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Urinary acidic hydrolases in renal diseases in children
Insights
Urinary acidic hydrolases are elevated in active childhood kidney diseases like nephrotic syndrome and glomerulonephritis. Enzyme levels normalize as disease activity decreases, suggesting they originate from injured kidney tissue.
Area of Science:
- Pediatric Nephrology
- Biochemistry
- Clinical Enzymology
Background:
- Acidic hydrolases play roles in cellular metabolism and degradation.
- Their role in pediatric renal diseases, specifically idiopathic nephrotic syndrome (INS) and glomerulonephritides (GN), requires further elucidation.
Purpose of the Study:
- To investigate the excretion patterns of urinary acidic hydrolases in children with active renal diseases.
- To determine if elevated hydrolase levels correlate with disease activity or other urinary parameters.
- To identify the potential source of these enzymes in the context of renal pathology.
Main Methods:
- Assay of urinary and plasma acidic hydrolases, including beta-galactosidase and beta-N-hexosaminidase.
- Analysis in cohorts of normal children, children with INS, GN, persistent proteinuria/hematuria, and orthostatic proteinuria.
- Comparison of enzyme excretion with disease activity and urinary markers like white blood cells (WBC), hematuria, and proteinuria.
Main Results:
- Significantly elevated urinary acidic hydrolases excretion (P < 0.01) was observed in active INS and GN.
- Hydrolase levels normalized with disease regression, independent of proteinuria, hematuria, or WBC counts.
- Elevated beta-galactosidase and beta-N-hexosaminidase excretion was noted in active renal diseases compared to normals.
Conclusions:
- Increased urinary acidic hydrolases reflect active renal disease in children, not merely proteinuria or inflammation.
- The injured renal parenchyma is the likely source of elevated urinary acidic hydrolases.
- These enzymes may serve as potential biomarkers for renal disease activity.
Abstract:
Acidic hydrolases were assayed in urines of 19 normal children, 33 children with idiopathic nephrotic syndrome of childhood (INS), 21 children with glomerulonephritides (GN) and 7 children with persistent proteinuria/hematuria, and in plasma of 10 children each with INS or GN. Both plasma and urinary acidic hydrolases were studied in intermittent orthostatic proteinuria. Cbeta-galactosidase and Cbeta-N-hexosaminidase were done in normals and children with active renal disease. Significantly (P less than 0.01) elevated urinary acidic hydrolases excretion in active renal diseases, both in INS and GN, returned to a normal range with regression of the diseases. Increased postural proteinuria was associated with normal urinary acidic hydrolases. Both beta-galactosidase and beta-N-hexosaminidase excretion was higher than similar mol wt proteins in normals and increased further in active renal diseases. The data suggests that increased urinary acidic hydrolases is related to the activity of the renal disease, and not to urinary WBC, hematuria or proteinuria. The likely source of urinary acidic hydrolases thus appears to be the injured renal parenchyma itself.