Renal pathologic spectrum in an autopsy series of patients with plasma cell dyscrasia

Arch Pathol Lab Med. 2004 Aug;128(8):875-9. doi: 10.5858/2004-128-875-RPSIAA.


Context: Renal dysfunction in plasma cell dyscrasias is common. It is the second most common cause of death in patients with myeloma.

Objective: We evaluated 77 sequential autopsies performed on patients dying from complications of plasma cell dyscrasias during an 11-year period at the University of Arkansas for Medical Sciences. These consisted of 15% of all the autopsies performed during this time.

Design: The kidneys were evaluated by light microscopy using hematoxylin-eosin-stained sections as well as Congo red and thioflavin T stains when amyloidosis was in the differential diagnosis. Immunofluorescence was performed on selected cases.

Results: The most common lesion identified was cast nephropathy (30%). Other findings included acute tubulopathy, AL-amyloidosis, light chain deposition disease, tubulointerstitial nephritis associated with monotypic light chain deposits, thrombotic microangiopathy, renal infarction, fungal infection, and plasma cell tumor nodules. Autolysis, an expected finding in autopsy evaluations, was significant in 25 cases.

Conclusions: Renal lesions are heterogeneous in these patients. In some cases, combined pathologic lesions were noted. Myeloma cast nephropathy predominated among all the renal lesions noted.

Publication types

  • Review

MeSH terms

  • Adult
  • Aged
  • Amyloid / analysis
  • Amyloidosis / etiology
  • Amyloidosis / pathology
  • Female
  • Humans
  • Kidney / chemistry
  • Kidney / pathology*
  • Kidney Diseases / etiology
  • Kidney Diseases / pathology
  • Kidney Glomerulus / pathology
  • Kidney Tubular Necrosis, Acute / etiology
  • Kidney Tubular Necrosis, Acute / pathology
  • Male
  • Middle Aged
  • Multiple Myeloma / complications
  • Multiple Myeloma / pathology
  • Paraproteinemias / complications
  • Paraproteinemias / pathology*
  • Retrospective Studies


  • Amyloid
  • amyloid protein AL