Mechanisms of light chain injury along the tubular nephron

J Am Soc Nephrol. 2012 Nov;23(11):1777-81. doi: 10.1681/ASN.2012040388. Epub 2012 Sep 20.


The tubular nephron is responsible for reabsorption and catabolism of filtered low molecular weight proteins that include Ig free light chains. In the setting of a plasma cell dyscrasia, significant amounts of free light chains, now monoclonal proteins, present to the tubular nephron for disposal. The result may be clinical renal dysfunction in the form of AKI, progressive CKD, and end-stage kidney disease. Here, I review the mechanisms involved in these processes that result in tubular injury, including proximal tubulopathy and cast nephropathy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / immunology
  • Fanconi Syndrome / etiology
  • Fanconi Syndrome / immunology
  • Humans
  • Immunoglobulin Light Chains / chemistry
  • Immunoglobulin Light Chains / metabolism*
  • Kidney Tubules / immunology*
  • Kidney Tubules / injuries*
  • Models, Molecular
  • Nephrons / immunology*
  • Nephrons / injuries*
  • Renal Insufficiency, Chronic / etiology
  • Renal Insufficiency, Chronic / immunology


  • Immunoglobulin Light Chains