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Myeloma Nephropathy

Human Kidneys
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What is Myeloma Nephropathy

Multiple Myeloma is a cancer that affects certain white blood cells called plasma cells.

This cells are found in the bone marrow, producing large amounts proteins which are actually small fragments of antibody proteins called light chains. Myeloma kidney disease may take many forms, as a number of metabolic derangement are caused by multiple myeloma, which may have deleterious effects on the kidney. The most significant of these derangements are:

  1. Hypercalaemia: May result in hypercalaemic nephropathy.
  2. Increased protein production: May lead to classic myeloma nephropathy, light chain deposition disease or amyloid nephropathy.

Statistics on Myeloma Nephropathy

Approximately 13,000 new cases of myeloma bone disease are diagnosed each year. The incidence of thise condition is 4 per 100,000 which holds true for the great majority of the world’s population. Males are slightly more affected than females and African/African Americans have almost twice the incidence as caucasians.

Renal disease is found clinically in 20% of patients at diagnosis, with 50% of patients affected throughout the course of their disease.

Risk Factors for Myeloma Nephropathy

The cause of multiple myeloma is unknown. Like most forms of cancer, a genetic and environmental component is thought to contribute to the development of this condition.

The condition seems to occur more commonly with increasing age and is more common in African/African Americans than caucasians, with a ratio of approximately 10:1 respectively. Males have a slightly increased risk of developing multiple myeloma. The “light-chain” variant of multiple myeloma is most commonly associated with myeloma renal disease.

Progression of Myeloma Nephropathy

With the development of myeloma nephropathy, patients will develop Bence Jones proteinuria, which essentially describes the loss of specific proteins in the urine. These proteins may by excreted without having developed myeloma kidney disease. In some patients, these proteins may cause kidney disease but depositing within the kidney tubules. The reason why some patients develop kidney disease and some patients do not is unknown. Once acquired, myeloma disease of the kidney reduces renal function, such that the kidneys may fail if stressed by dehydration and kidney toxic drugs. The renal failure is usually progressive, with the rate of progression variable, dependent upon the severity and nature of disease at diagnosis.

How is Myeloma Nephropathy Diagnosed?

General investigation of myeloma kidney disease should include other investigations to assess the seveity of the entire disease. A number of blood tests should be taken to assess disease activity and response to chemotherapy. These blood tests will also allow assessment of renal function, allowing guidance of support for renal failure. Urine tests and x-rays may also be required to assess the nature and severity of myeloma disease.

Prognosis of Myeloma Nephropathy

The prognosis of mmultiple myeloma is disappointing, with the median surivial time from diagnosis being 30-40 months. With the presence of renal failure, this survival rate is markedly reduced. The oerall prognosis of this condition depends upon the mass of the primary tumour and its subsequent response to chemotherapy.

How is Myeloma Nephropathy Treated?

There are two main aims of therapy:

  1. Prevent further deterioration of renal function: Avoid kidney toxic drugs, prevent dehydration, control high blood calcium levels and alkalinise the urine. The latter two objectives are achieved with medications such as bisphosphonates and bicarbonate preparations.
  2. Support through renal failure: Renal failure should be sought and identified early, with appropriate management initiated to prevent the metabolic consequences oy multiple myeloma. Any urinary obstruction caused by stones must be treated.

Diet advice is necessary which should involve increased calories and protein level of 0.5-1kg/day.

Myeloma Nephropathy References

  1. Kumar P, Clark M. Clinical Medicine. WB Saunders 2002.
  2. Longmore M, Wilkinson I, Torok E. Oxford Handbook of Clinical Medicine. Oxford University Press. 2001.
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Posted On: 30 December, 2003
Modified On: 26 August, 2008


Created by: myVMC