpose of the Study:
- To investigate urinary N-acetyl-beta-glucosaminidase (NAG) excretion in children with hypercalciuria.
- To determine if hypercalciuria is associated with renal tubular injury.
- To assess the effect of hydrochlorothiazide therapy on NAG excretion and urinary calcium levels.
Main Methods:
- Collected and analyzed urinary samples from 33 children diagnosed with hypercalciuria and 13 healthy controls.
- Measured urinary N-acetyl-beta-glucosaminidase to creatinine ratio (NAG/Cr) as an indicator of renal tubular damage.
- Monitored urinary calcium to creatinine ratio (UCa/Cr) and NAG/Cr in a subset of patients undergoing hydrochlorothiazide therapy.
Main Results:
- Children with hypercalciuria exhibited significantly higher urinary NAG/Cr levels compared to healthy children.
- Elevated NAG/Cr levels were observed in both renal and absorptive hypercalciuria subtypes.
- Hydrochlorothiazide therapy reduced UCa/Cr but did not significantly alter NAG/Cr levels in children with renal hypercalciuria.
Conclusions:
- Increased urinary calcium excretion in children is associated with renal tubular injury.
- Urinary NAG/Cr is a potential biomarker for detecting renal tubular damage in pediatric hypercalciuria.
- Short-term reduction of urinary calcium via hydrochlorothiazide therapy may not reverse established renal tubular injury.
Abstract:
Urinary excretion of N-acetyl-beta-glucosaminidase (NAG), a lysosomal enzyme, was examined in 33 children with hypercalciuria. Urinary NAG excretion in 13 healthy children was 5.84 +/- 9.35 nmole/hr/mg of creatinine (NAG/Cr) (mean +/- SD) compared with 35.61 +/- 42.04 nmole/hr/mg of creatinine in 23 children with renal hypercalciuria, and 28.99 +/- 13.69 nmole/hr/mg of creatinine in ten children with absorptive hypercalciuria. In children with renal hypercalciuria, NAG/Cr excretion was not statistically different between children with either urolithiasis or hematuria without calculi. In six children with renal hypercalciuria, no significant change in NAG/Cr excretion occurred after a mean duration of 25 weeks of hydrochlorothiazide therapy although urinary calcium to creatinine ratios (UCa/Cr) decreased from 0.24 +/- 0.11 to 0.16 +/- 0.11. We conclude that increased urinary calcium excretion produces renal tubular injury and that the renal injury may not be reversed by short-term alterations in urinary calcium excretion.