Case 5
Diagnosis and discussion
Versión en Español

Go back to clinical information and images


Myeloma cast nephropathy (myeloma kidney)

Cast nephropathy is the most common and significant form of renal pathology in multiple myeloma and is found in one third to 86% of patients. Other types of myeloma- induced renal disease include AL amyloidosis, light chain deposition disease, and parenchymal infiltration by neoplastic cells.

In the present case, bone marrow biopsy confirmed the diagnosis of multiple mieloma (Figure 8, see below). Protein electrophoresis showed a monoclonal component, and immunoelectrophoresis demonstrated high levels of IgA and Kappa light chains in serum.

Figure 8. Left: Bone marrow with infiltration by neoplastic cells, some with plasm cell features (H&E, X400). Right: Immunohistochemistry for Kappa light chain. Lamba was negative in neoplastic cells. (Immunoperoxidase for Kappa, X400).

In the present case the differential diagnosis would include acute tubular necrosis and tubulointerstitial nephritis. Acute or rapidly progressive glomerulonephritis would have been other clinical possibility. Hypercalcemia is a more suggestive feature in this patient.

Even if the evidence for multiple myeloma had been known, would a renal biopsy have been of value for confirming the presence of myeloma cast nephropathy versus some other cause for acte renal failure, or some other type of myeloma induced renal disease.

The pathologic findings in the present biopsy are diagnostic of myeloma cast nephropathy: angular and fractured casts with adjacent multinucleated giant cells and preferential staining for one light chain by immunofluorescence. The casts of myeloma cast nephropathy have much more angular edges and are more often fractured than the casts usually observed with other renal diseases. It is very very inusual to find simultaneous occurrence of myeloma cast nephropathy and renal tissular deposits of paraproteins.

In the treatment of cast nephropathy is important limit cast formation by counteracting any precipitating factors such as correcting dehydration or hypercalcemia, discontinuing NSAIDs, and treating infections; and inducing alkaline diuresis with a goal of >3 liters/day of urine at a pH of approximately 7 if the patient can tolerate fluid volume expansion. Reduce elevated paraprotein concentration, e.g. with chemotherapy, and possibly plasmapheresis. Early institution of dialysis.

See the chapter [Amiloidosis, mieloma múltiple, enfermedad por depósitos de cadenas ligeras... ] (only in spanish).

Go back to clinical information and images


  • Iggo N, Winearls CG, Davies DR. The development of cast nephropathy in multiple myeloma. QJM. 1997; 90: 653-6. [PubMed link] [Free full text]
  • Gertz MA. Managing myeloma kidney. Ann Intern Med. 2005; 143: 835-7. [PubMed link] [Free full text]
  • Basic-Jukic N, Kes P, Labar B. Myeloma kidney: pathogenesis and treatment. Acta Med Croatica. 2001; 55: 169-75. [PubMed link]
  • Pote A, Zwizinski C, Simon EE, Meleg-Smith S, Batuman V. Cytotoxicity of myeloma light chains in cultured human kidney proximal tubule cells. Am J Kidney Dis. 2000; 36: 735-44. [PubMed link]


Go back to clinical information and images