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The role of polymorphonuclear leucocytes in the autologous phase of nephrotoxic nephritis
Abstract:
The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.
Insights
Polymorphonuclear leucocytes (PMN) are key players in nephrotoxic nephritis (NTN). Reducing PMN levels protected kidney function and reduced glomerular damage in rabbits, highlighting their injurious role.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Nephrotoxic nephritis (NTN) is an autoimmune kidney disease.
- The role of polymorphonuclear leucocytes (PMN) in NTN pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of PMN in the autologous phase of NTN in a rabbit model.
- To determine if PMN depletion can protect renal function and reduce kidney damage.
Main Methods:
- Rabbits with NTN were treated with nitrogen mustard or anti-PMN serum (APS) to deplete circulating PMN.
- Renal function, proteinuria, and glomerular histology/immunofluorescence were assessed.
- Antibody response was measured in APS-treated rabbits.
Main Results:
- Depletion of PMN by either method protected renal function.
- APS treatment significantly reduced proteinuria and glomerular PMN infiltration, extracapillary cell proliferation, and fibrin deposition.
- Nitrogen mustard's protective effect may involve immunosuppression, but APS did not reduce antibody response.
Conclusions:
- PMN are the principal injurious agents in this NTN model.
- PMN directly or indirectly cause proteinuria and glomerular fibrin deposition in NTN.