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Effect of prednisone on nephrotic peripheral blood mononuclear cell mediated increase in 35sulfate uptake in rat

E H Garin1

  • 1Department of Pediatrics, Medical University of South Carolina, Charleston.

Nephron
|January 1, 1989
PubMed

Insights

Prednisone therapy reversed increased glomerular basement membrane sulfate uptake caused by peripheral blood mononuclear cells in patients with idiopathic minimal-lesion nephrotic syndrome. This suggests a link between GBM sulfate metabolism and proteinuria.

Area of Science:

  • Nephrology
  • Immunology
  • Biochemistry

Background:

  • Idiopathic minimal-lesion nephrotic syndrome (IMLNS) is characterized by proteinuria and effacement of podocyte foot processes.
  • Peripheral blood mononuclear cells (PBMC) from IMLNS patients in relapse significantly increase 35sulfate uptake in rat glomerular basement membrane (GBM).
  • This effect is absent in PBMC from IMLNS patients in remission or on prednisone therapy.

Purpose of the Study:

  • To investigate the effect of prednisone therapy on PBMC-mediated 35sulfate uptake in rat GBM.
  • To explore the role of GBM sulfated compounds in glomerular permeability.
  • To support the hypothesis that PBMC-derived lymphokines alter GBM metabolism in IMLNS.

Main Methods:

  • Coculturing rat glomeruli with PBMC from IMLNS patients in relapse and remission.
  • Measuring 35sulfate uptake in GBM.
  • Comparing GBM sulfate uptake in glomeruli cultured alone versus with PBMC, before and during prednisone treatment.

Main Results:

  • GBM 35sulfate uptake was significantly higher when cocultured with PBMC from IMLNS patients in relapse compared to glomeruli cultured alone.
  • Prednisone therapy abolished the PBMC-mediated increase in GBM 35sulfate uptake.
  • No significant difference in GBM 35sulfate uptake was observed with PBMC from patients on prednisone or in remission.

Conclusions:

  • Prednisone therapy effectively inhibits the PBMC-induced increase in GBM 35sulfate uptake.
  • GBM sulfated compounds are implicated in regulating glomerular permeability.
  • PBMC from relapsed IMLNS patients may secrete lymphokines that increase glomerular permeability by altering GBM sulfated compound metabolism.

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