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The role of cathepsin D in pathogenesis of acute post-streptococcal glomerulonephritis
Insights
Elevated urinary Cathepsin D levels were observed in children with acute post-streptococcal glomerulonephritis (APSGN). This enzyme activity originates from polymorphonuclear leukocytes, not blood or pus cells, and shows no correlation with serum complement C3 levels.
Area of Science:
- Nephrology
- Biochemistry
- Immunology
Background:
- Acute post-streptococcal glomerulonephritis (APSGN) is a common kidney disease in children.
- Lysosomal enzymes, such as Cathepsin D, play a role in inflammatory processes.
- Understanding the source of urinary enzymes in APSGN can aid in diagnosis and understanding pathogenesis.
Purpose of the Study:
- To investigate urinary Cathepsin D activity in pediatric APSGN patients.
- To determine the cellular origin of elevated Cathepsin D in APSGN urine.
- To explore the relationship between urinary Cathepsin D and serum complement C3 levels.
Main Methods:
- Fluorescent assay to measure Cathepsin D activity in urine.
- Comparison of enzyme activity in APSGN patients versus control groups (including hematuric and pyuric controls).
- Analysis of serum complement C3 levels.
Main Results:
- Urinary Cathepsin D activity was significantly elevated in APSGN patients compared to controls.
- Elevated activity was not due to erythrocytes or leukocytes, ruling out hematuria and pyuria as the source.
- Cathepsin D activity is likely derived from lysosomal enzymes from polymorphonuclear leukocytes interacting with the glomerular basement membrane.
- No correlation was found between serum complement C3 levels and urinary Cathepsin D activity.
Conclusions:
- Urinary Cathepsin D is a potential biomarker for APSGN in children.
- The enzyme originates from polymorphonuclear leukocytes, indicating local renal inflammation.
- Cathepsin D levels do not correlate with complement C3, suggesting distinct pathogenic pathways.
Abstract:
Cathepsin D activity has been studied by a fluoremetric assay in the urine of acute post-streptococcal glomerulonephritic (APSGN) patients aged from 3 to 14 years and has been found elevated when compared with four groups of controls. This activity cannot be accounted for by erythrocytes and/or leukocytes in the urine of these patients since haematuric and pyuric controls did not exhibit an amount of enzyme activity greater than the normal control group. Cathepsin D activity can be attributed to lysosomal enzymes released from polymorphonuclear leukocytes which are in close contact with glomerular basement membrane. Complement C3 levels in serum and cathepsin D activity in urine of these patients showed no correlation.