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Updated: Feb 19, 2026

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Dysproteinemias and Glomerular Disease.

Nelson Leung1,2, Maria E Drosou1, Samih H Nasr3

  • 1Divisions of Nephrology and Hypertension and.

Clinical Journal of the American Society of Nephrology : CJASN
|November 9, 2017
PubMed
Summary

Monoclonal proteins from B cell dysproteinemia can cause significant kidney damage through deposition or other mechanisms. Clone-directed therapies targeting these proteins are more effective than traditional immunosuppression for preserving renal function.

Keywords:
AmyloidosisB-LymphocytesImmunoglobulinsKidney DiseasesKidney GlomerulusMGRSParaproteinemiasThrombotic Microangiopathiescytokinesdysproteinemiaglomerular diseaseglomerulonephritiskidneymonoclonal gammopathy

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Area of Science:

  • Nephrology
  • Hematology
  • Immunology

Background:

  • Dysproteinemia involves immunoglobulin (Ig) overproduction by B cell clones.
  • Monoclonal proteins are increasingly implicated in kidney injury across glomerular, tubular, and vascular compartments.
  • Kidney damage can occur with or without a malignant state, including conditions termed monoclonal gammopathy of renal significance.

Purpose of the Study:

  • To review the mechanisms by which monoclonal proteins cause kidney disease.
  • To highlight the role of monoclonal gammopathy of renal significance in nephrotoxicity.
  • To discuss the efficacy of clone-directed therapies in managing these conditions.

Main Methods:

  • Review of literature on dysproteinemia and kidney disease.
  • Analysis of pathogenic mechanisms including Ig deposition, complement activation, and cytokine involvement.
  • Evaluation of therapeutic strategies targeting B cell and plasma cell clones.

Main Results:

  • Monoclonal proteins injure kidneys via deposition (e.g., Ig amyloidosis, monoclonal Ig deposition disease) or non-deposition mechanisms (e.g., complement activation, thrombotic microangiopathy).
  • Both malignant and non-malignant monoclonal gammopathies can lead to renal impairment.
  • Clone-directed therapies (e.g., rituximab, bortezomib) demonstrate superior efficacy compared to general immunosuppression.

Conclusions:

  • Substantial reduction of monoclonal protein is crucial for preserving renal function.
  • Targeted therapies offer a more effective approach to treating monoclonal protein-related kidney diseases.
  • Understanding pathogenesis guides the development of novel, clone-specific treatment strategies.