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Hypocomplementemic proliferative glomerulonephritis with C3 nephritic-factor-like activity in multiple myeloma.
E Bourke1, W G Campbell, M Piper
1Department of Medicine, Emory University School of Medicine, Atlanta, Ga.
Nephron
|January 1, 1989
Summary
A young male with multiple myeloma experienced severe kidney failure and proteinuria. Treatment with plasmapheresis and chemotherapy resolved the condition by reducing paraproteins and C3 nephritic factor-like activity.
Area of Science:
- Nephrology
- Immunology
- Hematology
Background:
- Multiple myeloma can cause kidney damage through various mechanisms.
- Proliferative glomerulonephritis is a serious kidney disease that can lead to renal failure.
- Complement system dysregulation, particularly involving C3, plays a role in certain kidney diseases.
Observation:
- A 31-year-old male presented with advanced renal failure and nephrotic-range proteinuria.
- The patient had multiple myeloma with circulating IgG2 lambda and free lambda light-chain paraproteins.
- Kidney biopsy showed proliferative glomerulonephritis with heavy granular glomerular deposition of C3, decreased serum C3, and increased C3c.
Findings:
- C3 nephritic factor (C3 NeF)-like activity was detected in the patient's serum.
- Plasmapheresis and chemotherapy significantly reduced paraprotein levels (up to 90%) and C3 NeF-like activity.
- These treatments normalized serum complement levels and markedly improved renal function and proteinuria.
Implications:
- This case suggests a potential syndrome linking paraproteinemia, C3 NeF-like activity, and glomerulonephritis.
- Understanding this association could lead to new diagnostic and therapeutic strategies for myeloma-related kidney disease.
- Targeting complement pathways may be beneficial in managing specific cases of glomerulonephritis associated with paraproteinemias.