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Idiopathic calcium oxalate nephrolithiasis: a cellular disease
1Institute of Internal Medicine, Division of Nephrology, University of Padova Medical School, Italy.
Scanning Microscopy
|March 1, 1992
Summary
Idiopathic calcium oxalate stone disease may stem from a cellular defect in erythrocyte anion exchange. Oral glycosaminoglycans corrected abnormal oxalate transport and erythrocyte band 3 phosphorylation in stone formers.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Current theories on calcium oxalate nephrolithiasis pathogenesis are insufficient.
- Idiopathic calcium oxalate stone formers exhibit abnormal erythrocyte oxalate transport and band 3 phosphorylation.
Purpose of the Study:
- To investigate the hypothesis that nephrolithiasis is a cellular disease linked to anion-exchange defects.
- To explore the role of glycosaminoglycans in regulating erythrocyte band 3 function and oxalate transport.
Main Methods:
- Analysis of erythrocyte oxalate self-exchange and band 3 phosphorylation in stone formers.
- In vivo trial administering oral glycosaminoglycans to stone formers.
- Measurement of urinary oxalate excretion and renal clearance before and after treatment.
Main Results:
- Stone formers showed faster erythrocyte oxalate exchange and higher band 3 phosphorylation.
- Oral glycosaminoglycan administration reduced urinary oxalate excretion and renal clearance.
- Treatment corrected abnormal erythrocyte oxalate flux and band 3 phosphorylation.
Conclusions:
- Nephrolithiasis may be a cellular disease with a genetically controlled defect in erythrocyte anion exchange.
- Reduced glycosaminoglycans in erythrocyte membranes may contribute to the disease.
- Therapeutic intervention with glycosaminoglycans shows potential for managing calcium oxalate nephrolithiasis.